Glaucoma is a leading cause of irreversible blindness worldwide. Toll-like receptor 4 (TLR4) is a pattern-recognition transmembrane receptor that induces neuroinflammatory processes in response to injury. Tlr4 is highly expressed in ocular tissues and is known to modulate inflammatory processes in both anterior and posterior segment tissues. TLR4 activation can lead to mitochondrial dysfunction and metabolic deficits in inflammatory disorders. Due to its effects on inflammation and metabolism, TLR4 is a candidate to participate in glaucoma pathogenesis. It has been suggested as a therapeutic target based on studies using acute models, such as experimentally raising IOP to ischemia-inducing levels. Nevertheless, its role in chronic glaucoma needs further evaluation. In the current study, we investigated the role of TLR4 in an inherited mouse model of chronic glaucoma, DBA/2J. To do this, we analyzed the effect of Tlr4 knockout (Tlr4-/-) on glaucoma in DBA/2J mice. Our studies found no significant differences in intraocular pressure, iris disease, or glaucomatous progression in Tlr4-/- compared to Tlr4+/+ DBA/2J mice. Our data do not support a role for TLR4 as a treatment target in chronic glaucoma.

Obesity is closely related to human metabolism and a variety of diseases. The association between weight-waist-adjustment index (WWI, a new index for obesity) and serum folate has not been sufficiently explored. Data from the National Health and Nutrition Examination Survey (2013-2018) was used to explore the correlation between WWI and serum folate. 12,757 adult participants were included in our study. In order to discern the relationship, we conducted weighted multiple linear regression analysis, generalized weighted smooth curve fitting and threshold effect analyses. Additionally, we executed subgroup analysis and interaction tests. There was a negative correlation between WWI and serum folate. In subgroup analysis, the relationship between WWI and serum folate were more pronounced among females, the elderly (65-80 years), nonsmokers, and those with hypertension or stroke. Furthermore, a nonlinear association between WWI and serum folate was found using smooth curve fitting (likelihood ratio = 0.014), with a threshold identified at WWI of 7.42. We discovered a stronger association between WWI and serum folate than other obesity markers including body mass index and waist circumference. Our study could help obese people predict serum folate and manage their nutrition well.

Polysaccharides, as macromolecular carbohydrates present in various medicine and food homology, have gained growing recognition for their potential in combating obesity through multiple mechanisms. Their natural origin and favorable safety profile have made polysaccharides from medicine and food homology (PMFH) an area of significant research interest, particularly in the context of developing effective, safe, and sustainable interventions for obesity management. This review summarized the classification and biological properties of PMFH and then elucidated the pathological characteristics of obesity. We primarily focused on the effects of PMFHs on obesity, with particular attention to the potential mechanisms mediated through the gut-liver axis. These mechanisms encompassed the improvement of fat metabolism imbalances, manager of appetite and energy balance, adjustment of intestinal microbial imbalances, and alleviation of oxidative stress and inflammation. The findings provided critical theoretical insights and data to support the development of anti-obesity dietary and pharmaceutical products. In brief, this review outlined future research directions regarding the potential mechanisms underlying the anti-obesity effects of PMFH, particularly those involving the gut-liver axis.

The consumption of nuts has beneficial effects on cardiovascular health, body composition, cognitive functions, the intestinal microbiota, and satiety control, but how nuts and their nutrients impact related gene expression is unclear.

We analyzed the effects of nut consumption on human gene expression as investigated in controlled clinical trials.

This systematic review was conducted according to the PRISMA guidelines. The databases used in the search were MEDLINE/PubMed, Embase, and the Cochrane Library.

Randomized and nonrandomized controlled trials conducted to date that evaluated the effect of nut consumption on the mRNA expression of human genes were evaluated according to eligible criteria. Two authors screened and determined the quality of the studies; disagreements were resolved by the third author between May and June 2024. All authors were involved in analyzing the compiled data.

We selected 13 original articles. Most studies evaluated the effects of Brazil nuts, followed by studies using combinations of two or more nuts, with an interventional duration of six weeks to one year. The consumption of hazelnuts and Brazil nuts increased expression in antioxidant-related genes, while beneficial regulation of proinflammatory pathways (tumor necrosis factor - TNF, interleukin-6 - IL-6, and toll-like receptors 2 and 4 - TLR2 and TLR4) was reported after consumption of Brazil nuts. Genes involved in vascular inflammation (eg, ciclooxygenase-2 - COX-2) were downregulated after the consumption of mixed nuts, and the expression of selenoprotein - SELENOP and glutathione peroxidase 1 - GPX1 were regulated according to the presence of single nucleotide polymorphisms after the consumption of Brazil nuts. Finally, pistachio consumption reduced telomere oxidation (telomerase reverse transcriptase - TERT and WD repeat containing antisense to TP53 - WRAP53) and downregulated resistin and IL-6 genes.

The consumption of nuts has beneficial effects on human health, modulating gene expression involved in the progression of chronic diseases, with emphasis on the pathways of inflammation, oxidative stress, and cardiovascular health.

PROSPERO registration No. CRD42024505199.

Obesity is a condition of chronic low-grade inflammation affecting peripheral organs of the body, as well as the central nervous system. The adipose tissue dysfunction occurring under conditions of obesity is a key factor in the onset and progression of a variety of diseases, including neurodegenerative disorders. Mitochondria, key organelles in the production of cellular energy, play an important role in this tissue dysfunction. Numerous studies highlight the close link between obesity and adipocyte mitochondrial dysfunction, resulting in excessive ROS production and adipose tissue inflammation. This inflammation is transmitted systemically, leading to metabolic disorders that also impact the central nervous system, where pro-inflammatory cytokines impair mitochondrial and cellular functions in different areas of the brain, leading to neurodegenerative diseases. To date, several bioactive compounds are able to prevent and/or slow down neurogenerative processes by acting on mitochondrial functions. Among these, some molecules present in the Mediterranean diet, such as polyphenols, carotenoids, and omega-3 PUFAs, exert a protective action due to their antioxidant and anti-inflammatory ability. The aim of this review is to provide an overview of the involvement of adipose tissue dysfunction in the development of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and multiple sclerosis, emphasizing the central role played by mitochondria, the main actors in the cross-talk between adipose tissue and the central nervous system.

Probiotics are increasingly recognized for promoting beneficial effects on intestinal health. However, most probiotic strains have been insufficiently researched, underscoring the need for further studies to fully understand their potential health benefits, especially in metabolic conditions. Therefore, this study aimed to explore the role and possible mechanism of Lactiplantibacillus plantarum YDJ-03 (YDJ-03) and Limosilactobacillus fermentum YDJ-6 (YDJ-6) in metabolic syndrome (MetS) and hyperuricemia.

Twelve mice per group were fed a high-fat, high-fructose, high-cholesterol (HFFC) diet for 90 days. Mice in both the YDJ-03 and YDJ-6 groups were administered a dose of 1.2 × 109 colony-forming units (CFU) intragastrically per mouse for 28 days before being injected with hypoxanthine (400 mg/kg) to induce hyperuricemia. Blood lipids (triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C)), liver injury markers (aspartate aminotransferase (AST) and alanine aminotransferase (ALT)), oxidative stress indicators (malondialdehyde (MDA) and superoxide dismutase (SOD)), and renal injury markers (uric acid (UA) and creatinine (CREA)) levels were analyzed after the conclusion of the study.

In contrast to the model group, the YDJ-03 group exhibited a marked decrease in liver TGs (p = 0.033), MDA (p = 0.0041), serum UA (p = 0.0071) and CREA (p = 0.0072). The mRNA levels of renal toll-like receptor 2 (Tlr2) (p = 0.0018), tumor necrosis factor receptor-associated factor 6 (Traf6) (p = 0.0013), and nuclear factor kappa B subunit 1 (Nfkb1) (p = 0.032) were downregulated, accompanied by marked attenuation of inflammatory cell infiltration in renal tissues and alleviation of glomerular epithelial cell swelling. Furthermore, YDJ-6 treatment promoted significant downward adjustments in hepatic TG (p = 0.0055), serum TG (p = 0.0082), and LDL-C (p = 0.0233) levels. YDJ-6 treatment also decreased serum ALT (p = 0.0458) and AST (p = 0.029) concentrations, downregulated the gene expression levels of inflammation-related adhesion G protein-coupled receptor E1 (Adgre1) (p = 0.033) and prostaglandin-endoperoxide synthase 2 (Ptgs2) (p = 0.0077), and effectively ameliorated hepatocellular lipid deposition and ballooning degeneration with hepatocyte necrosis.

YDJ-03 may exert nephroprotective effects by regulating the TLR2-mediated NF-κB pathway, and YDJ-6 can effectively reduce hepatic fat deposition and inflammation to alleviate liver injury.

Obesity is a chronic metabolic disease responsible for causing various health problems. Obese individuals experience disrupted homeostasis, thus making them more vulnerable to environmental pollutants. This study investigated the effect of pre-existing obesity on respiratory toxicity and explored whether sex differences exist in the response to titanium dioxide nanoparticles (TiO2-NPs), a component of air pollutants.

Male and female mice were fed a normal diet (ND) or a high-fat diet (HFD) for 26 weeks and then intratracheally instilled with TiO2-NPs at concentrations of 0, 0.1, 0.2, and 0.4 mg/50 μL on days 1, 4, 6, 9, 11, and 13. Mice were sacrificed 24 h after the final administration.

In HFD-fed obese mice, TiO2-NPs exposure led to respiratory inflammation through the toll-like receptor 4-mediated mitogen-activated protein kinase signaling pathway and a subsequent inflammatory response induced by oxidative stress. These effects were more pronounced in females than in males, and this was attributed to the higher sensitivity of females to HFD consumption and early depletion of antioxidant defenses.

Our findings suggest an increased risk of respiratory toxicity in individuals with pre-existing obesity and highlight that these effects are sex-specific.

Introduction: food contains both inflammatory and anti-inflammatory components. The higher the concentration of inflammatory components, the greater the likelihood of developing obesity and other chronic conditions linked to low-grade chronic inflammation. Consequently, various indices have been developed to quantify dietary inflammation, such as the Empirical Dietary Inflammatory Pattern (EDIP-SP), which has been validated in Brazil. This study aimed to examine the potential association between EDIP-SP and the nutritional status of college students. Methodology: the study involved 97 undergraduate nutrition students from Fortaleza, Ceará, in Northeast Brazil. Participants completed a food frequency questionnaire to assess their intake of EDIP-SP components, including processed meats, vegetables, fruits, rice, and beans. Anthropometric measurements (weight, height, and waist circumference) were taken to calculate body mass index (BMI) and to categorize nutritional status and abdominal adiposity. Results: the diet consumed by the participants was primarily anti-inflammatory, with a mean score of -1.57 ± 0.69. Most participants were not classified as overweight (59.79 %) and did not exhibit abdominal adiposity (91.75 %). No significant association was observed between EDIP-SP scores and BMI (r = -0.11; p = 0.297) or waist circumference (r = -0.07; p = 0.489). However, a weak but direct association was found between the inflammatory score of processed meat intake and abdominal adiposity in female participants (r = 0.27; p = 0.019). Conclusion: the Empirical Dietary Inflammation Pattern (EDIP-SP) does not appear to significantly influence the nutritional status of students. Nevertheless, the inflammatory impact of processed meat intake may contribute to excess abdominal adiposity, particularly among women.

Oral mucositis (OM) is a serious complication of anticancer therapy that can substantially affect patient quality of life and treatment outcomes. This meta-analysis evaluated the efficacy of omega-3 fatty acids in the prevention and treatment of OM in patients diagnosed with cancer undergoing anticancer therapy. A systematic literature search of the PubMed, Embase, Web of Science, Cochrane Library, CNKI, and Wanfang databases for relevant studies, published up to September 24, 2024, was performed. Risk ratio (RR) or standardized mean difference (SMD) with corresponding 95% confidence interval (CIs) were calculated using Review Manager version 5.3. Five studies, including 337 patients, were included in this meta-analysis. Results of analysis revealed that, although omega-3 fatty acids did not significantly reduce the overall incidence of OM (RR 0.50, 95% CI 0.25-1.01), it significantly reduced the incidence of severe OM (RR 0.31, 95% CI 0.17-0.56), with no heterogeneity was observed (p = 0.96; I2= 0%). Furthermore, omega-3 fatty acids were found to significantly alleviate OM-associated pain (SMD -1.61, 95% CI -2.79 to -0.43), with no heterogeneity was detected (p = 0.32; I2 = 0%). Omega-3 fatty acids effectively reduced the incidence of severe OM and alleviated OM-related pain in patients undergoing anticancer therapy.

The development of asthma is impacted by fat. Asthma is more common in obese persons. The purpose of the experimental study is to determine how chromium, formoterol, and their combination can improve the quality of life for obese people with lung anomalies. Thirty-six male Wistar rats were divided into six groups: control (C), obesity (CO), obese-asthma (COA), and obese-asthma groups treated with formoterol (OAF), chromium (OACR), or both (OACRF). Except for group C, all groups received a high-fat diet for 4 weeks. Subsequently, ovalbumin (OVA) was administered subcutaneously (s.c.) to all groups except C and CO to induce sensitization. Asthma was triggered via 1% OVA aerosol challenges on days 26-28. Over 5 days, OAF and OACRF received daily formoterol inhalations (50 μg/kg), while OACR and OACRF were given chromium (400 μg/kg). Treatments were timed to align with asthma induction protocols. Lipid profile and inflammatory indicators were examined at the end of the trial-Immunohistochemical analysis of lung tissue, Histopathological and lung tissue stained with Hematoxylin and Eosin. The combination therapy (OACRF) significantly reduced body weight (p < 0.05), lowered LDL and triglycerides, increased HDL, and normalized lung tissue architecture compared to controls. Immunohistochemistry revealed reduced IL-1β and IL-17α expression. The (OACRF) group demonstrated superior asthma control by reducing body weight, improving inflammatory indicators, and restoring lung tissue to its normal state by administering chromium and formoterol therapy. The most effective strategy for treating both obesity and asthma is to address their two connected conditions. These findings demonstrate that combined chromium and formoterol therapy effectively addresses metabolic and inflammatory components of obesity-induced asthma, offering a promising dual-target therapeutic strategy.

Insulin resistance (IR) is a metabolic disorder characterized by an impaired response to insulin. This condition is associated with excess adiposity and metabolic inflammation, contributing to an increased risk for related chronic diseases. Single-nucleotide polymorphisms (SNPs) can affect genes related to metabolic pathways which are related to IR and the individual response to nutrients and dietary patterns, affecting metabolic inflammation and insulin sensitivity. This narrative review explores the current evidence on interactions between genetic variants and dietary factors, specifically their effects in modulating IR and metabolic inflammation. A comprehensive search of the literature was conducted in PubMed, Google Scholar, and Web of Science, and a total of 95 articles were reviewed. The key findings reveal that SNPs in the TCF7L2, ADIPOQ, and TNF genes significantly influence metabolic responses and modulate the effects of the Mediterranean diet on biomarkers of inflammation and IR. Genotype-dependent variations in IR and inflammation biomarkers were observed in the response to different diets for SNPs in the TCF7L2, ADIPOQ, and TNF genes. Additionally, polygenic risk scores (PRSs) can also predict the response to the intake of nutrients and specific diets, and offer a promising tool for assessing genetic predisposition to IR. This review underscores the pivotal role of an individual's genetic background in the effects of their nutrient intake and in the responses to dietetic interventions, thereby laying the foundation for personalized and effective nutritional strategies tailored to each individual's necessity in mitigating IR and its associated risk factors for chronic diseases.

Psoriasis is a chronic immune-mediated skin disease characterized by cytokine dysregulation. Pro-inflammatory mediators, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-17, and IL-23, play pivotal roles in the pathogenesis of psoriasis. Emerging evidence suggests that dietary interventions can modulate cytokine activity, providing a complementary approach to standard therapies. This narrative review examines the impact of various dietary strategies, including a Mediterranean diet, ketogenic diet, gluten-free diet, and fasting-mimicking diet, on cytokine profiles and clinical outcomes in psoriasis. Research insights reveal that dietary components such as omega-3 fatty acids, polyphenols, and short-chain fatty acids influence immune signaling pathways. These pathways include nuclear factor-kappa B (NF-κB) and Signal Transducer and Activator of Transcription 3 (STAT3). Additionally, these dietary components promote anti-inflammatory effects mediated by gut microbiota. Clinical studies demonstrate significant reductions in psoriasis severity, improved quality of life, and modulation of key cytokines associated with disease activity. Despite these advancements, significant challenges persist in effectively integrating these findings into clinical practice. These challenges include variability in patient responses, adherence issues, and the need for robust biomarkers to monitor efficacy. Future directions emphasize the potential of personalized nutrition and precision medicine approaches to optimize dietary interventions tailored to individual cytokine profiles and genetic predispositions. Integrating these strategies into psoriasis care could transform treatment paradigms by simultaneously addressing both systemic inflammation and comorbid conditions.

Metabolic syndrome is the occurrence of at least three of the five conditions diabetes, overweight and obesity, triglyceridemia, hypercholesterolemia, and hypertension. Dietary interventions have been one of the first lines of treatment indicated for improving conditions related to metabolic syndrome. The growing interest in plant-based diets and foods with health-promoting qualities has increased significantly. Due to its excellent nutritional and bioactive value, chia seeds have a significant market share, characterized by their high content of proteins, essential fatty acids, fiber, vitamins, minerals, phenolic compounds, and antioxidants. These constituents promote potential positive effects on improving health, especially blood pressure, and reducing oxidative stress and the inflammatory state installed by metabolic syndrome and its risk conditions. However, the ten studies in humans that were reviewed generally showed no effect on anthropometric parameters and biochemical parameters related to glucose and lipid homeostasis. Thus, although chia seeds have a high potential to combat metabolic syndrome, this review found few studies, highlighting a gap in the area and a possible future topic for researchers.

Cancer is a disease influenced by both genetic and environmental factors, with dietary lipids being a significant contributing factor. This review summarizes the role of polyunsaturated fatty acids (PUFAs) in the mechanism of tumor occurrence and development, and elucidate the role of PUFAs in tumor treatment.

PUFAs exert their impact on cancer through altering lipid composition in cell membranes, interacting with cell membrane lipid receptors, directly modulating gene expression in the cell nucleus, and participating in the metabolism of lipid mediators. Most omega-3 PUFAs are believed to inhibit cell proliferation, promote cancer cell death, suppress cancer metastasis, alter energy metabolism, inhibit tumor microenvironment inflammation, and regulate immune responses involving macrophages, T cells, NK cells, and others. However, certain omega-6 PUFAs exhibit weaker anti-tumor effects and may even promote tumor development, such as by fostering inflammatory tumor microenvironment and enhancing tumor cell proliferation. PUFAs play important roles in hallmarks of cancer including tumor cell proliferation, cell death, migration and invasion, energy metabolism remodeling, epigenetics, and immunity. These findings provide insights into the mechanisms of cancer development and offers options for dietary management of cancer.

Obesity and obesity-related metabolic diseases are causally linked to inflammatory activation. Proinflammatory macrophage infiltration and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome activation contribute to chronic inflammation and insulin resistance. Alleviating inflammatory responses is a reliable method to restore insulin sensitivity and reduce the severity of metabolic syndrome. Solanesol, rich in anti-inflammatory foods (potato, tomato, eggplant, chili peppers), has demonstrated anti-inflammatory properties, but whether it plays a beneficial role in obesity-induced chronic inflammation remains poorly understood. In this study, we investigated the effects of solanesol on the NLRP3 inflammasome and inflammatory responses both in vitro and in high-fat diet (HFD)-fed mice. We found that oral administration of solanesol reduced weight gain, insulin resistance, and inflammation in epididymal white adipose tissue (eWAT) in both HFD-fed obese mice and mice concurrently treated with a HFD. This effect was involved with reducing macrophage inflammation and inactivating the NLRP3 inflammasome by reducing the K+ efflux and reactive oxygen species (ROS) production in macrophages. Solanesol also reprogrammed the phenotype of inflammatory macrophages. Taken together, our study suggests that solanesol may be a promising candidate for treating obesity and obesity-related metabolic diseases.

Saturated fat has been linked to cardiovascular diseases, leading to an increase in polyunsaturated fat consumption. The aim of the present study was to investigate the effects of three fat sources (coconut oil, lard and soybean oil) on metabolic and reproductive parameters in heterogenic mice. Female Swiss mice (5-6 weeks old; n = 9/group) were divided into four experimental groups: control (CC), coconut oil (CO), lard (LA), and soybean oil (SO), and were orally given 0.6 mL of the corresponding fat daily for 6 weeks to further investigate morphological, biochemical, and molecular parameters. SO females showed the highest glucose intolerance (P < 0.05), and all experimental groups were highly insulin resistant, with no statistical differences among them (P > 0.05). Moreover, all fat supplemented groups presented increased proportion in bile ducts, and CO and SO females presented higher LDL-cholesterol levels compared to CC (P < 0.05). Regarding reproductive parameters, estrous cycle alterations were observed mainly in the SO group, showing extended luteal phase duration (longer diestrus), and higher numbers of atretic follicles per area compared to the CC females (P < 0.05). Furthermore, higher proportion of active Casp-3 positive cells in the granulosa layers of preantral follicles were observed in the LA compared to the CO group (P < 0.05). The gene expression data revealed downregulation of Igf1r and Acvr1 in SO, upregulation of Igf1r in LA and Lhcgr in CO compared to CC females (P < 0.05). Thus, excessive fat intake may have deleterious effects on metabolism and reproductive function, but lard may be the least harmful source.

Although coconut oil has attracted great attention as a functional food, enough supportive scientific evidence is lacking. In addition, the beneficial effects of coconut oil consumption on the prevention of metabolic disorders are controversial. Fetuin-A is a plasma glycoprotein secreted by hepatocytes and adipocytes. Circulating fetuin-A levels relate to insulin resistance due to macrophage-mediated adipose tissue inflammation. This study demonstrated that coconut oil feeding significantly downregulated the hepatic expression of fetuin-A and reduced its plasma level in KK mice-an obese diabetic model animal. The expression of monocyte chemoattractant protein-1, a potent inducer for macrophage infiltration, decreased in epididymal white adipose tissue in coconut oil-fed KK mice. The expression of CD68 and CD11c, markers of proinflammatory M1 macrophages, was significantly reduced by coconut oil feeding in epididymal white adipose tissue of KK mice. However, the mice did not exhibit improved insulin resistance. Our results may further support the potential of coconut oil as a dietary trigger that can reduce both circulating fetuin-A levels and infiltration of proinflammatory macrophages in visceral adipose tissue.

The low-carbohydrate high-fat (LCHF) diet lipids are often overlooked for obesity management. We hypothesized that unsaturated lipids enhance fatty acid metabolism, and influence obesity-related metainflammation.

Male Swiss mice were fed an obesity-inducing diet for ten weeks. Subsequently, the obese mice were divided into four groups, each receiving a LCHF diet enriched with different types of lipids: saturated fatty acids (SFA), polyunsaturated fatty acids (PUFA) ω-3, PUFA ω-6, and monounsaturated fatty acids (MUFA) ω-9 during six weeks as an obesity intervention. For comparison, a lean control (CTL) group and an obesity control (HFC) group were also included, spanning the entire 16-week experimental protocol. We evaluated body mass gain, fatty acid profiles via gas chromatography, elongase, and desaturase activities, NFκBp65 expression by western blotting, and cytokine by ELISA kits in serum, liver, and retroperitoneal adipose tissue (RET) samples. Our results highlight that ω-3 and ω-9 LCHF diets facilitate weight loss and enhance unsaturated fatty acid incorporation in liver, RET, and serum compared to the other groups. The ω-3 LCHF diet notably reduced the ω-6/ω-3 ratio and improved inflammatory status by reducing cytokines such as IL-4, IL-17, IL-33, CXCL1/KC, and inhibiting NFκBp65 activity compared to the HFC group. Desaturase (delta-9 desaturase-18, delta-6 desaturase) and elongase (ELOVL5 and ELOVL6) activities were modulated in liver, RET, and serum samples by ω-3 and ω-9 compared to the HFC group.

ω-3 and ω-9 fats were most effective in obesity treatment with the LCHF diet, highlighting the significance of lipid type in carbohydrate-restriction for obesity management.

Sulforaphane (SFN) is a phytochemical bioactive substance commonly found in cruciferous plants, such as broccoli and mustard. It has been reported to possess antibacterial, anti-inflammatory, anti-oxidant, anti-cancer and autophagy regulating properties. Recent studies have revealed that SFN regulates fat metabolism both in vivo and in vitro through various mechanisms, including alleviating endoplasmic reticulum stress, inhibiting inflammatory response and improving mitochondrial dysfunction, involving Nrf2/ARE, NF-κB, NLRP3 inflammasome, HDAC8-PGC1α axis and other signaling pathways. By curbing complications associated with abnormal fat metabolic diseases, SFN exhibits therapeutic effects on conditions like obesity, fatty liver disease, atherosclerosis, type 2 diabetes, etc., with minimal side effects. Therefore, it holds promise as a potential alternative treatment for lipid metabolism-related diseases. Although its extraction method has been matured, the thermal instability and preservation difficulties of SFN limit its clinical promotion. More effective and low-cost methods to improve the stability and production of SFN remain to be further studied. This paper reviews the physiological and biological activities of SFN, and summarizes the protective effects and molecular mechanisms of SFN in diseases related to abnormal lipid metabolism. Additionally, it proposes potential challenges, possible solutions and future research directions in the clinical application of SFN.

Short-chain fatty acids (SCFAs) produced from microbial fermentation of non-digestible carbohydrates and protein have been shown to modulate adipocyte adipokine secretion and metabolic function, which has implications for mitigating dysfunction in obese adipose tissue; however, the individual effects of different SCFAs and the optimal concentration required is unknown. The purpose of this study was to dose-dependently determine the effects of individual SCFAs on adipocyte adipokine secretion and metabolic function.

We recapitulated the obese adipocyte inflammatory conditions using mature 3T3-L1 adipocytes and a physiological concentration of lipopolysaccharide (LPS) ± individual SCFAs, namely acetate, propionate, and butyrate, in a dose-dependent manner (0.25 mM, 0.5 mM, and 1 mM) for 24 h.

SCFAs dose-dependently affected inflammatory adipokine secretion, wherein at 1 mM, all three SCFAs reduced the secretion of leptin, IL-6 and IL-1β, but only propionate and butyrate reduced MCP-1/CCL2 and MIP-1α/CCL3 compared to control (p < 0.05). Interestingly, 1 mM acetate increased RANTES/CCL5 secretion versus control, whereas propionate and butyrate decreased RANTES/CCL5 secretion, and only 1 mM propionate reduced MCP-3/CCL7 secretion (p < 0.05). At the lower 0.5 mM concentration, both propionate and butyrate reduced IL-6 and IL-1β secretion compared to control (p < 0.05), and there was no difference in adipokine secretion between groups at the 0.25 mM SCFA concentration (p > 0.05). Intracellular protein expression in the ratio of phosphorylated-to-total STAT3 was reduced by all SCFAs at 1 mM and by propionate and butyrate at 0.5 mM versus control (p < 0.05). The ratio fo phosphorylated-to-total NFκB p65 expression was reduced by propionate and butyrate at 1 mM and by butyrate alone at 0.5 mM compared to control (p < 0.05). Basal (no insulin stimulation) and insulin-stimulated glucose uptake did not differ between control and any 1 mM SCFA treatment conditions (p > 0.05).

Individual SCFAs exert different dose-dependent effects on LPS-stimulated adipocyte function.

The metabolome and lipidome comprise the thousands of molecular compounds in an organism. Molecular compounds consist of the upstream metabolic components of intracellular reactions or the byproducts of cellular pathways. Molecular and biochemical perturbations are associated with disorders in newborns and infants. The diagnosis of inborn errors of metabolism has relied on targeted metabolomics for several decades. Newer approaches offer the potential to identify novel biomarkers for common diseases of the newborn and infant. They may also elucidate novel predictive or diagnostic measures for a variety of health trajectories. Here, we review the relevance of the metabolome and lipidome for common disorders and highlight challenges and opportunities for future investigations.

Activation of innate immune signaling occurs during the progression of immunometabolic diseases, including type 2 diabetes (T2D), yet the impact of innate immune signaling on glucose homeostasis is controversial. Here, we report that the E3 ubiquitin ligase TRAF6 integrates innate immune signals following diet-induced obesity to promote glucose homeostasis through the induction of mitophagy. Whereas TRAF6 was dispensable for glucose homeostasis and pancreatic β-cell function under basal conditions, TRAF6 was pivotal for insulin secretion, mitochondrial respiration, and increases in mitophagy following metabolic stress in both mouse and human islets. Indeed, TRAF6 was critical for the recruitment and function of machinery within both the ubiquitin-mediated (Parkin-dependent) and receptor-mediated (Parkin-independent) mitophagy pathways upon metabolic stress. Intriguingly, the effect of TRAF6 deficiency on glucose homeostasis and mitophagy was fully reversed by concomitant Parkin deficiency. Thus, our results implicate a role for TRAF6 in the cross-regulation of both ubiquitin- and receptor- mediated mitophagy through the restriction of Parkin. Together, we illustrate that β-cells engage innate immune signaling to adaptively respond to a diabetogenic environment.

Consumption of the Mediterranean diet (MedDiet) has beneficial effects on cardiometabolic health and aging.

This systematic review aimed to critically investigate the effect of the MedDiet on glycation markers in healthy or overweight individuals with type 2 diabetes or cardiovascular disease.

MEDLINE, EMBASE, Web of Science, and the Cochrane Library were searched, using the terms "Mediterranean diet" AND "glycation end products, advanced".

Three randomized and 3 nonrandomized clinical trials, containing data on 2935 adult and elderly individuals with normal weight or overweight, were included. All extracted data were compiled, compared, and critically analyzed.

The authors of most of the studies demonstrated a reduction in serum concentrations of advanced glycation end products (AGEs), such as εN-carboxymethyllysine and methylglyoxal, and in skin autofluorescence levels after at least 4 weeks of adherence to the MedDiet. The MedDiet also led to positive effects on gene expression of receptors for AGEs, as RAGE and AGER1, and an enzyme involved in detoxification (glyoxalase I). There is no evidence that short-term adherence affects glycation markers.

Glycation markers improved in response to the MedDiet. The possible mechanisms involved may be related to the low AGE and refined sugars content of the diet, as well as its high monounsaturated fatty acid, phenolic compound, and dietary fiber contents.

PROSPERO registration no. CRD42021284006.

Obesity is known to be associated with inflammation and impaired sleep quality. In addition, the anti-inflammatory properties of the daily diet provide positive effects on health. The aim of this study was to investigate the relationship between the inflammatory index of the diet consumed by people with obesity and inflammatory biomarkers and sleep quality.

This study included 124 people with obesity (F: 75; M: 49) with a mean age of 42.20 ± 11.00 years, who presented to a dietary outpatient clinic in Malatya between November 2021 and May 2022. Three-day dietary intake records were collected to calculate Dietary Inflammatory Index (DII) scores, which were then compared with inflammatory biomarkers, anthropometric measurements, and sleep quality measures.

Among the biochemical parameters, C-reactive protein (CRP) was found to be significantly higher in the groups with higher DII score (p = 0.006), and CRP (r = 0.258; p = 0.004) and total cholesterol (r = -0.243; p = 0.007) increased significantly with increasing inflammatory score of the diet. As the inflammatory burden of the diet consumed by the participants increased, their Body Mass Index (BMI) also increased (p = 0.009). No significant correlation was found between DII and sleep quality (p = 0.348).

These findings suggest that an anti-inflammatory diet can effectively reduce inflammation and BMI in people with obesity, but has a limited effect on sleep quality. Therefore, it is recommended that dietitians integrate anti-inflammatory dietary strategies for people with obesity into their clinical practice.

Portulaca oleracea L. (purslane) is a dietary plant and a botanical drug with antioxidant, antidiabetic, and anti-inflammatory activities. However, the effects of purslane against intestinal-inflammation-associated obesity are yet to be studied. In the present study, we hypothesized that purslane extract could reduce intestinal inflammation associated with metabolic disorder.

Male C57BL/6J mice were fed a high-fat diet (HFD, 60% kcal% of fat) for a total duration of 14 weeks to establish an obesity model; further, the treatment group was orally administered purslane extract (200 mg/kg/day) during the last 4 weeks. Then, intestinal tissues were detached from the mice for detecting protein expressions through Western blot and immunohistochemical analyses. Pro-inflammatory cytokines were determined using ELISA kits, whereas the components of purslane extract were detected by ultra performance liquid chromatography/electrospray ionization quadrupole time-of-flight mass spectrometry. Chronic oral administration of purslane extract ameliorated colon shortening syndrome and reduced bowel inflammation in HFD-induced obese mice through suppression of the toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway to downregulate TLR4, myeloid differentiation factor 88 (MyD88), Ser32 phosphorylation of NF-κB inhibitor alpha (IκBα), and Ser536 phosphorylation of NF-κB p65 expression levels, thereby inhibiting the pro-inflammatory cytokines, tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels.

The present study supports the anti-inflammatory potential of purslane extract for modulating bowel inflammation under obesity through inhibition of the TLR4/NF-κB signaling pathway.

An elevated level of saturated fatty acids (SFAs) can cause non-alcoholic fatty liver disease (NAFLD). While n-3 polyunsaturated fatty acids (PUFAs) were shown to improve NAFLD, the effects of n-6 PUFAs in the liver have not been fully elucidated. We examined the association between NAFLD and n-6 PUFAs, particularly dihomo-γ-linolenic acid (DGLA), in patients with type 2 diabetes. A total of 60 patients with type 2 diabetes were included in the study. Patients were categorized into the NAFLD group (n = 35) and non-NAFLD group (n = 25) based on the presence of fatty liver as determined by abdominal ultrasound. We demonstrated that the levels of serum SFAs, specifically palmitic acid and stearic acid, and the levels of n-6 PUFAs, specifically DGLA, and arachidonic acid (AA), were significantly higher in the NAFLD group. The serum palmitic acid, stearic acid, DGLA and AA levels were positively correlated with liver enzyme gamma-glutamyl transpeptidase (GGT). We further demonstrated by multivariate analysis that serum DGLA was a predictor of NAFLD. The serum DGLA level was negatively correlated with blood adiponectin and was positively correlated with blood leptin, high-sensitivity CRP, C-peptide index, and triglyceride-glucose index. Furthermore, delta-5-desaturase (D5D), the AA (product)/DGLA (precursor) ratio calculated from the product-to-precursor ratio of fatty acids, was significantly lower in the NAFLD group. These findings suggest that high serum DGLA levels in NAFLD group may be due to an excessive intake of n-6 PUFAs and changes in desaturase in the human body. High serum DGLA levels may also be associated with insulin resistance and inflammatory factors.

As a type of macronutrient, fatty acids (FA) play significant roles in the bone health of elderly people. However, the specific association between different types of FA and bone health is not fully understood, especially in rural elderly populations. To address this gap, a study was conducted in rural areas of Qingdao, China. Participants aged 65 and older were randomly recruited from 11 rural villages in Licha town, Qingdao City. The levels of serum FA in their serum were measured to investigate the associations between FA and bone mass. The results showed that levels of saturated fatty acids (SFA), n-3 polyunsaturated fatty acids (n-3 PUFA), and n-6 polyunsaturated fatty acids (n-6 PUFA) were all significantly associated with bone mass. Specifically, higher levels of SFA were positively correlated with low bone mass (LBM), while PUFA levels were inversely correlated with LBM. Furthermore, the odds ratio (OR) for LBM exhibited a significant nonlinear dose-response relationship (pnonlinearity = 0.1989) with SFA levels, and a significant nonlinear dose-dependent relationship was also observed with the levels of n-3PUFA and n-6PUFA (pnonlinearity = 0.6183, 0.5808, respectively), indicating that increasing dietary PUFA intake appropriately and controlling SFA intake may benefit the bone health of elderly individuals in rural areas.

Carrageenan, a naturally occurring polysaccharide derived from red seaweed, has been utilized extensively in the food industry as a stabilizer, thickener, and emulsifier due to its unique gel-forming properties. This versatile compound exists in various forms, including kappa, iota, and lambda, each with distinct characteristics suitable for different applications. Its widespread use as a food additive has raised concerns regarding its safety, particularly its potential inflammatory effects on the gastrointestinal tract. While carrageenan has been deemed safe for consumption by regulatory agencies in small amounts, studies have suggested its association with intestinal inflammation and gastrointestinal disturbances, particularly in susceptible individuals. Animal models, including rodents and non-human primates, have been employed to investigate the inflammatory response induced by carrageenan ingestion. These models have provided valuable insights into the molecular mechanisms underlying its pro-inflammatory properties. At the molecular level, carrageenan is believed to trigger inflammation by activating toll-like receptor 4 (TLR4) signaling pathways, leading to the production of pro-inflammatory cytokines and the recruitment of immune cells to the site of exposure. Furthermore, carrageenan-induced inflammation may disrupt the intestinal barrier function, facilitating the translocation of luminal antigens and exacerbating immune responses. This review provides a comprehensive examination of the current understanding of carrageenan's role in inflammation, encompassing its diverse applications in the food industry, safety concerns, experimental findings from animal models, and molecular mechanisms underlying its pro-inflammatory effects.

The present study explored the possible antiobesogenic and osteoprotective properties of the gut metabolite ginsenoside CK to clarify its influence on lipid and atherosclerosis pathways, thereby validating previously published hypotheses. These hypotheses were validated by harvesting and cultivating 3T3-L1 and MC3T3-E1 in adipogenic and osteogenic media with varying concentrations of CK. We assessed the differentiation of adipocytes and osteoblasts in these cell lines by applying the most effective doses of CK that we initially selected. Using 3T3-L1 adipocytes in vitro assessments, CK could effectively decrease intracellular lipid accumulation, inhibit α-glucosidase enzyme, increase 2-NBDG glucose uptake, reduce inflammation-associated cytokines (TNFα, and IL-6), adipogenic regulatory genes (PPARγ, FAS, C/EBPα), lipogenic gene LPL, and increase the expression of thermogenic gene UCP1. Additionally, CK treatment induced osteoblast development in MC3T3-E1 cells as shown by increased mineralization and calcium distribution, collagen content, alkaline phosphatase activity, and decreased inflammatory cytokines TNFα, and IL-6 and increased the regulated expressions of osteogenic genes including Runx2, ALP, BGLAP, OCN, and Col1a1. Significantly, as a major inhibitory regulator, the TP53 gene was down-regulated in both 3T3-L1 and MC3T3E1 cells after the treatment of CK. These encouraging results demonstrate the possible use of CK as an innovative treatment for controlling obesity and osteoporosis, targeting the underlying mechanisms of obesogenic and bone loss. Further studies are necessary to explore the clinical implications of these results and the potential of CK in future treatment strategies. This research highlights the promise of CK in addressing significant health issues.

The type 2 scavenger receptor CD36 functions not only as a long chain fatty acid transporter, but also as a pro-inflammatory mediator. Ceramide is the simple N-acylated form of sphingosine and exerts distinct biological activity depending on its acyl chain length. Six ceramide synthases (CerS) in mammals determine the chain length of ceramide species, and CerS6 mainly produces C16-ceramide. Endotoxin-induced septic shock shows high mortality, but the pathophysiologic role of sphingolipids involved in this process has been hardly investigated. This paper aims to highlight the different role of CerS isoforms in endotoxin-induced inflammatory responses and the regulatory role of CD36 in CerS6 protein degradation with an emphasis as the potential therapeutic candidates in humans. Lipopolysaccharide (LPS), the endotoxin of the Gram-negative bacterial cell wall, was treated to induce endotoxin-induced inflammation both in vitro and in vivo. CerS6-derived C16-ceramide propagated LPS-induced inflammatory responses activating various intracellular signaling pathways, such as mitogen-activated protein kinase and nuclear factor-κB, resulting in the formation of inflammasome complex and pro-inflammatory cytokines. Mechanistically, CerS6-derived C16-ceramide augmented inflammatory responses via endoplasmic reticulum stress, and CerS6 protein stability was regulated by CD36. Finally, CerS6 protein expression and LPS-induced lethality were strikingly reduced in CD36 knockout mice. Collectively, our findings show that CerS6-derived C16-ceramide plays a pivotal role in endotoxin-induced inflammation and suggest CerS6 and its regulator CD36 as possible targets for therapy under life-threatening inflammation such as septic shock.

Inflammation plays a critical role in the pathophysiology of many diseases, and dysregulation of the involved signaling cascades often culminates in uncontrollable disease progression and, ultimately, chronic manifestation. Addressing these disorders requires balancing inflammation control while preserving essential immune functions. Cyclodextrins (CDs), particularly β-CD, have gained attention as biocompatible biomaterials with intrinsic anti-inflammatory properties, and chemical modification of their backbone offers a promising strategy to enhance their physicochemical properties, adaptability, and therapeutic potential. This study evaluated and characterized the immunomodulatory effects of amphiphilic CD derivatives, which self-assemble into nanoparticles, compared to soluble parent β-CD. In a human macrophage model, CD nanoparticles demonstrated superior anti-inflammatory activity, with derivative-specific effects tied to their physicochemical properties, surpassing the soluble β-CD control. Alongside the downregulation of key pro-inflammatory markers, significant reductions in inflammasome activation and changes in lipid profiles were observed. The findings of this study underscore the potential of cyclodextrin-based nanoparticles as versatile biomaterials for treating the complex pathophysiology of various acute and chronic inflammation-associated disorders.

Clinical mastitis (CM) is a prevalent and severe inflammatory disease in dairy cows affecting the mammary glands. Fatty acid (FA) metabolism and associated enzymes are crucial for many physiological and pathological processes in dairy cows. However, the relationships among FA metabolism, FA-associated enzymes, and CM, as well as the mechanisms underlying their interactions, in dairy cows are not fully understood. The aim of this study was to characterize biological process (BP) terms, pathways, and differentially expressed proteins (DEPs) related to FA metabolism from our previous data-independent acquisition proteomic study. Six BPs involving 14 downregulated and 20 upregulated DEPs, and four pathways involving 10 downregulated and 11 upregulated DEPs related to FA synthesis and metabolism were systematically identified. Associated analysis suggested that 12 candidate DEPs obtained from BPs and pathways, especially acyl-CoA thioesterase 7 (ACOT7), regulate long-chain FA (LCFA) elongation and the biosynthesis of unsaturated FAs. Immunohistochemical and immunofluorescence staining results showed that ACOT7 was present mainly in the cytoplasm of mammary epithelial cells. The qRT-PCR and Western blotting results showed that ACOT7 mRNA and protein levels in the mammary glands of the CM group were significantly upregulated compared to those in the healthy group. This evidence indicates that ACOT7 is positively correlated with CM onset and progression in Holstein cows. These findings offer novel insights into the role of FA metabolism and related enzymes in CM and offer potential targets for the development of therapeutic strategies and biomarkers for the prevention and treatment of CM in dairy cows.

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe respiratory condition associated with elevated morbidity and mortality. Understanding their complex pathophysiological mechanisms is crucial for developing new preventive and therapeutic strategies. Recent studies highlight the significant role of inflammation involved in ALI/ARDS, particularly the hyperactivation of the NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome in macrophages. This activation drives pulmonary inflammation by releasing inflammatory signalling molecules and is linked to metabolic reprogramming, marked by increased glycolysis and reduced oxidative phosphorylation. However, the relationship between NLRP3 inflammasome activation and macrophage glycolytic reprogramming in ALI/ARDS, as well as the molecular mechanisms regulating these processes, remain elusive. This review provides a detailed description of the interactions and potential mechanisms linking NLRP3 inflammasome activation with macrophage glycolytic reprogramming, proposing that glycolytic reprogramming may represent a promising therapeutic target for mitigating inflammatory responses in ALI/ARDS. KEY POINTS: NLRP3 inflammasome activation is pivotal in mediating the excessive inflammatory response in ALI/ARDS. Glycolytic reprogramming regulates NLRP3 inflammasome activation. Therapeutic potential of targeting glycolytic reprogramming to inhibit NLRP3 inflammasome activation in ALI/ARDS.

Higher maternal body mass index (BMI) is associated with metabolic disturbances and pregnancy complications. We aimed to examine whether metabolic profiles in early pregnancy were associated with metabolic pregnancy complications in women with obesity (BMI ≥ 30 kg/m2).

Nested cohort study from a prospective longitudinal cohort (n = 1031) of women who were healthy prior to pregnancy and gave birth at Oslo University Hospital from 2002-2008. The sample comprised 81 women with obesity. Metabolic pregnancy complications included gestational diabetes mellitus, gestational hypertension and preeclampsia. In plasma samples from gestational weeks 14-16, 91 metabolites were analyzed by nuclear magnetic resonance spectroscopy. We performed a principal component analysis to reduce the metabolic dimensions. Logistic regression models were fitted to estimate crude and adjusted odds ratios (ORs) of metabolic pregnancy complications.

Twenty-four out of 81 women developed metabolic pregnancy complications (gestational hypertension, preeclampsia, and/or gestational diabetes). Two of five principal components (80 % explained variance) were significantly associated with metabolic pregnancy complications. The ratio of monounsaturated to total fatty acids increased the risk of metabolic pregnancy complications (OR 2.09, 95 % confidence interval [CI] 1.25-3.75), while the ratio of polyunsaturated to monounsaturated fatty acids decreased the risk (OR 0.54, 95 % CI 0.30-0.89). The ratio of omega-3 to total fatty acids (OR 0.59, 95 % CI 0.34-0.98) and the ratio of docosahexaenoic acid to total fatty acids (OR 0.57, 95 % CI 0.31-0.97) also decreased the risk of metabolic pregnancy complications.

Metabolic profile in early pregnancy was associated with risk of metabolic pregnancy complications in women with obesity. We observed the strongest associations between fatty acid composition and metabolic pregnancy complications.

Edible Astraeus mushrooms are known for their nutritional and culinary benefits and potential therapeutic properties. However, more investigation and discussion are still needed to understand their mechanisms of action regarding observed biological activities and thorough chemical analysis of bioactive compounds. This review provides a comprehensive summary and discussion of the bioactive properties and mode of action of Astraeus extracts and their isolated compounds. It covers their reported antioxidant, anti-inflammatory, antidiabetic, anticancer, anti-tuberculosis, antimalarial, antiviral and antileishmanial activities, as well as their potential benefits on metabolic and cardiovascular health and immune function. The review highlights the significance of the biological potential of isolated compounds, such as sugar alcohols, polysaccharides, steroids, and lanostane triterpenoids. Moreover, the review identifies under-researched areas, such as the chemical analysis of Astraeus species, which holds immense research potential. Ultimately, the review aims to inspire further research on the nutraceuticals or therapeutics of these mushrooms.

This study explored how the weight-adjusted waist index (WWI) and a body shape index (ABSI) are related to serum neurofilament light chain (sNfL) levels among U.S. adults. We aimed to evaluate sNfL, which plays key roles in neuronal injury in neurological diseases, given its understudied connection to obesity.

We used cross-sectional data from the 2013-2014 National Health and Nutrition Examination Survey (NHANES) of people with complete information on the weight-adjusted waist index (WWI), a body shape index (ABSI), and serum neurofilament light chain (sNfL). Multiple linear regression analysis allowed us to investigate the separate connections among the WWI, ABSI, and sNfL. Moreover, interaction testing and subgroup analysis were performed to improve the general validity of our results. To assess any nonlinear correlations, we also performed threshold effect analysis and smoothed curve fitting.

WWI and ABSI were positively linked with sNfL (WWI: β = 0.05, 95% CI 0.01-0.09; ABSI: β = 1.65, 95% CI 3.53-13.72). There was no clear reliance on this association according to subgroup analysis and interaction tests. Smoothed curve fitting and saturation effects also demonstrated nonlinear associations between WWI and ABSI and sNfL, with inflection points of 10.38 and 0.38, respectively.

In the adult American population, while the WWI and ABSI are linearly positively correlated with serum neurofilament light protein (sNfL), the effect size is greater for the ABSI. This correlation provides fresh evidence connecting obesity to neurological conditions, deepening our comprehension of the extensive health impacts associated with obesity. Level of Evidence Level I, experimental studies.

Background: Microbial fermentation of non-digestible carbohydrates and/or protein produces short-chain fatty acids (SCFA), whereas branched-chain fatty acids (BCFA) are produced from protein fermentation. The effects of individual SCFA and BCFA of comparable carbon chain length on adipocyte inflammation have not been investigated. Objective: To compare the effects of SCFA and BCFA on inflammatory mediator secretion in an adipocyte cell culture model designed to recapitulate obesity-associated adipocyte inflammation under normoxic and hypoxic conditions. Methods: The 3T3-L1 adipocytes were cultured (24 h) without (Control, Con) and with 1 mmol/L of SCFA (butyric acid (But) or valeric acid (Val)) or 1 mmol/L of BCFA (isobutyric acid (IsoBut) or isovaleric acid (IsoVal)) and were unstimulated (cells alone, n = 6/treatment), or stimulated with 10 ng/mL lipopolysaccharide (LPS, inflammatory stimulus, n = 8/treatment) or 10 ng/mL LPS + 100 µmol/L of the hypoxia memetic cobalt chloride (LPS/CC, inflammatory/hypoxic stimulus, n = 8/treatment). Results: Compared to Con + LPS, But + LPS reduced secreted protein levels of interleukin (IL)-1β, IL-6, macrophage chemoattractant protein (MCP)-1/chemokine ligand (CCL)2, MCP3/CCL7, macrophage inflammatory protein (MIP)-1α/CCL3 and regulated upon activation, normal T cell expressed, and secreted (RANTES)/CCL5 and decreased intracellular protein expression of the ratio of phosphorylated to total signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa B (NFκB) p65 (p < 0.05). Val + LPS reduced IL-6 secretion and increased MCP-1/CCL2 secretion compared to Con + LPS and exhibited a different inflammatory mediator secretory profile from But + LPS (p < 0.05), indicating that individual SCFA exert individual effects. There were no differences in the secretory profile of the BCFA IsoBut + LPS and IsoVal + LPS (p > 0.05). Alternatively, under inflammatory hypoxic conditions (LPS/CC) Val, IsoVal, and IsoBut all increased secretion of IL-6, MCP-1/CCL2 and MIP-1α/CCL3 compared to Con (p < 0.05), whereas mediator secretion did not differ between But and Con (p > 0.05), indicating that the proinflammatory effects of SCFA and BCFA was attenuated by But. Interestingly, But + LPS/CC decreased STAT3 activation versus Con + LPS/CC (p < 0.05). Conclusions: The decreased secretion of inflammatory mediators that is attributable to But highlights the fact that individual SCFA and BCFA exert differential effects on adipocyte inflammation under normoxic and hypoxic conditions.

Polyphenols have antioxidant and anti-inflammatory properties and maintain the immune system in balance; therefore, the aim of the study was to investigate the effect of polyphenols present in pomegranate peel extract on the spleens of rats with metabolic syndrome. The study objects were adult male Zucker Diabetic Fatty (ZDF-Leprfa/Crl, fa/fa) rats. The rats were divided into a control group (MetS) consisting of rats with metabolic syndrome and four study groups consisting of rats with metabolic syndrome (MetS + 100 mg and MetS + 200 mg) or healthy animals (H + 100 mg and H + 200 mg) receiving polyphenol extract at a dose of 100 mg or 200 mg/kg, respectively. Concentrations of IL-6, NF-κB, NFATc1, Cyt-C, TNFα, MMP-2, ROS/RNS, and MDA were measured; the activities of GPX, SOD, CAT, MMP-2, and MMP-9 were assessed; and the expression of the BAX and BCL-2 genes was evaluated in homogenized spleens. In conclusion, pomegranate extract may lead to an increase in catalase and glutathione peroxidase activity. Additionally, it may have a reducing effect on the ROS/RNS level, leading to a reduction in the activity of SOD in the MetS groups with PPE administration. Moreover, the BCL-2 gene showed lower expression in the MetS + 100 mg group compared to the H + 100 mg group, indicating that the balance between pro- and antiapoptotic factors of the BCL-2 family may be disrupted by the metabolic syndrome promoting the proapoptotic pathway.

Dietary patterns have been shown to worsen or alleviate several dermatological diseases. A well-balanced, plant-based diet is known to have anti-inflammatory, probiotic, and antioxidant properties, along with weight loss-promoting effects. Moreover, a plant-based diet has a low glycemic load, improving metabolic disease. Due to these qualities, plant-based diets may have beneficial effects on inflammatory skin conditions. In this review, we aim to discuss the possible mechanisms by which a plant-based diet reduces disease severity in psoriasis, acne, hidradenitis suppurativa, and atopic dermatitis. We also aim to clarify how a plant-based diet may influence skin healing and identify sources of vitamins, nutrients, fatty acids, and protein in a well-balanced, plant-based diet. We performed a literature search on PubMed/MEDLINE databases with the following keywords: "plant-based" OR "vegan" OR "vegetarian" OR "meat" OR "diet" AND "psoriasis" OR "hidradenitis suppurativa" OR "acne" OR "atopic dermatitis" OR "skin healing" OR "dermatology". Our findings demonstrate that plant-based foods may improve inflammatory skin diseases by supporting the gut microbiome, exerting anti-inflammatory effects, providing barrier support, and improving glycemic control. With the proper education, there is an abundance of plant-based food sources or supplements that contain riboflavin, vitamin B12, vitamin A, omega-3 fatty acids, and protein, thereby ameliorating the risk of nutritional deficiencies. Thus, a plant-based diet may have therapeutic potential in dermatology. In spite of the evidence available, there is a paucity of clinical studies focusing specifically on plant-based diets and dermatologic conditions and further investigation is warranted.

The prevalence of type 2 diabetes is increasing worldwide. Various molecular mechanisms have been proposed to interfere with the insulin signaling pathway. Recent advances in proteomics and genomics indicate that one such mechanism involves the post-transcriptional regulation of insulin signaling by microRNA (miRNA). These noncoding RNAs typically induce messenger RNA (mRNA) degradation or translational repression by interacting with the 3' untranslated region (3'UTR) of target mRNA. Dietary components and patterns, which can either enhance or impair the insulin signaling pathway, have been found to regulate miRNA expression in both in vitro and in vivo studies. This review provides an overview of the current knowledge of how dietary components influence the expression of miRNAs related to the control of the insulin signaling pathway and discusses the potential application of these findings in precision nutrition.