The hemoglobin glycation index (HGI) represents the discrepancy between the glucose management indicator (GMI) based on mean blood glucose levels and laboratory values of glycated hemoglobin (HbA1c). The HGI is a promising indicator for identifying individuals with excessive glycosylation, facilitating personalized evaluation and prediction of diabetic complications. However, the factors influencing the HGI in patients with type 1 diabetes (T1D) remain unclear. Autoimmune destruction of pancreatic β cells is central in T1D pathogenesis, yet insulin resistance can also be a feature of patients with T1D and their coexistence is called "double diabetes" (DD). However, knowledge regarding the relationship between DD features and the HGI in T1D is limited.

To assess the association between the HGI and DD features in adults with T1D.

A total of 83 patients with T1D were recruited for this cross-sectional study. Laboratory HbA1c and GMI from continuous glucose monitoring data were collected to calculate the HGI. DD features included a family history of type 2 diabetes, overweight/obesity/central adiposity, hypertension, atherogenic dyslipidemia, an abnormal percentage of body fat (PBF) and/or visceral fat area (VFA) and decreased estimated insulin sensitivity. Skin autofluorescence of advanced glycation end products (SAF-AGEs), diabetic complications, and DD features were assessed, and their association with the HGI was analyzed.

A discrepancy was observed between HbA1c and GMI among patients with T1D and DD. A higher HGI was associated with an increased number of SAF-AGEs and a higher prevalence of diabetic microangiopathy (P = 0.030), particularly retinopathy (P = 0.031). Patients with three or more DD features exhibited an eight-fold increased risk of having a high HGI, compared with those without DD features (adjusted odds ratio = 8.12; 95% confidence interval: 1.52-43.47). Specifically, an elevated PBF and/or VFA and decreased estimated insulin sensitivity were associated with high HGI. Regression analysis identified estimated insulin sensitivity and VFA as factors independently associated with HGI.

In patients with T1D, DD features are associated with a higher HGI, which represents a trend toward excessive glycosylation and is associated with a higher prevalence of chronic diabetic complications.

Obesity, accumulation of adipose tissue, is a global disease that can lead to cardiovascular and metabolic complications. The aim of this study was to investigate the relationship between obesity indicators and metabolic risk factors in type 2 diabetes mellitus (T2DM) patients.

A total of 337 T2DM subjects were included in our study. The metabolic risk factors including diabetes duration, fast plasma glucose (FPG), height, weight, systolic blood pressure (SBP), diastolic blood pressure (DBP), estimated average glucose (eAG), glycated hemoglobin (HbA1c), total cholesterol (TC), high-density lipoprotein-cholesterol (HDL-c), low-density lipoprotein-cholesterol (LDL-c), triglyceride (TG), blood urea nitrogen (BUN), serum creatinine (Scr), free fatty acid (FFA), uric acid (UA), cystatin c (cysc), albumin (Alb), urinary albumin creatinine ratio (UACR) were recorded. The obesity indicators included body surface area (BSA), body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), para-perirenal fat thickness (PRFT), total abdominal fat (TAF), subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT). The association between obesity indicators and metabolic risk factors was investigated by univariate and multivariate analysis.

HDL-c was independently associated with WHR and PRFT (β = -0.126 vs. -0.214, both p < 0.05). TG and Scr were both independently associated with PRFT (β = 0.173 vs. 0.218, both p < 0.01, respectively). UA was independently associated with BSA (β = 0.172, p < 0.01) and PRFT (β = 0.151, p < 0.01). cysc, Alb and UACR were independently associated with WC (β = 0.274 vs. 0.204 vs. 0.182, all p < 0.01).

In T2DM patients, obesity indicators were significantly associated with metabolic risk factors.

Although gout is one of the most common rheumatic diseases, world data are lacking because most studies have focused on industrialized countries. Therefore, we aimed to investigate the global burden of gout and its associations with the year of diagnosis, age, geographical region, sociodemographic status and various further risk factors.

Retrospective data from the Global Burden of Disease (GBD) were used, initially collected between 1990 and 2019. Raw numbers and age-standardized rates (per 100,000 persons) of prevalence, incidence and years lived with disability (YLDs) of gout were extracted from GBD 2019 for 204 countries and territories and stratified by sex, age, year, sociodemographic index and geographic region. Correlations between gout and other chronic diseases were identified, and the burden attributable to high body mass index (BMI) and kidney dysfunction was described.

The total number of patients and gout age-standardized prevalence rate increased between 1990 and 2019. Gout was most prevalent in Australasia and high-income North America, and a higher sociodemographic index (SDI) was associated with higher age-standardized prevalence, incidence and YLDs. High BMI and kidney dysfunction were risk factors for gout, while gout was correlated with other kidney diseases.

The global prevalence of gout, as well as incidence, and YLDs increased worldwide from 1990 to 2019 and had a significant association with sex, age, geographic region, SDI and risk factors. Understanding the complex interplay of environmental, sociodemographic and geographic risk factors is essential in mitigating the ever-rising disease burden of gout.

Visceral fat has been considered an important risk factor of elevated serum uric acid (SUA). Perirenal fat is a unique visceral fat around the kidneys that has special morphological and physiological features while its relationship with SUA remains incompletely elucidated. This study aimed to assess the association between perirenal fat volume (PrFV) and SUA.

A cross-sectional study was conducted in 102 subjects aged ≥ 18 years old recruited from Nanjing,China. The clinical characteristics including age, sex, drinking behavior, history of hypertension, body mass index, waist circumference, total cholesterol, fast plasma glucose, urea, serum creatinine, C-reactive protein, and SUA were recorded. PrFV was measured by ultrasonography. Multivariate linear models and the restricted cubic spline were used to investigate the association between PrFV and SUA.

The median age of this study population was 52.5 (42.0-60.0) years and 56.9% were female. The median value of SUA was 5.73 mg/dL (4.58-6.80 mg/dL). The subjects were divided by PrFV tertiles and we found that the subjects in the highest PrFV tertile had a higher level of SUA compared to those in the lowest tertile (β=1.86, 95%CI 1.23-2.48, P for trend <0.001).The positive association also remained after adjustment for potential covariates (tertile3 versus tertile1: β=0.99, 95%CI 0.35-1.63, P for trend =0.005). There was an increase of approximately 0.53 mg/dL in SUA per 1-fold increase in PrFV (β=0.53, 95%CI 0.02-1.04, P for nonlinearity = 0.637).

Our results confirmed a positive independent relationship between PrFV and SUA in Chinese adults. This study suggested that perirenal fat might constitute a potential risk factor for elevated serum uric acid levels.

Morbidity of hyperuricemia has constantly increased in population in decades, and hyperuricemia has proved to be an important risk factor for gout, cardiovascular diseases and others. Many urate-lowering drugs have unfavorable side effects and drug interactions. Quzhuotongbi decoction (QZTBD) is an empirical traditional Chinese medicine prescription for clinical therapy of hyperuricemia without serious adverse effects. In the study, we investigated the effects of QZTBD on urate and other metabolites in the sera of hyperuricemia model rats. Hyperuricemia model was established by orally administering yeast extract paste, and allopurinol served as a positive control drug. Serum metabolomics was performed by using a gas chromatography-mass spectrometry (GC-MS) method. Student's t-test and the principal component analysis (PCA) were employed to find the metabolic perturbations in hyperuricemia model rats. The levels of urate, lactate, pyruvate and ornithine were significantly increased, and xanthine, glyconic acids (ribonate, galactonate), amino acids (aspartate, proline, glutamine, serine, pyroglutamate, glutamate) and glucose were down-regulated greatly in the model rats. It demonstrated that nucleotide metabolism, amino acid metabolism and glycolytic pathway were disturbed by yeast administration. An orthogonal signal correction-partial least-squares discriminant analysis (OSC-PLS DA) was performed to assess the effects of yeast administering and drug treatment. 11 significantly distinctive metabolites among four groups were defined according to the variable importance for project values (VIP>1) and univariate ANOVA (p value<0.05). As compared to the model rats, the serum uric acid levels were lowered markedly under the treatment of allopurinol or QZTBD. Aspartate and glutamine involved in purine metabolism, were raised to normal level as well. The different influences on xanthine, glutamate pyroglutamate and galactonate suggested there were different mechanisms of two drugs in urate-lowering therapy. Our finding proved that QZTBD can efficiently lower the level of serum uric acid in a different way from allopurinol, which suggested that QZTBD based on the theory of TCM could be an effective therapeutic option for hyperuricemia.

Gout patients are frequently complicated with hypertension, obesity, dyslipidemia, and/or impaired glucose tolerance, which are components of the metabolic syndrome and risks for atherosclerotic diseases.

To determine the relationship between metabolic syndrome and gout, as well as plasma concentrations of adipocytokines in gout patients.

The frequency of metabolic syndrome as well as its constituents were investigated in 258 male gout patients and 111 males who attended an annual check-up examination. In addition, plasma concentrations of adipocytokines were measured in 107 of the patients.

Gout patients had a higher prevalence of metabolic syndrome as compared with the controls (36.4% vs. 15.3%, P < 0.0001). In addition, frequencies of individual metabolic abnormalities, such as waist circumference >85 cm, hypertension, and hypertriglyceridemia, were significantly increased in the gout patients as compared with the controls. Furthermore, uric acid over-production gout had a significantly higher prevalence of metabolic syndrome as compared with uric acid under-excretion gout (48.6% vs. 32.4%, P < 0.001). The plasma concentrations of leptin and plasminogen activator inhibitor-1 were significantly higher in the patients (P < 0.05, respectively), while that of adiponectin and the adiponectin/leptin ratio were significantly decreased in the gout patients as compared with the controls (P < 0.05, respectively).

A higher prevalence of metabolic syndrome in gout patients may in part contribute to susceptibility to atherosclerotic diseases. Therefore, more attention should be paid to the presence of metabolic syndrome in gout patients to reduce their risk for cardiovascular disease complications.

We investigated the relationship between serum uric acid (SUA) and body fat area, serum lipid level, insulin resistance, and metabolic syndrome in Japanese men.

We studied 508 Japanese man industrial workers who underwent an annual medical examination and agreed to participate in the CT scanning examination. Body fat area was measured at the umbilical level. Metabolic syndrome was defined by the presence of visceral fat Accumulation (> or = 100 cm2) accompanied by two or more disorders; dyslipidemia, hypertension, and hyperglycemia.

SUA was positively correlated with visceral fat area, subcutaneous fat area, serum total cholesterol level, serum triglyceride level, the Homeostasis Model Assessment index, and was negatively correlated with the high-density lipoprotein cholesterol level. In multiple regression analysis, the most influential factor for SUA was visceral fat area (p=0.0027), followed by the serum triglyceride level (p=0.0245). We clarified a higher SUA in the metabolic syndrome group as compared with the non-metabolic syndrome group: 6.67+/-1.14 mg, 6.09+/-1.14 mg, respectively (p<0.0001). The median SUA was elevated with increasing metabolic syndrome factors (p<0.0001).

The present study indicated that SUA is related to visceral fat accumulation. Patients with metabolic syndrome revealed a higher SUA.

Data with regard to serum uric acid levels in HIV-infected subjects are scarce. A high prevalence of hyperuricaemia was identified in a prospective analysis of urate levels in 2287 visits made by a cohort of 270 HIV-positive patients. In univariate and multivariate analysis, hyperuricaemia was associated with factors previously identified in HIV-uninfected individuals, but also with the use of some antiretroviral drugs, particularly with the use of stavudine.

The accumulation of risk factors for central retinal artery occlusion can be seen in a single person and might be explained by the metabolic syndrome.

We presented the case of a 52-year-old man with no light perception in his right eye. The visual loss was monocular and painless, fundoscopy showed central retinal artery occlusion and the laboratory investigation showed the raised erythrocyte sedimentation rate of 105 mm/h and the raised C-reactive protein of 22 mg/l. Specific laboratory investigations and fluorescein angiography excluded the presence of vasculitis, collagen vascular diseases, hypercoagulable state and antiphospholipid syndrome.

The patient met all the five of the National Cholesterol Education Program (NCEP) criteria for the metabolic syndrome: hypertension, abnormal lipid profile, abnormal glucose metabolism, obesity and hyperuricemia. Measurement of C-reactive protein is useful for the assessment of therapeutic systemic effect on any abnormality in the metabolic syndrome. Individual therapy for all risk factors in the metabolic syndrome is necessary to prevent complications such as cardiovascular, retinal vascular diseases and stroke.

The world is increasingly threatened by a global epidemic of chronic diseases. Almost half of the global morbidity and almost two thirds of global mortality is due to these diseases-approximately 35 million die each year from chronic diseases. And they continue to increase. Increasing evidence suggest that these diseases are associated with lifestyle, stress, lack of physical exercise, over-consumption of calorie-condensed foods rich in saturated fat, sugar and starch, but also under-consumption of antioxidant-rich fruits and vegetables. As a result the function of the innate immune system is severe impaired. This review discusses the changes induced in response to mental and physical stress and their association with the subsequent development of metabolic syndrome, and its association with various chronic diseases. The endothelial cells and their function appears to be of great importance, and the function of their cellular membranes of special importance to the function of the underlying cells; their ability to obtain nutrients and antioxidants and to eliminate waste products. The abdominal adipocytes seen to play a key role, as they have the ability to in stressful situations release much of proinflammatory cytokines, PAI-1 and free fatty acids compared to elsewhere in the body. The load on the liver of these various substances in often of greater magnitude than the liver can handle. Some of the most common chronic diseases and their potential association with acute and "chronic" phase response, and with metabolic syndrome are discussed separately. The need for studies with lifestyle modifications is especially emphasized.

There are many factors that contribute to hyperuricemia, including obesity, insulin resistance, alcohol consumption, diuretic use, hypertension, renal insufficiency, genetic makeup, etc. Of these, alcohol (ethanol) is the most important. Ethanol enhances adenine nucleotide degradation and increases lactic acid level in blood, leading to hyperuricemia. In beer, purines also contribute to an increase in plasma uric acid. Although rare, dehydration and ketoacidosis (due to ethanol ingestion) are associated with the ethanol-induced increase in serum uric acid levels. Ethanol also increases the plasma concentrations and urinary excretion of hypoxanthine and xanthine via the acceleration of adenine nucleotide degradation and a possible weak inhibition of xanthine dehydrogenase activity. Since many factors such as the ALDH2*1 gene and ADH2*2 gene, daily drinking habits, exercise, and dehydration enhance the increase in plasma concentration of uric acid induced by ethanol, it is important to pay attention to these factors, as well as ingested ethanol volume, type of alcoholic beverage, and the administration of anti-hyperuricemic agents, to prevent and treat ethanol-induced hyperuricemia.

To evaluate the effect of weight reduction on parameters of the metabolic syndrome in obese patients according to their pattern of abdominal fat distribution.

A longitudinal intervention study, consisting of a 12-week weight reduction programme, including lifestyle modification and adjuvant appetite suppressant, in 38 subjects with visceral obesity and 47 subjects with subcutaneous obesity. Visceral, subcutaneous and total adipose tissue areas were determined by CT scan at the level of L4-L5. Parameters for components of the metabolic syndrome were measured before and after weight reduction.

Reductions in body weight, BMI and subcutaneous adipose tissue area were greater in the subcutaneous than in the visceral obesity group. In contrast, changes in fasting plasma glucose, insulin, and HOMA score were higher in the visceral than in the subcutaneous obesity group. Changes in visceral adipose tissue area were significantly related to changes in fasting plasma glucose, triglycerides and HOMA score.

Visceral fat reduction induced greater beneficial effects on parameters of the metabolic syndrome than subcutaneous fat reduction. Evaluation of changes in abdominal fat distribution is necessary when obese subjects enter a weight reduction programme.

Uric acid is a strong scavenger of reactive oxygen species, which are known to contribute to the development of atherosclerosis, while the incidence of atherosclerotic diseases is rather high in patients with gout. Among the established risk factors for atherosclerosis, oxidized LDL is believed to play a major role in its development and progression. Allopurinol and its active metabolite, oxypurinol, have been suggested to possess an antioxidant ability to scavenge the hydroxyl radical. Therefore, allopurinol may be beneficial in the prevention of LDL oxidation, as well as in the treatment of hyperuricemia. The objective of this work was to determine the degree of LDL oxidation in gout and the effect of allopurinol on LDL oxidation.

Age-matched male patients with primary intercritical gout and healthy male adults were included in the study. The serum concentrations of oxidized LDL autoantibodies and total antioxidant status were measured using an enzyme immunoassay.

Serum concentrations of oxidized LDL autoantibodies were significantly higher in patients with gout than the control subjects (p < 0.05) and were significantly decreased after allopurinol treatment (p < 0.05), but not by benzbromarone treatment, in spite of the similar concentrations of uric acid and total antioxidant status in serum following their separate administration.

Although the exact mechanism remains unclear, increased serum concentrations of oxidized LDL may play a role in the high incidence of coronary artery disease in gout. In addition, allopurinol may be more preferable to benzbromarone for treatment of gout in light of its inhibitory action toward LDL oxidation.

To assess the effect of a combination treatment using anti-hyperuricaemic agents with fenofibrate and/or losartan on uric acid metabolism in hypertriglyceridaemic and/or hypertensive patients with gout.

Twenty seven patients with gout were included in a fenofibrate plus anti-hyperuricaemic agents combination study, and 25 in a losartan plus anti-hyperuricaemic agents combination study. Serum uric acid concentration, uric acid clearance, and 24 hour urinary uric acid excretion were measured before and two months after the addition of fenofibrate (300 mg once daily) or losartan (50 mg once daily) to anti-hyperuricaemic agents.

Combination therapy of fenofibrate or losartan with anti-hyperuricaemic agents, which included benzbromarone (50 mg once daily) or allopurinol (200 mg twice a day), significantly reduced serum uric acid concentrations in accordance with increased uric acid excretion.

A combination of fenofibrate or losartan with anti-hyperuricaemic agents is a good option for the treatment of gout patients with hypertriglyceridaemia and/or hypertension, though the additional hypouricaemic effect may be modest.

Gout continues to be a health problem around the world despite the availability of effective therapies. Although the prevalence is influenced by genetic factors, the associations of alcohol consumption, obesity, and hypertension appear to be partially responsible for the increased prevalence of gout and hyperuricemia in African and Oriental countries. The association between hyperuricemia and cardiovascular disease seems linked to insulin resistance. This relation, in part, explains the common coexistence of hyperlipidemia and glucose intolerance in patients with gout. Accordingly, it is recommended that one pay more attention to dietary manipulation in patients with gout in addition to managing hypertension, obesity, and other medical problems. Although acute gout attacks can be treated, eliminating gout requires effective removal of urate from the body. Allopurinol remains a dominant urate-lowering agent, however its use may be limited by allergic reactions. Uricosuric agents are also effective urate-lowering agents and provide an alternative to allopurinol. Strategies to treat patients who are sensitive to allopurinol continue to evolve.