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ObjectivesObesity is a risk factor for type 2 diabetes mellitus. Among obesity, visceral fat obesity, and ectopic fat obesity, it has been unclear which has the greatest effect on incident diabetes.MethodsIn this historical cohort study of 8430 men and 7034 women, we investigated the effect of obesity phenotypes on incident diabetes. Obesity, visceral fat obesity, and ectopic fat obesity were defined as body mass index ≥25 kg/m2, waist circumference ≥90 cm in men or ≥80 cm in women, and having fatty liver diagnosed by abdominal ultrasonography, respectively. We divided the participants into eight groups according to the presence or absence of the three obesity phenotypes.ResultsDuring the median 5.8 years follow-up for men and 5.1 years follow-up for women, 286 men and 87 women developed diabetes. Compared to the non-obese group, the hazard ratios (HRs) of incident diabetes in the only-obesity, only-visceral fat obesity, only-ectopic fat obesity groups, and with all-three types of obesity group were 1.85 (95%CI 1.06–3.26, p = 0.05) in men and 1.79 (0.24–13.21, p = 0.60) in women, 3.41 (2.51–4.64, p < 0.001) in men and 2.30 (0.87–6.05, p = 0.12) in women, 4.74 (1.91–11.70, p < 0.001) in men and 13.99 (7.23–27.09, p < 0.001) in women and 10.5 (8.02–13.8, p < 0.001) in men and 30.0 (18.0–50.0, p < 0.001) in women. Moreover, the risk of incident diabetes of the groups with ectopic fat obesity were almost higher than that of the four groups without ectopic fat obesity.ConclusionEctopic fat obesity presented the greatest risk of incident type 2 diabetes.

The number of patients with type 2 diabetes mellitus is increasing, and its prevention and management are important. One of the factors contributing to the increased incidence of type 2 diabetes mellitus is the change in dietary habits, including a Westernized diet. Fermented foods are foods that are transformed by the action of microorganisms to produce beneficial effects in humans and have been consumed for thousands of years. The production and consumption of fermented soy foods, including natto, miso, douchi, cheonggukjang, doenjang, tempeh, and fermented soy milk, are widespread in Asian countries. This review focuses on fermented soybean foods and summarizes their effects on diabetes. Fermentation increases the content of ingredients originally contained in soybeans and adds new ingredients that are not present in the original soybeans. Recent studies have revealed that fermented soybean food modifies the gut microbiota‐related metabolites by modifying dysbiosis. Furthermore, it has been reported that fermented soybean foods have antioxidant, anti‐inflammatory, and anti‐diabetic effects. In recent years, fermented foods, including fermented soybeans, have shown various beneficial effects. Therefore, it is necessary to continue focusing on the benefits and mechanisms of action of fermented foods. The number of patients with type 2 diabetes mellitus is increasing, and its prevention and management are important. Fermented soybean food modifies the gut microbiota‐related metabolites by modifying dysbiosis. Fermented soybean foods also have antioxidant, anti‐inflammatory, and anti‐diabetic effects.

Background Previous studies have investigated the association between the ratio of triglycerides (TG) to high-density lipoprotein cholesterol (HDL-C) and the incidence of diabetes in adults and discovered that a high TG/HDL-C ratio was linked to an elevated risk of new-onset diabetes. However, the comparison of predicting diabetes development among lipid profiles including the TG/HDL-C ratio, and the ratio of TG/HDL-C cut-off value has received limited attention. We examined the relationship between diabetes onset and the TG/HDL-C ratio in addition to the applicable cut-off value for predicting diabetes onset. Methods This study included 120,613 participants from the health examination database at Panasonic Corporation from 2008 to 2017. Cox regression analysis employing multivariable models was used to investigate the association between lipid profiles, particularly the ratio of TG/HDL-C and the development of type 2 diabetes (T2D). The multivariable model was adjusted for age, sex, BMI, systolic blood pressure, plasma glucose levels after fasting, smoking status, and exercise habits. Areas under time-dependent receiver operating characteristic (ROC) curves (AUCs) were employed to assess the prediction performance and cut-off values of each indicator. A fasting plasma glucose level of 126 mg/dL, a self-reported history of diabetes, or usage of antidiabetic medicines were used to identify T2D. Results During the course of the study, 6,080 people developed T2D. The median follow-up duration was 6.0 (3–10) years. Multivariable analysis revealed that the ratio of TG/HDL-C (per unit, HR; 1.03 [95% CI 1.02–1.03]) was substantially linked to the risk of incident T2D. AUC and cut-off points for the ratio of TG/HDL-C for T2D development after 10 years were 0.679 and 2.1, respectively. Furthermore, the AUC of the ratio of TG/HDL-C was considerably larger compared to that of LDL-C, HDL-C, and TG alone (all P < 0.001). We discovered an interaction effect between sex, BMI, and lipid profiles in subgroup analysis. Females and participants having a BMI of < 25 kg/m 2 showed a higher correlation between lipid profile levels and T2D onset. Conclusions The ratio of TG/HDL-C was found to be a stronger predictor of T2D development within 10 years than LDL-C, HDL-C, or TG, indicating that it may be useful in future medical treatment support.

Nonalcoholic steatohepatitis (NASH) is a progressive disorder with aberrant lipid accumulation and subsequent inflammatory and profibrotic response. Therapeutic efforts at lipid reduction via increasing cytoplasmic lipolysis unfortunately worsens hepatitis due to toxicity of liberated fatty acid. An alternative approach could be lipid reduction through autophagic disposal, i.e., lipophagy. We engineered a synthetic adaptor protein to induce lipophagy, combining a lipid droplet-targeting signal with optimized LC3-interacting domain. Activating hepatocyte lipophagy in vivo strongly mitigated both steatosis and hepatitis in a diet-induced mouse NASH model. Mechanistically, activated lipophagy promoted the excretion of lipid from hepatocytes, thereby suppressing harmful intracellular accumulation of nonesterified fatty acid. A high-content compound screen identified alpelisib and digoxin, clinically-approved compounds, as effective activators of lipophagy. Administration of alpelisib or digoxin in vivo strongly inhibited the transition to steatohepatitis. These data thus identify lipophagy as a promising therapeutic approach to prevent NASH progression. Nonalcoholic steatohepatitis (NASH) starts with lipid droplet accumulation in the liver that eventually causes inflammation and fibrosis. Here, authors use lipophagy activators to limit the accumulation of lipids in the liver and show that this can prevent disease progression in a mouse model of nonalcoholic steatohepatitis.

Microplastics (MPs) are small particles of plastic ( in diameter). In recent years, oral exposure to MPs in living organisms has been a cause of concern. Leaky gut syndrome (LGS), associated with a high-fat diet (HFD) in mice, can increase the entry of foreign substances into the body through the intestinal mucosa. We aimed to evaluate the pathophysiology of intestinal outcomes associated with consuming a high-fat diet and simultaneous intake of MPs, focusing on endocrine and metabolic systems. C57BL6/J mice were fed a normal diet (ND) or HFD with or without polystyrene MP for 4 wk to investigate differences in glucose tolerance, intestinal permeability, gut microbiota, as well as metabolites in serum, feces, and liver. In comparison with HFD mice, mice fed the HFD with MPs had higher blood glucose, serum lipid concentrations, and nonalcoholic fatty liver disease (NAFLD) activity scores. Permeability and goblet cell count of the small intestine (SI) in HFD-fed mice were higher and lower, respectively, than in ND-fed mice. There was no obvious difference in the number of inflammatory cells in the SI lamina propria between mice fed the ND and mice fed the ND with MP, but there were more inflammatory cells and fewer anti-inflammatory cells in mice fed the HFD with MPs in comparison with mice fed the HFD without MPs. The expression of genes related to inflammation, long-chain fatty acid transporter, and cotransporter was significantly higher in mice fed the HFD with MPs than in mice fed the HFD without MPs. Furthermore, the genus was significantly more abundant in the intestines of mice fed the HFD with MPs in comparison with mice fed the HFD without MPs. gene expression was decreased when palmitic acid and microplastics were added to the murine intestinal epithelial cell line MODE-K cells, and Muc2 gene expression was increased when IL-22 was added. Our findings suggest that in this study, MP induced metabolic disturbances, such as diabetes and NAFLD, only in mice fed a high-fat diet. These findings suggest that LGS might have been triggered by HFD, causing MPs to be deposited in the intestinal mucosa, resulting in inflammation of the intestinal mucosal intrinsic layer and thereby altering nutrient absorption. These results highlight the need for reducing oral exposure to MPs through remedial environmental measures to improve metabolic disturbance under high-fat diet conditions. https://doi.org/10.1289/EHP11072.

Background. The triglyceride and glucose index (TyG), defined as the product of triglycerides (TG) and fasting plasma glucose (FPG), is reported as a surrogate index for insulin resistance. Although a cross-sectional study revealed the association between the TyG-index and the prevalence of nonalcoholic fatty liver disease (NAFLD), few studies have investigated the association between the TyG-index and incident NAFLD. Here we investigated whether the TyG-index can be used to predict incident NAFLD. Methods. This historical cohort study included 16,093 apparently healthy Japanese individuals. The TyG-index was calculated by the established formula: TyG = Ln [TG (mg/dl) × FPG (mg/dl)/2]. Fatty liver was diagnosed based on the subjects’ abdominal ultrasonography results. We divided the subjects into tertiles according to the levels of TyG-index. Hazard ratios (HRs) of the TyG-index for incident NAFLD were calculated by a Cox proportional hazards regression model. Results. During the observation period, 27.4% of the men and 11.0% of the women developed NAFLD. The highest TyG-index tertile (men, 8.48 ≤ TyG and women, 7.97 ≤ TyG) (adjusted HR 1.67, 95% CI 1.44–1.94, p<0.001 in the men and 2.06, 1.59–2.70, p<0.001 in the women) and the middle TyG-index tertile (men, 8.00 < TyG ≤ 8.48 and women, 7.53 

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