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Abstract Context Consuming calories later in the day is associated with obesity and metabolic syndrome. We hypothesized that eating a late dinner alters substrate metabolism during sleep in a manner that promotes obesity. Objective The objective of this work is to examine the impact of late dinner on nocturnal metabolism in healthy volunteers. Design and Setting This is a randomized crossover trial of late dinner (LD, 22:00) vs routine dinner (RD, 18:00), with a fixed sleep period (23:00-07:00) in a laboratory setting. Participants Participants comprised 20 healthy volunteers (10 male, 10 female), age 26.0 ± 0.6 years, body mass index 23.2 ± 0.7 kg/m2, accustomed to a bedtime between 22:00 and 01:00. Interventions An isocaloric macronutrient diet was administered on both visits. Dinner (35% daily kcal, 50% carbohydrate, 35% fat) with an oral lipid tracer ([2H31] palmitate, 15 mg/kg) was given at 18:00 with RD and 22:00 with LD. Main Outcome Measures Measurements included nocturnal and next-morning hourly plasma glucose, insulin, triglycerides, free fatty acids (FFAs), cortisol, dietary fatty acid oxidation, and overnight polysomnography. Results LD caused a 4-hour shift in the postprandial period, overlapping with the sleep phase. Independent of this shift, the postprandial period following LD was characterized by higher glucose, a triglyceride peak delay, and lower FFA and dietary fatty acid oxidation. LD did not affect sleep architecture, but increased plasma cortisol. These metabolic changes were most pronounced in habitual earlier sleepers determined by actigraphy monitoring. Conclusion LD induces nocturnal glucose intolerance, and reduces fatty acid oxidation and mobilization, particularly in earlier sleepers. These effects might promote obesity if they recur chronically.

In this large clinical trial, the angiotensin-receptor blocker valsartan reduced the risk of diabetes in patients with impaired glucose tolerance. However, the effect was small, and there was no reduction in the rate of cardiovascular events. Thus, impaired glucose tolerance is probably best managed with lifestyle intervention. In this large clinical trial, the angiotensin-receptor blocker valsartan reduced the risk of diabetes in patients with impaired glucose tolerance. However, the effect was small, and there was no reduction in the rate of cardiovascular events. Patients with impaired glucose tolerance have an increased risk of type 2 diabetes mellitus and cardiovascular disease. 1 – 3 Interventions that might reduce the incidence of diabetes and associated rates of death and complications from cardiovascular causes in such patients are therefore of importance. 3 Several trials have shown that lifestyle modification, including increased physical activity and weight loss, reduces the risk of diabetes, although these trials did not evaluate cardiovascular outcomes. 3 – 8 Certain drugs, including metformin, acarbose, and rosiglitazone, also reduce the incidence of diabetes, although their effect on cardiovascular events is uncertain. 6 , 9 , 10 Another pharmacologic approach to reducing the . . .

Among patients with impaired glucose tolerance, the short-acting insulin secretagogue nateglinide did not reduce the incidence of diabetes over the course of 5 years. Nateglinide also did not reduce the risk of cardiovascular events. Therefore, nateglinide does not have a place in the management of impaired glucose tolerance. Among patients with impaired glucose tolerance, the short-acting insulin secretagogue nateglinide did not reduce the incidence of diabetes over the course of 5 years. Nateglinide also did not reduce the risk of cardiovascular events. Persons with impaired glucose tolerance are at increased risk for type 2 diabetes mellitus and cardiovascular disease 1 – 3 ; therefore, treatments that might reduce the incidence of diabetes and associated cardiovascular disease and death are potentially important. 3 The risk of diabetes is reduced with lifestyle interventions that involve increasing physical activity and reducing weight 4 – 6 and with metformin, 6 acarbose, 7 or rosiglitazone 8 therapy, but no trials to date have been powered to consider cardiovascular outcomes. Among persons with type 2 diabetes, reducing glycemia results in a small reduction in the risk of major macrovascular events. 9 Glucose levels after a glucose challenge, . . .

Foxtail millet has relatively low starch digestibility and moderate glycemic index compared to other grains. Since there are still no clinical researches regarding its long-term effect on blood glucose, this self-controlled study was conducted to investigate the glucose-lowering effect of foxtail millet in free-living subjects with impaired glucose tolerance (IGT). Fifty g/day of foxtail millet was provided to enrolled subjects throughout 12 weeks and the related clinical parameters were investigated at week 0, 6 and 12, respectively. After 12 weeks of foxtail millet intervention, the mean fasting blood glucose of the subjects decreased from 5.7 ± 0.9 mmol/L to 5.3 ± 0.7 mmol/L (p < 0.001) and the mean 2 h-glucose decreased from 10.2 ± 2.6 mmol/L to 9.4 ± 2.3 mmol/L (p = 0.003). The intake of foxtail millet caused a significant increase of serum leptin (p = 0.012), decrease of insulin resistance (p = 0.007), and marginal reduction of inflammation. Furthermore, a sex-dependent difference in glucose-lowering effect of foxtail millet was observed in this study. Foxtail millet could improve the glycemic control in free-living subjects with IGT, suggesting that increasing the consumption of foxtail millet might be beneficial to individuals suffering from type 2 diabetes mellitus.

In this study with a 2-by-2 factorial design, patients with cardiovascular risk factors and dysglycemia or type 2 diabetes received insulin glargine or standard care. Insulin treatment did not affect cardiovascular events, the primary outcome. An elevated fasting plasma glucose level is an independent risk factor for adverse cardiovascular outcomes. 1 – 7 Basal insulin secretion is required to maintain fasting plasma glucose levels below 100 mg per deciliter (5.6 mmol per liter), and an elevated fasting plasma glucose level indicates that there is insufficient endogenous insulin secretion to overcome underlying insulin resistance. 8 , 9 The correction of this deficiency may reduce cardiovascular outcomes. Such a possibility has not been formally tested; however, large outcomes trials of more versus less intense glucose lowering in which insulin was used in both study groups have not shown a clear cardiovascular . . .

The anti-hyperglycemic effect of metformin is believed to be caused by its direct action on signaling processes in hepatocytes, leading to lower hepatic gluconeogenesis. Recently, metformin was reported to alter the gut microbiota community in humans, suggesting that the hyperglycemia-lowering action of the drug could be the result of modulating the population of gut microbiota. However, the critical microbial signaling metabolites and the host targets associated with the metabolic benefits of metformin remained elusive. Here, we performed metagenomic and metabolomic analysis of samples from individuals with newly diagnosed type 2 diabetes (T2D) naively treated with metformin for 3 d, which revealed that Bacteroides fragilis was decreased and the bile acid glycoursodeoxycholic acid (GUDCA) was increased in the gut. These changes were accompanied by inhibition of intestinal farnesoid X receptor (FXR) signaling. We further found that high-fat-diet (HFD)-fed mice colonized with B. fragilis were predisposed to more severe glucose intolerance, and the metabolic benefits of metformin treatment on glucose intolerance were abrogated. GUDCA was further identified as an intestinal FXR antagonist that improved various metabolic endpoints in mice with established obesity. Thus, we conclude that metformin acts in part through a B. fragilis –GUDCA–intestinal FXR axis to improve metabolic dysfunction, including hyperglycemia. Metformin decreases the levels of Bacteroides fragilis while increasing the bile acid GUDCA to antagonize intestinal FXR and improves the metabolic health of humans and mice.

In a 2-by-2 factorial design, participants without cardiovascular disease but with impaired fasting glucose levels or impaired glucose tolerance received ramipril or placebo (with or without rosiglitazone) for a median of 3 years. The results suggest that ACE inhibitors may modestly improve glucose metabolism, though ramipril failed to change the rate of death or newly diagnosed diabetes. ACE inhibitors may modestly improve glucose metabolism, though ramipril failed to change the rate of death or newly diagnosed diabetes. Diabetes, ranked as the fifth leading cause of death worldwide, is a major risk factor for various cardiovascular and renal disorders. 1 The prevalence of diabetes is increasing, which in turn increases the risk of premature cardiovascular disease and death. 2 Therefore, strategies to reduce the incidence of diabetes are needed. Physical activity, weight loss, 3 , 4 and some glucose-lowering agents 4 , 5 reduce the incidence of diabetes in people with elevated glucose levels that are just below the diagnostic threshold for diabetes. Several trials involving people with hypertension or cardiovascular disease have suggested that agents that block or inhibit the renin–angiotensin system may . . .

Context: The effects of energy-balanced bed rest on metabolic flexibility have not been thoroughly examined.Objective: We investigated the effects of 21 days of bed rest, with and without whey protein supplementation, on metabolic flexibility while maintaining energy balance. We hypothesized that protein supplementation mitigates metabolic inflexibility by preventing muscle atrophy.Design and Setting: Randomized crossover longitudinal study conducted at the German Aerospace Center, Cologne, Germany.Participants and Interventions: Ten healthy men were randomly assigned to dietary counter-measure or isocaloric control diet during a 21-day bed rest.Outcome Measures: Before and at the end of the bed rest, metabolic flexibility was assessed during a meal test. Secondary outcomes were glucose tolerance by oral glucose tolerance test, body composition by dual energy X-ray absorptiometry, ectopic fat storage by magnetic resonance imaging, and inflammation and oxidative stress markers.Results: Bed rest decreased the ability to switch from fat to carbohydrate oxidation when transitioning from fasted to fed states (i.e., metabolic inflexibility), antioxidant capacity, fat-free mass FFM), and muscle insulin sensitivity along with greater fat deposition in muscle (P < 0.05 for all). Changes in fasting insulin and inflammation were not observed. However, glucose tolerance was reduced during acute overfeeding. Protein supplementation did not prevent FFM loss and metabolic alterations.Conclusions: Physical inactivity triggers metabolic inflexibility, even when energy balance is maintained. Although reduced insulin sensitivity and increased fat deposition were observed at the muscle level, systemic glucose intolerance was detected only in response to a moderately high-fat meal. This finding supports the role of physical inactivity in metabolic inflexibility and suggests that metabolic inflexibility precedes systemic glucose intolerance.

The aim of the study was to find out whether participation in earlier intervention had an effect on the occurrence of retinopathy in study participants. We also examined risk factors (age, sex, weight, fasting and 2 h glucose, fasting insulin, blood pressure, serum lipids) for early retinal changes. The study included 522 individuals (mean 55 years old, range 40–64 years) with impaired glucose tolerance who were randomized into intervention (weight loss, healthy diet, and physical activity, N = 265) and control groups (N = 257). Intervention lasted for median of four years in 1993–2000, after which annual follow-up visits at study clinics were conducted. In the years 2002–2006 (at least five years after stopping intervention), fundus photography was offered for all study participants in four of five study clinics. Photographs were assessed by two experienced ophthalmologists (A.A. and K.K.), masked for the group assignment. After exclusion of poor quality photographs, the data of 211 individuals (N = 113 for intervention and N = 98 for control group) were included in the present study. The occurrence of microaneurysms was significantly higher in the control (37/98, 38%) than in the intervention group (27/113, 24%; p = 0.029). In the model, including age, sex, diabetes diagnosis before the retinal assessment, body mass index (BMI), and treatment group, the odds ratio for microaneurysms was markedly lower in intervention group (OR 0.52; 0.28–0.97, p = 0.039). The only risk factor that predicted the occurrence of microaneurysms was serum triglycerides at baseline (mean ± SD 1.9 ± 0.9 vs. 1.6 ± 0.7, mmol/L, with and without microaneurysms, respectively, p = 0.003). Triglycerides associated with decreased microaneurysms in regression analysis for age, sex, fasting glucose, and intervention group (OR 1.92, p = 0.018). Lifestyle intervention in overweight and obese individuals with impaired glucose tolerance showed decreased occurrence of retinal microaneurysms. Elevated serum triglycerides were associated to the development of early diabetic microangiopathy.

AbstractObjectiveTo assess the prevalence of diabetes and its risk factors.DesignPopulation based, cross sectional study.Setting31 provinces in mainland China with nationally representative cross sectional data from 2015 to 2017.Participants75 880 participants aged 18 and older—a nationally representative sample of the mainland Chinese population.Main outcome measuresPrevalence of diabetes among adults living in China, and the prevalence by sex, regions, and ethnic groups, estimated by the 2018 American Diabetes Association (ADA) and the World Health Organization diagnostic criteria. Demographic characteristics, lifestyle, and history of disease were recorded by participants on a questionnaire. Anthropometric and clinical assessments were made of serum concentrations of fasting plasma glucose (one measurement), two hour plasma glucose, and glycated haemoglobin (HbA1c).ResultsThe weighted prevalence of total diabetes (n=9772), self-reported diabetes (n=4464), newly diagnosed diabetes (n=5308), and prediabetes (n=27 230) diagnosed by the ADA criteria were 12.8% (95% confidence interval 12.0% to 13.6%), 6.0% (5.4% to 6.7%), 6.8% (6.1% to 7.4%), and 35.2% (33.5% to 37.0%), respectively, among adults living in China. The weighted prevalence of total diabetes was higher among adults aged 50 and older and among men. The prevalence of total diabetes in 31 provinces ranged from 6.2% in Guizhou to 19.9% in Inner Mongolia. Han ethnicity had the highest prevalence of diabetes (12.8%) and Hui ethnicity had the lowest (6.3%) among five investigated ethnicities. The weighted prevalence of total diabetes (n=8385) using the WHO criteria was 11.2% (95% confidence interval 10.5% to 11.9%).ConclusionThe prevalence of diabetes has increased slightly from 2007 to 2017 among adults living in China. The findings indicate that diabetes is an important public health problem in China.