Prevailing dietary guidelines recommend replacing saturated fatty acids (SFAs) with unsaturated fatty acids (USFAs). However, the relationship between specific types of SFA consumption and the risk of incident diabetes in China remains unclear.

We analyzed data from 15,021 apparently healthy Chinese adults, aged ≥ 20 years, participating in the China Health and Nutrition Survey (CHNS). Cumulative averages of SFA intake were calculated using 3-day, 24-h dietary recalls from each survey cycle. Multivariable Cox proportional hazard models were employed to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs) for diabetes risk associated with isocaloric substituting carbohydrate or PUFAs with SFAs.

Over 167,698 person-years of follow-up, 1014 incident diabetes were identified. After adjustment for multiple variables, isocaloric substitution of carbohydrates with total SFAs was associated with a lower risk of diabetes (P < 0.001 for trend). The HR (95% CI) among the highest quartile of SFA intake individuals compared to the lowest quartile was 0.56 (0.40-0.79) for even-chain SFAs and 0.53 (0.37-0.76) for long-chain SFAs. Specifically, an inverse association with diabetes risk was observed for isocaloric substituting carbohydrates with lauric acid (12:0) [HRs for increasing quartiles (95% CIs): 0.62 (0.47-0.82), 0.62 (0.44-0.86), and 0.36 (0.24-0.53); P < 0.001 for trend]. No significant association were found between diabetes risk and isocaloric substitutions of carbohydrates with myristic acid (14:0), palmitic acid (16:0), or stearic acid (18:0). Alternations of PUFAs with total SFAs or subtypes of SFAs present similar results.

Isocaloric substituting carbohydrates with lauric acid (12:0) was associated with a lower risk of incident diabetes. Given the strong correlation between lauric acid and diabetes, further research is needed to clarify the association and underlying mechanisms.

Polycystic Ovary Syndrome (PCOS) is a common health condition related to a woman's hormonal problems. Hormonal imbalance, metabolic disorders, and an increased insulin level mainly characterize the ailment. This detailed review focuses on dietary strategies, macromolecules, macromolecules, and herbal interventions that exception-ally work in PCOS treatment. Research has shown that Mediterranean, low-glycemic index, and ketogenic diets that are modified with individuals in mind are the best ways to resolve insulin resistance, obesity, and lack of ovulation. The other nutrients shown to affect glucose metabolism and play a role in hormone regulation are the macromolecules, such as increased protein and reduced refined carbs. Among the different micronutrients, vitamin D, omega-3 fatty acids, and inositol were shown to be the most vital supplements in the treatment of PCOS-induced oxidative damage, hyperandrogenism, and infertility. Not to mention, cinnamon, curcumin, sage, fennel, and traditional Chinese herbal medicine are among some of the herbal remedies that so far show good potential to be the perfect complementary therapy tools as they create better glycemic control, inflammation reduction, and menstrual cycle regularization. Even though the findings are promising, the current supply of clinical trials for standardizing these nutritional and herbal protocols is lacking. Overall, this report stresses the fact that a customized, holistic diet regime is the best treatment for women with PCOS to make them feel well and live a long and healthy life.

Polycystic ovary syndrome (PCOS) is a gynecological, endocrine condition characterized by ovulatory disorders, clinical or biochemical hyperandrogenism, and polycystic ovarian morphology. PCOS has significant metabolic and reproductive implications that affect the quality of life of women. This PCOS guideline summary is based on the Indonesian Reproductive Endocrinology and Fertility Association guidelines for PCOS. This guideline is expected to guide the diagnosis and long-term management of PCOS.

We searched scientific evidence on the Cochrane and PubMed databases using the keyword "polycystic ovary syndrome". This evidence was reviewed by experts in the field of obstetrics and gynecology, and recommendations were made based on scientific evidence while considering patient values, costs, and resources.

A total of 127 recommendations and practice points were made regarding the diagnosis and management of PCOS. The levels of available health services and management algorithms for PCOS in Indonesia are also included.

The first-line treatment for managing hyperandrogenism and menstrual disorders in patients with PCOS is combined oral contraceptives. The first-line treatment for ovulation induction is letrozole, while clomiphene citrate, metformin, gonadotropins, and ovarian surgery serve as the second-line treatment. The third-line treatments included in vitro fertilization, with or without in vitro maturation.

Dietary fat composition has changed substantially during the obesity epidemic. As adipocyte hyperplasia is a major mechanism of adipose expansion, we aim to ascertain how dietary fats affect adipogenesis during obesity. We employ an unbiased dietary screen to identify oleic acid (OA) as the only dietary fatty acid that induces obesogenic hyperplasia at physiologic levels and show that plasma monounsaturated fatty acids (MUFAs), which are mostly OA, are associated with human obesity. OA stimulates adipogenesis in mouse and human adipocyte precursor cells (APCs) by increasing AKT2 signaling, a hallmark of obesogenic hyperplasia, and reducing LXR activity. High OA consumption decreases LXRα Ser196 phosphorylation in APCs, while blocking LXRα phosphorylation results in APC hyperproliferation. As OA is increasingly being incorporated into dietary fats due to purported health benefits, our finding that OA is a unique physiologic regulator of adipose biology underscores the importance of understanding how high OA consumption affects metabolic health.

This paper provides a summary of the 2023 British Nutrition Foundation Annual Lecture by Professor Julie Lovegrove. Professor Lovegrove is the head of the Hugh Sinclair Unit of Human Nutrition at the University of Reading. Professor Lovegrove, who was nominated for the BNF Prize for her outstanding contribution to nutritional sciences has published over 300 scientific papers and made a major contribution to establishing the relevance of dietary fat quality in the development and prevention of cardiometabolic disease.

Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide, driven by complex interactions among genetic, environmental, and lifestyle factors, with diet playing a pivotal role. Extra Virgin Olive Oil (EVOO), a cornerstone of the Mediterranean diet (MedDiet), is a plant-based fat that has garnered attention for its robust cardiovascular benefits, which are attributed to its unique composition of monounsaturated fatty acids (MUFAs), particularly oleic acid (OA); and bioactive polyphenols, such as Hydroxytyrosol (HT) and oleocanthal. These compounds collectively exert antioxidant, anti-inflammatory, vasodilatory, and lipid-modulating effects. Numerous clinical and preclinical studies have demonstrated that EVOO's properties reduce major modifiable cardiovascular risk factors, including hypertension, dyslipidemia, obesity, and type 2 diabetes. EVOO also promotes endothelial function by increasing nitric oxide (NO) bioavailability, thus favoring vasodilation, lowering blood pressure (BP), and supporting vascular integrity. Furthermore, it modulates biomarkers of cardiovascular health, such as C-reactive protein, low-density lipoprotein (LDL) cholesterol, and NT-proBNP, aligning with improved hemostatic balance and reduced arterial vulnerability. Emerging evidence highlights its interaction with gut microbiota, further augmenting its cardioprotective effects. This review synthesizes current evidence, elucidating EVOO's multifaceted mechanisms of action and therapeutic potential. Future directions emphasize the need for advanced extraction techniques, nutraceutical formulations, and personalized dietary recommendations to maximize its health benefits. EVOO represents a valuable addition to dietary strategies aimed at reducing the global burden of cardiovascular diseases.

Type 2 diabetes mellitus (T2DM) is a multifactorial metabolic disorder characterized by insulin resistance and beta cell dysfunction, resulting in hyperglycemia. Olive oil, a cornerstone of the Mediterranean diet, has attracted considerable attention due to its potential health benefits, including reducing the risk of developing T2DM. This literature review aims to critically examine and synthesize existing research regarding the impact of olive oil on the expression of genes relevant to T2DM. This paper also seeks to provide an immunological and genetic perspective on the signaling pathways of the main components of extra virgin olive oil. Key bioactive components of olive oil, such as oleic acid and phenolic compounds, were identified as modulators of insulin signaling. These compounds enhanced the insulin signaling pathway, improved lipid metabolism, and reduced oxidative stress by decreasing reactive oxygen species (ROS) production. Additionally, they were shown to alleviate inflammation by inhibiting the NF-κB pathway and downregulating pro-inflammatory cytokines and enzymes. Furthermore, these bioactive compounds were observed to mitigate endoplasmic reticulum (ER) stress by downregulating stress markers, thereby protecting beta cells from apoptosis and preserving their function. In summary, olive oil, particularly its bioactive constituents, has been demonstrated to enhance insulin sensitivity, protect beta cell function, and reduce inflammation and oxidative stress by modulating key genes involved in these processes. These findings underscore olive oil's therapeutic potential in managing T2DM. However, further research, including well-designed human clinical trials, is required to fully elucidate the role of olive oil in personalized nutrition strategies for the prevention and treatment of T2DM.

Gestational diabetes mellitus (GDM) and preeclampsia (PE) are commonly observed medical complications in pregnancy. Dietary total fat and fatty acids associated with GDM and PE risk have been examined in several epidemiological studies. In some instances, systematic reviews and meta-analyses might provide more accurate dietary recommendations.

This systematic review and dose-response meta-analysis was conducted to investigate the association between dietary total fat and fatty acids and the risk of GDM and PE.

Research on dietary fat intake and the risk of GDM and PE was conducted through systematic searches of the PubMed, Scopus, and Web of Science databases for articles published up to August 19, 2023. An investigation of associations between dietary intake of total fat and fatty acids and the risk of GDM and PE was performed using prospective cohort study designs.

Twenty-one prospective cohort studies were considered eligible. Findings indicated that higher intakes of total fat (relative risk [RR], 1.08; 95% confidence interval [CI], 1.02-1.14), animal fat (RR, 1.56; 95%CI, 1.34-1.89), vegetable fat (RR, 1.23; 95%CI, 1.05-1.45), dietary cholesterol (RR, 1.48; 95%CI, 1.10-2.00), and omega-3 fatty acid (RR, 1.11; 95%CI, 1.02-1.20) are associated with a greater risk of GDM. However, no significant association was found between dietary total fat and fatty acids and the risk of PE. Dose-response meta-analyses suggested every 10% increment in total energy intake from total fat, 5% from animal fat, 5% from vegetable fat, and 100 mg from cholesterol was related to 15%, 12%, 7%, 14%, and 20% higher GDM risk, respectively.

Overall, total fat, animal fat, vegetable fat, dietary cholesterol, and omega-3 fatty acid consumption are associated with a small but statistically significant increase in GDM risk.

PROSPERO (CRD42023466844).

Fatty acid metabolism, exercise, and insulin action play critical roles in maintaining vascular health, especially relevant in metabolic disorders such as obesity, type 2 diabetes, and cardiovascular disease. Insulin, a vasoactive hormone, induces arterial vasodilation throughout the arterial tree, increasing arterial compliance and enhancing tissue perfusion. These effects, however, are impaired in individuals with obesity and type 2 diabetes, and evidence suggests that vascular insulin resistance contributes to the pathogenesis of type 2 diabetes and its cardiovascular complications. Elevated plasma levels of free fatty acids in people with insulin resistance engender vascular inflammation, endothelial dysfunction, and vascular insulin resistance. Importantly, these effects are both functionally and structurally dependent, with saturated fatty acids as the primary culprits, while polyunsaturated fatty acids may support insulin sensitivity and endothelial function. Exercise enhances fatty acid oxidation, reduces circulating free fatty acids, and improves insulin sensitivity, thereby mitigating lipotoxicity and promoting endothelial function. Additionally, exercise induces beneficial vascular adaptations. This review examines the complex interplay among fatty acid metabolism, exercise training-induced vascular adaptations, and insulin-mediated vascular changes, highlighting their collective impact on vascular health and underlying mechanisms in both healthy and insulin-resistant states. It also explores the therapeutic potential of targeted exercise prescriptions and fatty acid-focused dietary strategies for enhancing vascular health, emphasizing tailored interventions to maximize metabolic benefits. Future research should investigate the pathways linking fatty acid metabolism to vascular insulin resistance, with a focus on how exercise and dietary modifications can be personalized to enhance vascular insulin sensitivity, optimize vascular health, and reduce the risks of type 2 diabetes and associated cardiovascular complications.

The incidence rate of pancreatic cancer, a fatal illness with a meager 5-year survival rate, has been on the rise in recent times. When individuals accumulate excessive amounts of adipose tissue, the adipose organ becomes dysfunctional due to alterations in the adipose tissue microenvironment associated with inflammation and metabolism. This phenomenon may potentially contribute to the aberrant accumulation of fat that initiates pancreatic carcinogenesis, thereby influencing the disease's progression, resistance to treatment, and metastasis. This review presents a summary of the impact of pancreatic steatosis, visceral fat, cancer-associated adipocytes and lipid diets on the advancement of pancreatic cancer, as well as the reciprocal effects of pancreatic cancer on adipose tissue. Understanding the molecular mechanisms underlying the relationship between dysfunctional adipose tissue and pancreatic cancer better may lead to the discovery of new therapeutic targets for the disease's prevention and individualized treatment. This is especially important given the rising global incidence of obesity, which will improve the pancreatic cancer treatment options that are currently insufficient.

Most modern dietary guidelines recommend limiting lard and animal fats due to their potential link to metabolic diseases. Nevertheless, emerging evidence suggests that lard may not significantly contribute to diabetes and that moderate lard intake could even benefit lipid metabolism. This commentary suggests a reevaluation of lard’s classification as a “bad actor” in the context of diabetes, urging colleagues to give greater consideration to and empirically validate this intriguing hypothesis.

Introduction: The ketogenic diet (KD) is widely used for weight management by reducing appetite, enhancing fat oxidation, and facilitating weight loss. However, the high content of total and saturated fats in a conventional KD may elevate low-density lipoprotein (LDL)-cholesterol levels, a known risk factor for cardiovascular diseases, highlighting the need for healthier alternatives. This study aimed to investigate the effect of a newly developed Healthy Ketogenic Diet (HKD) versus an Energy-Restricted Diet (ERD) on weight loss and metabolic outcomes among adults with obesity. Methods: Multi-ethnic Asian adults (n = 80) with body mass index ≥ 27.5 kg/m2 were randomized either to HKD (n = 41) or ERD (n = 39) for 6 months. Both groups followed an energy-restricted healthy diet, emphasizing on reducing saturated and trans fats. The HKD group additionally limited net carbohydrate intake to no more than 50 g per day. Dietary adherence was supported via the Nutritionist Buddy app with dietitian coaching. The primary outcome was weight change from baseline at 6 months. Secondary outcomes included weight change at 3 months and 1 year, along with changes in metabolic profiles. Data were analyzed using linear regression with an intention-to-treat approach. Results: The HKD group achieved significantly greater mean weight loss at 6 months than the ERD group (-7.8 ± 5.2 kg vs. -4.2 ± 5.6 kg, p = 0.01). The mean weight loss percentage at 6 months was 9.3 ± 5.9% and 4.9 ± 5.8% for the HKD and ERD groups, respectively (p = 0.004). Improvements in metabolic profiles were also significantly better in the HKD group [glycated hemoglobin (-0.3 ± 0.3% vs. -0.1 ± 0.2%, p = 0.008), systolic blood pressure (-7.7 ± 8.9 mmHg vs. -2.6 ± 12.2 mmHg, p = 0.005), and aspartate transaminase (-7.6 ± 15.5 IU/L vs. 0.6 ± 11.5 IU/L, p = 0.01)], with no increase in LDL-cholesterol (-0.12 ± 0.60 mmol/L vs. -0.04 ± 0.56 mmol/L, p = 0.97) observed in either group. Conclusions: The HKD was more effective than the ERD in promoting weight loss and improving cardiometabolic outcomes without elevation in LDL-cholesterol. It can be recommended for therapeutic intervention in patients with obesity.

Excess dietary intake of saturated fatty acids (SFAs) induces glucose intolerance and metabolic disorders. In contrast, unsaturated fatty acids (UFAs) elicit beneficial effects on insulin sensitivity. However, it remains elusive how SFAs and UFAs signal differentially toward insulin signaling to influence glucose homeostasis. Here, using a croaker model, we report that dietary palmitic acid (PA), but not oleic acid or linoleic acid, leads to dysregulation of mTORC1, which provokes systemic insulin resistance. Mechanistically, we show that PA profoundly elevates acetyl-CoA derived from mitochondrial fatty acid β oxidation to intensify Tip60-mediated Rheb acetylation, which triggers mTORC1 activation by promoting the interaction between Rheb and FKBPs. Subsequently, hyperactivation of mTORC1 enhances IRS1 serine phosphorylation and inhibits TFEB-mediated IRS1 transcription, inducing impairment of insulin signaling. Collectively, our results reveal a conserved molecular insight into the mechanism by which Tip60-mediated Rheb acetylation induces mTORC1 activation and insulin resistance under the PA condition, which may provide therapeutic avenues to intervene in the development of T2D.

Lipoprotein(a) [Lp(a)] is recognized as an independent risk factor for cardiovascular diseases; however, the impact of fat-based diets on its levels remains unclear.

This study aims to assess and analyze current evidence on the impact of various types of fat-based diets on Lp(a) levels.

A comprehensive search of the PubMed database was conducted on 9 July 2024, focusing on clinical and randomized trials published since 2000. Out of 697 identified studies, 33 met the inclusion criteria and were selected for analysis.

The findings suggest that modifications in fat-based diets, particularly concerning the type and amount of consumed fats and fatty acids, can significantly influence plasma Lp(a) levels. Diets rich in unsaturated fats, including polyunsaturated and monounsaturated fatty acids, were associated with more favorable effects in lowering Lp(a) levels. In contrast, diets high in saturated fats were linked to elevated Lp(a) levels. However, these conclusions were not consistent across all studies considered.

This work highlights the importance of a personalized dietary approach, considering both genetic predispositions and dietary habits. While diet alone may not drastically alter Lp(a) levels due to their strong genetic determination, a comprehensive strategy involving a healthy diet rich in unsaturated fats, regular physical activity, and effective weight management is recommended to reduce the risk of cardiovascular diseases. Further research is needed to clarify the mechanisms through which different fats affect Lp(a) and to develop targeted dietary recommendations.

Liver phospholipid fatty acid composition depends on the dietary lipid intake and the efficiency of hepatic enzymatic activity. Our study aimed to simultaneously investigate the liver phospholipid fatty acid composition in response to chronic linseed, palm, or sunflower oil diets. We used adult female C57/BL6 mice and randomly divided them into control and three groups treated with 25 % dietary oils. Prior to treatment, we analyzed the fatty acid profiles in dietary oils and hepatocytes and, after 100 days, the fatty acid composition in the liver using gas-liquid chromatography. Linseed oil treatment elevated alpha-linolenic, eicosapentaenoic, and docosapentaenoic acids and reduced arachidonic and docosatetraenoic acids, consequently lowering the n-6/n-3 ratio. Palm oil treatment increased linoleic acid and decreased docosahexaenoic acid, contributing to an elevated n-6/n-3 ratio. Sunflower oil treatment elevated total monounsaturated fatty acids by increasing palmitoleic, oleic, and vaccenic acids. The estimated activity of Δ9 desaturase was significantly elevated in the sunflower oil group, while Δ5 desaturase was the highest, and Δ6 desaturase was the lowest after the linseed oil diet. Our findings demonstrate that chronic consumption of linseed, palm, or sunflower oil alters the distribution of liver phospholipid fatty acids differently. Sunflower oil diet elevated total monounsaturated fatty acids, proposing potential benefits for liver tissue health. Considering these outcomes, a substantial recommendation emerges to elevate linseed oil intake, recognized as the principal ALA source, thereby aiding in reducing the n-6/n-3 ratio. Moreover, modifying dietary habits to incorporate specific vegetable oils in daily consumption could substantially enhance overall health.

Diet is a contributing factor to CVD risk, but how diet quality changes over the long term and contributes to CVD risk is less well studied. Diet data were analysed from parents and offspring from the Princeton Lipid Research Study (24-h recall in the 1970s; Block FFQ in 1998). Diet quality was assessed using an 8-point Dietary Approaches to Stop Hypertension nutrient-based scoring index, including a new method for scoring in children, as well as examining twelve key macro/micronutrients. Outcomes included blood glucose, blood pressure, serum lipids and BMI. The analysis included 221 parents (39 % male, mean age 38·9 ± 6·5 at baseline and 66·6 ± 6·6 at follow-up) and 606 offspring (45 % male, 11·9 ± 3·2 at baseline and 38·5 ± 3·6 at follow-up). Parents' Dietary Approaches to Stop Hypertension score increased slightly from baseline to follow-up (1·4 ± 1·0 and 2·1 ± 1·3, respectively, P < 0·001), while offspring remained consistent (1·6 ± 0·9 and 1·6 ± 1·1, respectively, P = 0·58). Overall, the Dietary Approaches to Stop Hypertension score, adjusted for age, race, sex and BMI, was not significantly associated with any examined outcomes. Of the macro/micronutrients at follow-up, saturated and total fat were associated with increased diabetes and dyslipidaemia in parents, while the inverse was seen with niacin. Among offspring, niacin was associated with lower rates of hypertension and dyslipidaemia. In conclusion, no relationship was detected between Dietary Approaches to Stop Hypertension adherence and disease outcomes. However, both saturated fat and niacin were associated with components of CVD risk, highlighting the need for improved diet quality overall.

The role of fatty acids (FA) in the pathogenesis of insulin resistance and hyperlipidemia is a subject of intensive research. Several recent works have suggested cis-vaccenic acid (cVA) in plasma lipid compartments, especially in plasma phospholipids (PL) or erythrocyte membranes, could be associated with markers of insulin sensitivity and cardiovascular health. Nevertheless, not all the results of research work testify to these beneficial effects of cVA. Therefore, we decided to investigate the relations of proportion of cVA in plasma PL to markers of insulin resistance in hyperlipidemic men.

In 231 men (median age 50) with newly diagnosed hyperlipidemia, we analyzed basic clinical parameters together with FA composition of plasma PL and stratified them according to the content of cVA into upper quartile (Q4) and lower quartile (Q1) groups. We examined also small control group of 50 healthy men.

The individuals in Q4 differed from Q1 by lower plasma insulin (p < 0.05), HOMA-IR values (p < 0.01), and apolipoprotein B concentrations (p < 0.001), but by the higher total level of nonesterified FA (p < 0.01). Both groups had similar age, anthropometrical, and other lipid parameters. In plasma PL, the Q4 group had lower content of the sum of n-6 polyunsaturated FA, due to decrease of γ-linolenic and dihomo-γ-linolenic acids, whereas the content of monounsaturated FA (mainly oleic and palmitoleic) was in Q4 higher.

Our results support hypothesis that plasma PL cVA could be associated with insulin sensitivity in men with hyperlipidemia.

The understanding of bile acid (BA) and unsaturated fatty acid (UFA) profiles, as well as their dysregulation, remains elusive in individuals with type 2 diabetes mellitus (T2DM) coexisting with non-alcoholic fatty liver disease (NAFLD). Investigating these metabolites could offer valuable insights into the pathophy-siology of NAFLD in T2DM.

To identify potential metabolite biomarkers capable of distinguishing between NAFLD and T2DM.

A training model was developed involving 399 participants, comprising 113 healthy controls (HCs), 134 individuals with T2DM without NAFLD, and 152 individuals with T2DM and NAFLD. External validation encompassed 172 participants. NAFLD patients were divided based on liver fibrosis scores. The analytical approach employed univariate testing, orthogonal partial least squares-discriminant analysis, logistic regression, receiver operating characteristic curve analysis, and decision curve analysis to pinpoint and assess the diagnostic value of serum biomarkers.

Compared to HCs, both T2DM and NAFLD groups exhibited diminished levels of specific BAs. In UFAs, particular acids exhibited a positive correlation with NAFLD risk in T2DM, while the ω-6:ω-3 UFA ratio demonstrated a negative correlation. Levels of α-linolenic acid and γ-linolenic acid were linked to significant liver fibrosis in NAFLD. The validation cohort substantiated the predictive efficacy of these biomarkers for assessing NAFLD risk in T2DM patients.

This study underscores the connection between altered BA and UFA profiles and the presence of NAFLD in individuals with T2DM, proposing their potential as biomarkers in the pathogenesis of NAFLD.

We assessed the effect of a dietary pattern rich in unsaturated fatty acids (UFA), protein and fibers, without emphasizing energy restriction, on visceral adipose tissue (VAT) and cardiometabolic risk profile. Within the 36-months randomized controlled NutriAct trial, we randomly assigned 502 participants (50-80 years) to an intervention or control group (IG, CG). The dietary pattern of the IG includes high intake of mono-/polyunsaturated fatty acids (MUFA/PUFA 15-20% E/10-15% E), predominantly plant protein (15-25% E) and fiber (≥30 g/day). The CG followed usual care with intake of 30% E fat, 55% E carbohydrates and 15% E protein. Here, we analyzed VAT in a subgroup of 300 participants via MRI at baseline and after 12 months, and performed further metabolic phenotyping. A small but comparable BMI reduction was seen in both groups (mean difference IG vs. CG: -0.216 kg/m2 [-0.477; 0.045], partial η2 = 0.009, p = 0.105). VAT significantly decreased in the IG but remained unchanged in the CG (mean difference IG vs. CG: -0.162 L [-0.314; -0.011], partial η2 = 0.015, p = 0.036). Change in VAT was mediated by an increase in PUFA intake (ß = -0.03, p = 0.005) and induced a decline in LDL cholesterol (ß = 0.11, p = 0.038). The NutriAct dietary pattern, particularly due to high PUFA content, effectively reduces VAT and cardiometabolic risk markers, independent of body weight loss.

Chronic low-grade adipose tissue inflammation is associated with metabolic disorders. Inflammation results from the intertwined cross-talks of pro-inflammatory and anti-inflammatory pathways in the immune response of adipose tissue. In addition, adipose FABP4 levels and lipid droplet proteins are involved in systemic and tissue inflammation. Dysregulated adipocytes help infiltrate immune cells derived from bone marrow responsible for producing cytokines and chemokines. When adipose tissue expands in excess, adipocyte exhibits increased secretion of adipokines and is implicated in metabolic disturbances due to the release of free fatty acids. This review presents an emerging concept in adipose tissue fat metabolism, fatty acid handling and binding proteins, and lipid droplet proteins and their involvement in inflammatory disorders.

Avocados are a rich source of nutrients including monounsaturated fats, dietary fibre and phytochemicals. Higher dietary quality is reported in studies of consumers with higher avocado intakes. The present study aimed to examine avocado consumption and cardiometabolic risk measures in a representative sample of Australian adults.

A cross-sectional analysis was performed using Australian Health Survey 2011-2013 (n = 2,736 observations). Day 1 24-hour recall data was used to examine reported avocado intake (whole avocados and avocado-containing products excluding avocado oil) and cardiometabolic risk measures (LDL, HDL, and total cholesterol, triglycerides, apolipoprotein B, HbA1c, plasma glucose, systolic and diastolic blood pressure). T-tests and chi square analyses were conducted between low (5.21 [95% CI: 4.63, 5.79] grams/day) and high (44.11 [95% CI: 35.89, 52.33] grams/day) consumers of avocado.

14.7% of Australians were 'avocado consumers' (n = 403 observations). Mean avocado intake was 24.63 (95% CI: 20.11, 29.15) grams per day, with a median intake of 10.40 (IQR: 4.49-26.00) grams per day for those considered 'avocado consumers'. Consumers of avocados had a lower BMI and waist circumference (each, p ≤ 0.001), lower plasma glucose level (p = 0.03), and higher HDL cholesterol (p ≤ 0.001) when compared with non-consumers. A trend towards lower plasma glucose, HbA1c (each, p = 0.04) and higher dietary fibre intake (p = 0.05) was found between high and low consumers of avocado.

Our study suggests favourable outcomes for avocado intake and cardiometabolic characteristics of consumers. Future studies should explore glucose homeostasis using a clinical trial design to understand potential relationships between avocado intake and cardiometabolic risk factors.

The effect of dietary fats on type 2 diabetes (T2D) is not clear. This study aimed to determine the association between T2D and dietary fatty acids among Iranian adults.

This case-control study was performed on 4241 participants aged 35-70, including 1804 people with T2D and pre-diabetes as the case group and 2437 people without diabetes as the control group. Dietary intake was assessed using a food frequency questionnaire (FFQ).

The cases had higher age (48.36 ± 8.62 vs. 54.53 ± 7.75 y, P < 0.001), weight (73.7713.41 vs. 76.18 ± 13.49 kg, P = 0.001), body mass index (BMI) (28.02 ± 4.70 vs. 24 ± 4.74 kg/m2, P = 0.001), right systolic blood pressure (RSBP) (113.33 ± 16.7 vs. 121.61 ± 17.24 mmHg, P = 0.001), right diastolic blood pressure (RDBP) (71.41 ± 10.53 vs. 75.33 ± 9.92 mmHg, P = 0.001), fasting blood sugar (FBS) (96.87 ± 19.39 vs. 169.95 ± 69.28 mg/dl, P = 0.001), blood urine nitrogen (BUN) (13.65 ± 3.74 vs. 14.26 ± 4.03 mg/dl, P = 0.001), triglyceride (TG) (141.61 ± 99.37 vs. 175.96 ± 114.74 mg/dl, P = 0.001), alkaline phosphatase (ALP) (218.24 ± 66.35 vs. 246.97 ± 72.65 IU/L, P = 0.001), low-density lipoprotein cholesterol (LDL) (111.68 ± 33.02 vs. 101.97 ± 36.54 mg/dl, P = 0.001), serum glutamic-pyruvic transaminase (SGPT) (21.88 ± 15.15 vs. 23.55 ± 15.96 IU/L, P = 0.001), gamma-glutamyl transferase (GGT) (24.66 ± 20.42 vs. 30.72 ± 30.43 IU/L P = 0.001), and cholesterol (192.45 ± 39.1190 vs. 187.12 ± 46.19 mg/dl P = 0.001) compared to the control group. T2D was negatively associated with dietary intake of PUFAs (OR = 0.93, CI95%:0.84-1.03, P = 0.01) and positively associated with dietary cholesterol (OR: 1.01, CI95%:1.001-1.01, P = 0.02).

In summary, cholesterol was positively and PUFAs were negatively associated with diabetes. If the results of the present study on the effect of fat intake on diabetes are proven, future dietary recommendations for people at risk of diabetes may be corrected by providing diets rich in polyunsaturated fatty acids and low in cholesterol.

There are inconclusive results available on the association between dietary fatty acid intake and the risk of hypertension (HTN) incident. In this study, we investigate the relationship between baseline dietary fatty acids intake including polyunsaturated fatty acid (PUFA), trans fatty acids (TFA), monounsaturated fatty acid (MUFA), and saturated fatty acid (SFA), and the risk of first incidence hypertension. The current prospective cohort study was carried out from the Ravansar Non-Communicable Diseases (RaNCD) cohort. A food frequency questionnaire (FFQ) with 118 items was used for the assessment of dietary data. Cox proportional hazards analyses were done to estimate hazard ratios (HR) and 95% confidence intervals (CIs) of the highest versus lowest quartile intake of SFA, PUFA, MUFA, and SFA and risk of HTN. Out of 7359 eligible participants, 597 new cases of HTN were identified over an average of 6.4 ± 1.33 years of follow-up. No significant relationship was observed between the fourth compared to the first categories of dietary SFA (HR: 0.82, 95% CI 0.55, 1.21; P trend: 0.476), MUFA (HR: 0.71, 95% CI 0.48, 1.06; P trend: 0.252), PUFA (HR: 0.86, 95% CI 0.62, 1.19; P trend: 0.315) and TFA (HR: 0.99, 95% CI 0.76, 1.27; P trend: 0.675), and risk of HTN. However, a significant inverse association between each 1 g per day increase in dietary MUFA intake during 6.4 years of follow up and HTN incident (HR: 0.97; 95% CI 0.94, 0.99; P 0.044) was observed. In brief, our study revealed that higher dietary MUFA intake was protectively associated with HTN incident. Dietary MUFA-rich foods should be encouraged to improve blood pressure.

The popularity of vegetarian diets has increased the need for studies on long-term health outcomes. A limited number of studies, including only one study from a non-vegetarian population, investigated the risk of mortality with self-identified vegetarianism and reported inconsistent results. This study evaluated prospective associations between vegetarian diets and all-cause mortality among 117,673 participants from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial cohort study. Vegetarian diet status was self-identified on the questionnaire. Deaths were ascertained from follow-up questionnaires and the National Death Index database. Multivariable Cox regression models were used to estimate the risk of all-cause mortality in hazard ratio (HR) and 95% confidence intervals (CI). By diet group, there were 116,894 omnivores (whose diet does not exclude animal products), 329 lacto- and/or ovo-vegetarians (whose diet excludes meat, but includes dairy and/or eggs), 310 pesco-vegetarians (whose diet excludes meat except for fish and seafood) and 140 vegans (whose diet excludes all animal products). After an average follow-up of 18 years, 39,763 participants were deceased. The risk of all-cause mortality did not statistically significantly differ among the four diet groups. Comparing with the omnivore group, the HR (95% CI) were 0.81 (0.64-1.03) for pesco-vegetarian group, 0.99 (0.80-1.22) for lacto- and/or ovo-vegetarian group and 1.27 (0.99-1.63) for vegan group, respectively. Similarly, mortality risk did not differ when comparing lacto- and/or ovo-vegetarians plus vegans with meat/fish eaters (omnivores and pesco-vegetarians) (HR [95% CI] = 1.09 [0.93-1.28]). As this study is one of the two studies of vegetarianism and mortality in non-vegetarian populations, further investigation is warranted.

Insulin resistance is an important feature of metabolic syndrome and a precursor of type 2 diabetes mellitus (T2DM). Overnutrition-induced obesity is a major risk factor for the development of insulin resistance and T2DM. The intake of macronutrients plays a key role in maintaining energy balance. The components of macronutrients distinctly regulate insulin sensitivity and glucose homeostasis. Precisely adjusting the beneficial food compound intake is important for the prevention of insulin resistance and T2DM. Here, we reviewed the effects of different components of macronutrients on insulin sensitivity and their underlying mechanisms, including fructose, dietary fiber, saturated and unsaturated fatty acids, and amino acids. Understanding the diet-gene interaction will help us to better uncover the molecular mechanisms of T2DM and promote the application of precision nutrition in practice by integrating multi-omics analysis.

The impact of the dietary fat type on type 2 diabetes (T2D) remains unclear.

We aimed to evaluate the effects of replacing dietary saturated fatty acids (SFA) with mono- or poly-unsaturated fatty acids (MUFA and PUFA, respectively) on insulin sensitivity, pancreatic β-cell function, and glucose tolerance, as surrogate endpoints for T2D.

We conducted a systematic review and meta-analysis of randomized controlled trials that replaced ≥5% of total energy intake provided by SFA with MUFA or PUFA and reported indexes of insulin sensitivity, β-cell function, and/or glucose tolerance. We searched MEDLINE, Scopus, and the Cochrane Library (CENTRAL) up to 9 January, 2023. Eligible interventions had to be isocaloric, with no significant difference in other macronutrients. Data were synthesized using random-effects model meta-analysis.

Of 6355 records identified, 10 parallel and 20 crossover trials with 1586 participants were included. The mean age of the participants was 42 years, 47% were male, mean body mass index (BMI; in kg/m2) was 26.8, median baseline fasting glucose was 5.13 mmol/L, and the median duration of interventions was 5 weeks. Replacing SFA with MUFA or PUFA had no significant effects on insulin sensitivity [standardized mean difference (SMD) SFA compared with MUFA: 0.01, 95% confidence interval (CI): -0.06 to 0.09, I2 = 0% and SMD SFA compared with PUFA: 0, 95% CI: -0.15 to 0.14, I2 = 0%]. Replacing SFA with MUFA did not significantly impact the β-cell function, evaluated by the disposition index (mean difference: -12, 95% CI: -158 to 133, I2=0%). Evidence on glucose tolerance (SFA compared with MUFA or PUFA) and on β-cell function when SFA were replaced with PUFA was scant.

Short-term substitution of saturated with unsaturated fat does not significantly affect insulin sensitivity nor β-cell function (the latter in the SFA compared with MUFA comparison). Future studies are needed to elucidate longer term effects of dietary fat saturation on glucose homeostasis. This trial was registered at PROSPERO as CRD42020178382.

An increasing number of studies have evaluated the association between ultra-processed foods (UPF) consumption and metabolic disorders. However, the association between UPF intake and non-alcoholic fatty liver disease (NAFLD) remains unclear. In this study, we analysed data from 6545 participants who were recruited in National Health and Nutrition Examination Surveys 2011-2018. UPF were defined in light of the NOVA food classification system and divided into quartiles based on its proportion of total weight intake. Complex logistic regression models were used to assess the association between UPF and NAFLD. Mediation analyses were conducted to reveal underlying mediators. We found that NAFLD patients consumed more UPF than controls (925·92 ± 18·08 v. 812·70 ± 14·32 g/d, P < 0·001). Dietary intake of UPF (% weight) was negatively related to the Healthy Eating Index-2015 score (Spearman r = -0·32, P < 0·001). In the multivariable model, the highest quartile compared with the lowest, the OR (95 % CI) were 1·83 (1·33, 2·53) for NAFLD (OR per 10 % increment: 1·15; 95 % CI: 1·09, 1·22; P for trend < 0·001) and 1·52 (1·12, 2·07) for insulin resistance (OR per 10 % increment: 1·11; 95 % CI: 1·05, 1·18; P for trend = 0·002). Mediation analyses revealed that poor diet quality, high saturated fat and refined grain intake partly mediated the association between UPF and NAFLD. In conclusion, high UPF intake was associated with an increased risk of NAFLD in US adults. Further prospective studies are needed to verify these findings.

Gluten, which is found in cereals such as wheat, rye and barley, makes up a major dietary component in most western nations, and has been shown to promote body mass gain and peripheral inflammation in mice. In the current study, we investigated the impact of gluten on central inflammation that is typically associated with diet-induced obesity. While we found no effect of gluten when added to a low-fat diet (LFD), male mice fed high fat diet (HFD) enriched with gluten increased body mass and adiposity compared with mice fed HFD without gluten. We furthermore found that gluten, when added to the LFD, increases circulating C-reactive protein levels. Gluten regardless of whether it was added to LFD or HFD led to a profound increase in the number of microglia and astrocytes in the arcuate nucleus of the hypothalamus, as detected by immunohistochemistry for ionised calcium binding adaptor molecule 1 (Iba-1) and glial fibrillary acidic protein (GFAP), respectively. In mice fed LFD, gluten mimicked the immunogenic effects of HFD exposure and when added to HFD led to a further increase in the number of immunoreactive cells. Taken together, our results confirm a moderate obesogenic effect of gluten when fed to mice exposed to HFD and for the first-time report gluten-induced astro- and microgliosis suggesting the development of hypothalamic injury in rodents.

Our previous study uncovered potent inhibitory effects of two naphthoquinones from Impatiens balsamina, namely lawsone methyl ether (2-methoxy-1,4-naphthoquinone, LME) and lawsone (2-hydroxy-1,4-naphthoquinone), against α-glucosidase. This gave us the insight to compare the hypoglycemic and hypolipidemic effects of LME and lawsone in high-fat/high-fructose-diet- and nicotinamide-streptozotocin-induced diabetic rats for 28 days. LME and lawsone at the doses of 15, 30, and 45 mg/kg, respectively, produced a substantial and dose-dependent reduction in the levels of fasting blood glucose (FBG), HbA1c, and food/water intake while boosting the insulin levels and body weights of diabetic rats. Additionally, the levels of total cholesterol (TC), triglycerides (TGs), high-density lipoproteins (HDLs), low-density lipoproteins (LDLs), aspartate transaminase (AST), alanine transaminase (ALT), creatinine, and blood urea nitrogen (BUN) in diabetic rats were significantly normalized by LME and lawsone, without affecting the normal rats. LME at a dose of 45 mg/kg exhibited the most potent antihyperglycemic and antihyperlipidemic effects, which were significantly comparable to glibenclamide but higher than those of lawsone. Furthermore, the toxicity evaluation indicated that both naphthoquinones were entirely safe for use in rodent models at doses ≤ 50 mg/kg. Therefore, the remarkable antihyperglycemic and antihyperlipidemic potentials of LME make it a promising option for future drug development.

The effects of different dietary fatty acids (FA) on cardiovascular risk still needs clarification. Plasma lipids composition may be a biomarker of FA dietary intake.

To evaluate in a composite population the relationships between changes in dietary fat intake and changes in FA levels in serum cholesterol esters.

In a multinational, parallel-design, dietary intervention (KANWU study), dietary intakes (3-day food record) and FA composition of serum cholesterol esters (gas-liquid chromatography) were evaluated at baseline and after 3 months in 162 healthy individuals, randomly assigned to a diet containing a high proportion of saturated (SFA) or monounsaturated (MUFA) fat, with a second random assignment to fish oil or placebo supplements.

Main differences in serum lipid composition after the two diets included saturated (especially myristic, C14:0, and pentadecanoic, C15:0) and monounsaturated (oleic acid, C18:1 n-9) FA. C14:0 and C15:0 were related to SFA intake, while C18:1 n-9 was associated with MUFA intake. Fish oil supplementation induced a marked increase in eicosapentaenoic (C20:5 n-3) and docosahexaenoic (C22:6 n-3) acids. After the 3-month intervention, Δ-9 desaturase activity, calculated as palmitoleic acid/palmitic acid (C16:1/C16:0) ratio, was more reduced after the MUFA (0.31±0.10 vs 0.25±0.09, p<0.0001) than SFA diet (0.31±0.09 vs 0.29±0.08, p=0.006), with a statistically significant difference between the two groups (p<0.0001).

This study shows that serum cholesterol ester FA composition can be used during randomized controlled trials as an objective indicator of adherence to experimental diets based on saturated and monounsaturated fat modifications, as well as fish oil supplementation.

With rapid aging of the population worldwide, the number of people with dementia is dramatically increasing. Some studies have emphasized that metabolic syndrome, which includes obesity and diabetes, leads to increased risks of dementia and cognitive decline. Factors such as insulin resistance, hyperglycemia, high blood pressure, dyslipidemia, and central obesity in metabolic syndrome are associated with synaptic failure, neuroinflammation, and imbalanced neurotransmitter levels, leading to the progression of dementia. Due to the positive correlation between diabetes and dementia, some studies have called it "type 3 diabetes". Recently, the number of patients with cognitive decline due to metabolic imbalances has considerably increased. In addition, recent studies have reported that neuropsychiatric issues such as anxiety, depressive behavior, and impaired attention are common factors in patients with metabolic disease and those with dementia. In the central nervous system (CNS), the amygdala is a central region that regulates emotional memory, mood disorders, anxiety, attention, and cognitive function. The connectivity of the amygdala with other brain regions, such as the hippocampus, and the activity of the amygdala contribute to diverse neuropathological and neuropsychiatric issues. Thus, this review summarizes the significant consequences of the critical roles of amygdala connectivity in both metabolic syndromes and dementia. Further studies on amygdala function in metabolic imbalance-related dementia are needed to treat neuropsychiatric problems in patients with this type of dementia.

We aimed to examine the association between the quantity and quality of dietary fat in early pregnancy and gestational diabetes mellitus (GDM) risk. In total, 1477 singleton pregnant women were included from Sichuan Provincial Hospital for Women and Children, Southwest China. Dietary information was collected by a 3-d 24-h dietary recall. GDM was diagnosed based on the results of a 75-g, 2-h oral glucose tolerance test at 24-28 gestational weeks. Log-binomial models were used to estimate relative risks (RR) and 95% CI. The results showed that total fat intake was positively associated with GDM risk (Q4 v. Q1: RR = 1·40; 95 % CI 1·11, 1·76; Ptrend = 0·001). This association was also observed for the intakes of animal fat and vegetable fat. After stratified by total fat intake (< 30 %E v. ≥ 30 %E), the higher animal fat intake was associated with higher GDM risk in the high-fat group, but the moderate animal fat intake was associated with reduced risk of GDM (T2 v. T1: RR = 0·65; 95 % CI 0·45, 0·96) in the normal-fat group. Vegetable fat intake was positively associated with GDM risk in the high-fat group but not in the normal-fat group. No association between fatty acids intakes and GDM risk was found. In conclusion, total fat, animal and vegetable fat intakes were positively associated with GDM risk, respectively. Whereas when total fat intake was not excessive, higher intakes of animal and vegetable fat were likely irrelevant with increased GDM risk, even the moderate animal fat intake could be linked to lower GDM risk.

The Mediterranean Diet (MD) is plant-based and consists of multiple daily portions of vegetables, fruit, cereals, and olive oil. Although there are challenges with isolating the MD from the typical Mediterranean lifestyle and culture (including prolonged 'social' meals and siestas), much evidence supports the health benefits of the MD that include improved longevity, reduced metabolic risk of Diabetes Mellitus, obesity, and Metabolic Syndrome, reduced risk of malignancy and cardiovascular disease, and improved cognitive function. The MD is also associated with characteristic modifications to gut microbiota, mediated through its constituent parts (primarily dietary fibres, extra virgin olive oil, and polyunsaturated fatty acids [including ω-3]). These include enhanced growth of species that produce short-chain fatty acids (butyrate), such as Clostridium leptum and Eubacterium rectale, enhanced growth of Bifidobacteria, Bacteroides, and Faecalibacterium prausnitzii species, and reduced growth of Firmicutes and Blautia species. Such changes in gut microbiota are known to be associated favourably with inflammatory and oxidative status, propensity for malignancy and overall metabolic health. A key challenge for the future is to explore the extent to which the health benefits of the MD are mediated by such changes to gut microbiota. The MD confers both health and environmental benefits. Adoption of the MD should perhaps be encouraged and facilitated more generally and not just restricted to populations from Mediterranean regions. However, there are key challenges to this approach that include limited perennial availability of the constituent parts of the MD in some non-Mediterranean regions, intolerability of a high-fibre diet for some people, and potential cultural disconnects that juxtapose some traditional (including Western) diets with the MD.

Excessive adipose tissue (AT) lipolysis around parturition in dairy cows is associated with impaired AT insulin sensitivity and increased incidence of metabolic diseases. Supplementing cows with oleic acid (OA) reduces circulating biomarkers of lipolysis and improves energy balance. Nevertheless, it is unclear if OA alters lipid trafficking in AT. In the liver and skeletal muscle, OA improves mitochondrial function and promotes lipid droplet formation by activating perilipin 5 (PLIN5) and peroxisome proliferator-activated receptor α (PPARα). However, it is unknown if this mechanism occurs in AT. The objective of this study was to determine the effect of OA on AT lipolysis, systemic and AT insulin sensitivity, and AT mitochondrial function in periparturient dairy cows. Twelve rumen-cannulated Holstein cows were infused abomasally following parturition with ethanol (CON) or OA (60 g/d) for 14 d. Subcutaneous AT samples were collected at 11 ± 3.6 d before calving (-12 d), and 6 ± 1.0 d (7 d) and 13 ± 1.4 d (14 d) after parturition. An intravenous glucose tolerance test was performed on d 14. Adipocyte morphometry was performed on hematoxylin and eosin-stained AT sections. The antilipolytic effect of insulin (1 μg/L) was evaluated using an ex vivo explant culture following lipolysis stimulation. PLIN5 and PPARα transcription and translation were determined by real-time quantitative PCR and capillary electrophoresis, respectively. RNA sequencing was used to evaluate the transcriptomic profile of mitochondrial gene networks. In CON cows, postpartum lipolysis increased the percentage of smaller (<3,000 µm²) adipocytes at 14 d compared with -12 d. However, OA limited adipocyte size reduction at 14 d. Likewise, OA decreased lipolysis plasma markers nonesterified free fatty acids and β-hydroxybutyrate at 5 and 7 d. Over the 14-d period, compared with CON, OA increased the concentration of plasma insulin and decreased plasma glucose. During the glucose tolerance test, OA decreased circulating glucose concentration (at 10, 20, 30, 40 min) and the glucose clearance rate. Moreover, OA increased insulin at 10 and 20 min and tended to increase it at 30 min. Following lipolysis stimulation, OA improved the antilipolytic effect of insulin in the AT at 14 d. PLIN5 and PPARA gene expression decreased postpartum regardless of treatment. However, OA increased PLIN5 protein expression at 14 d and increased PPARA at 7 and 14 d. Immunohistochemical analysis of AT and RNA sequencing data showed that OA increased the number of mitochondria and improved mitochondrial function. However, OA had no effect on production and digestibility. Our results demonstrate that OA limits AT lipolysis, improves systemic and AT insulin sensitivity, and is associated with markers of mitochondrial function supporting a shift to lipogenesis in AT of periparturient dairy cows.

Type 2 diabetes mellitus (T2DM), one of the main types of Noncommunicable diseases (NCDs), is a systemic inflammatory disease characterized by dysfunctional pancreatic β-cells and/or peripheral insulin resistance, resulting in impaired glucose and lipid metabolism. Genetic, metabolic, multiple lifestyle, and sociodemographic factors are known as related to high T2DM risk. Dietary lipids and lipid metabolism are significant metabolic modulators in T2DM and T2DM-related complications. Besides, accumulated evidence suggests that altered gut microbiota which plays an important role in the metabolic health of the host contributes significantly to T2DM involving impaired or improved glucose and lipid metabolism. At this point, dietary lipids may affect host physiology and health via interaction with the gut microbiota. Besides, increasing evidence in the literature suggests that lipidomics as novel parameters detected with holistic analytical techniques have important roles in the pathogenesis and progression of T2DM, through various mechanisms of action including gut-brain axis modulation. A better understanding of the roles of some nutrients and lipidomics in T2DM through gut microbiota interactions will help develop new strategies for the prevention and treatment of T2DM. However, this issue has not yet been entirely discussed in the literature. The present review provides up-to-date knowledge on the roles of dietary lipids and lipidomics in gut-brain axis in T2DM and some nutritional strategies in T2DM considering lipids- lipidomics and gut microbiota interactions are given.

Prospective studies have failed to establish a causal relationship between animal fat intake and cardiovascular diseases in humans. Furthermore, the metabolic effects of different dietary sources remain unknown. In this four-arm crossover study, we investigated the impact of consuming cheese, beef, and pork meat on classic and new cardiovascular risk markers (obtained from lipidomics) in the context of a healthy diet. A total of 33 young healthy volunteers (23 women/10 men) were assigned to one out of four test diets in a Latin square design. Each test diet was consumed for 14 days, with a 2-week washout. Participants received a healthy diet plus Gouda- or Goutaler-type cheeses, pork, or beef meats. Before and after each diet, fasting blood samples were withdrawn. A reduction in total cholesterol and an increase in high density lipoprotein particle size were detected after all diets. Only the pork diet upregulated plasma unsaturated fatty acids and downregulated triglycerides species. Improvements in the lipoprotein profile and upregulation of circulating plasmalogen species were also observed after the pork diet. Our study suggests that, within the context of a healthy diet rich in micronutrients and fiber, the consumption of animal products, in particular pork meat, may not induce deleterious effects, and reducing the intake of animal products should not be regarded as a way of reducing cardiovascular risk in young individuals.

The number of diabetes mellitus patients is increasing rapidly worldwide. Diet and nutrition are strongly believed to play a significant role in the development of diabetes mellitus. However, the specific dietary factors and detailed mechanisms of its development have not been clearly elucidated. Increasing evidence indicates the intestinal microbiota is becoming abundantly apparent in the progression and prevention of insulin resistance in diabetes. Differences in gut microbiota composition, particularly butyrate-producing bacteria, have been observed in preclinical animal models as well as human patients compared to healthy controls. Gut microbiota dysbiosis may disrupt intestinal barrier functions and alter host metabolic pathways, directly or indirectly relating to insulin resistance. In this article, we focus on dietary fat, diabetes, and gut microbiome characterization. The promising probiotic and prebiotic approaches to diabetes, by favorably modifying the composition of the gut microbial community, warrant further investigation through well-designed human clinical studies.

Trials investigating the role of carbohydrate restriction in the management of glycaemia in type 2 diabetes (T2D) have been confounded by multiple factors, including degree of calorie restriction and dietary protein content, as well as by no clear definition of a low-carbohydrate diet. The present study aimed to provide insight into the relationship between carbohydrate restriction and glycaemia by testing the effect of varying doses of carbohydrate on continuous glucose concentrations within a range of intakes defined as low-carbohydrate at the same time as controlling for confounding factors.

This was a randomised crossover trial in participants with T2D (HbA1c: 6.6 ± 0.6%, 49 ± 0.9 mmol mol^-1 ) testing five different 6-day eucaloric dietary treatments with varying carbohydrate content (10%, 15%, 20%, 25%, and 30% kcal). Diets exchanged %kcal from carbohydrate with fat, keeping protein constant at 15% kcal. Daily self-weighing was employed to ensure weight stability throughout each treatment arm. Between dietary treatments, participants underwent a washout period of at least 7 days and were advised to maintain their habitual diet. Glycaemic control was assessed using a continuous glucose monitoring device.

Twelve participants completed the study. There were no differences in 24-h and post-prandial sensor glucose concentrations between the 30 and 10%kcal doses (7.4 ± 1.1 mmol L^-1 vs. 7.6 ± 1.3 mmol L^-1 [p = 0.28] and 8.1 ± 1.5 mmol L^-1 vs. 8.5 ± 1.4 mmol L^-1 [p = 0.28], respectively). In our exploratory analyses, we did not find any dose-response relationship between carbohydrate intake and glycaemia. A small amount of weight loss occurred in each treatment arm (range: 0.4-1.1 kg over the 6 days) but adjusting for these differences did not influence the primary or secondary outcomes.

Modest changes in dietary carbohydrate content in the absence of weight loss at the same time as keeping dietary protein intake constant do not appear to influence glucose concentrations in people with well-controlled T2D.

This study randomised people with T2D to receive five different doses of carbohydrate from 10% to 30% of calories in random order to see what effect it had on their blood glucose.

Nutrition and dietary interventions are a central component in the pathophysiology, but also a cornerstone in the management of patients with non-alcoholic fatty liver disease (NAFLD). Summarizing our rapidly advancing understanding of how our diet influences our metabolism and focusing on specific effects on the liver, we provide a comprehensive overview of dietary concepts to counteract the increasing burden of NAFLD. Specifically, we emphasize the importance of dietary calorie restriction independently of the macronutrient composition together with adherence to a Mediterranean diet low in added fructose and processed meat that seems to exert favorable effects beyond calorie restriction. Also, we discuss intermittent fasting as a type of diet specifically tailored to decrease liver fat content and increase ketogenesis, awaiting future study results in NAFLD. Finally, personalized dietary recommendations could be powerful tools to increase the effectiveness of dietary interventions in patients with NAFLD considering the genetic background and the microbiome, among others.

Lifestyle changes that emphasis on plant-based diets (PBD) are typically recommended for those at risk for type 2 diabetes mellitus (T2DM) to mitigate their cardo-metabolic risk. We examined the impact of the inclusion of eggs compared with their exclusion from PBD on diet quality among adults at risk for T2DM.

This was a randomized, controlled, single-blind, crossover trial of 35 adults (mean age 60.7 years; 25 women, 10 men; 34 Caucasians, 1 African-American) at risk for T2DM (i.e., pre- diabetes or metabolic syndrome) assigned to one of two possible sequence permutations of two treatments (PBD with eggs and exclusively PBD), with a 4-week washout period. Participants received dietary counseling from a dietitian to exclude or to include 2 eggs daily in the context of PBD for a 6-week period. Diet quality was assessed using the Healthy Eating Index 2015 (HEI-2015) at baseline and 6 weeks.

Compared with the exclusion of eggs, the inclusion of eggs in the context of PBD improved the diet quality score for intake of total protein foods (1.0 ± 1.1 vs. -0.4 ± 1.0; p <.0001); seafood and plant proteins (0.2 ± 1.2 vs. -0.4 ± 1.1; p = 0.0338); and fatty acids (0.8 ± 2.5 vs. -0.7 ± 2.7; p = 0.0260). Overall diet quality score depreciated with the adoption of exclusively PBD without eggs (-3.1 ± 8.3; p = 0.0411), while it was unaffected with the adoption of a PBD with the inclusion of eggs (-0.6 ± 7.9; p = 0.6892).

Eggs could be used as an adjuvant to enhance the diet quality among those at risk for T2DM who adopt plant-based dietary patterns.

Short-term trials indicate improvement of intrahepatic lipids (IHLs) and metabolism by dietary protein or unsaturated fatty acids (UFAs) beyond weight loss.

We aimed to assess the effect of a dietary intervention high in protein and UFAs on IHLs and metabolic outcome after 12 mo, as long-term effects of such a combined intervention are unknown.

Within a 36-mo randomized controlled trial, eligible subjects (aged 50 to 80 y, ≥1 risk factor for unhealthy aging) were randomly assigned to either intervention group (IG) with high intake of mono-/poly-UFAs [15-20 percent of total energy (%E)/10%-15%E, respectively], plant protein (15%-25%E), and fiber (≥30 g/d), or control group [CG, usual care, dietary recommendations of the German Nutrition Society (fat 30%E/carbohydrates 55%E/protein 15%E)]. Stratification criteria were sex, known cardiovascular disease, heart failure, arterial hypertension, type 2 diabetes, and cognitive or physical impairment. Nutritional counseling and supplementation of foods mirroring the intended dietary pattern were performed in the IG. Diet-induced effects on IHLs, analyzed by magnetic resonance spectroscopy, as well as on lipid and glucose metabolism were predefined secondary endpoints.

IHL content was analyzed in 346 subjects without significant alcohol consumption at baseline and in 258 subjects after 12 mo. Adjusted for weight loss, sex, and age, we observed a comparable decline of IHLs in IG and CG (-33.3%; 95% CI: -49.3, -12.3%; n = 128 compared with -21.8%; 95% CI: -39.7, 1.5%; n = 130; P = 0.179), an effect that became significant by comparing adherent IG subjects to adherent CG subjects (-42.1%; 95% CI: -58.1, -20.1%; n = 88 compared with -22.2%; 95% CI: -40.7, 2.0%; n = 121; P = 0.013). Compared with the CG, decline of LDL cholesterol (LDL-C) and total cholesterol (TC) was stronger in the IG (for LDL-C P = 0.019, for TC P = 0.010). Both groups decreased in triglycerides and insulin resistance (P for difference between groups P = 0.799 and P = 0.124, respectively).

Diets enriched with protein and UFAs have beneficial long-term effects on liver fat and lipid metabolism in adherent older subjects. This study was registered at the German Clinical Trials Register, https://www.drks.de/drks_web/setLocale_EN.do, DRKS00010049. Am J Clin Nutr 20XX;xx:xx-xx.

This systematic review and meta-analysis was conducted to pool findings of cohort studies that investigated hazards of type 2 diabetes mellitus (T2DM) in relation to intakes of SFAs. A systematic search was conducted in the PubMed, Scopus, and Embase databases up to June 2021 to find eligible studies. Review articles or commentaries, clinical trials, cross-sectional studies, studies on gestational or type 1 diabetes patients, animal studies, articles with no access to full-texts, articles published in non-English languages, and articles with missing critical data needed for the systematic review were excluded from the meta-analysis. A random-effects model was used to combine study-specific results. Thirteen cohort studies with 361,686 participants and 11,865 T2DM events were included. Dietary total SFA intake, as well as dietary palmitic acid (PA) or stearic acid (SA) were not associated with risk of T2DM when the highest was compared with the lowest intake category (HR = 0.99; 95% CI: 0.91, 1.09; n = 13 for total SFAs; HR = 0.96; 95% CI: 0.79, 1.15; n = 4 for PA; and HR = 1.08; 95% CI: 0.79, 1.49; n = 4 for SA). However, the risk of T2DM decreased by 11% in the highest compared with the lowest category of dietary lauric acid (HR = 0.89; 95% CI: 0.82, 0.97; n = 2), and by 17% in the highest compared with lowest category of dietary myristic acid (MA) (HR = 0.83; 95% CI: 0.74, 0.92; n = 3). There was evidence of publication bias among studies on dietary total SFAs and T2DM. Our results indicated no significant association between dietary total SFA and risk of T2DM. However, dietary intake of MA was negatively associated with developing T2DM.