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Global rates of obesity and Type 2 diabetes mellitus (T2DM) are increasing globally concomitant with a rising prevalence of sleep deprivation and sleep disorders. Understanding the links between sleep, obesity and T2DM might offer an opportunity to develop better prevention and treatment strategies for these epidemics. Experimental studies have shown that sleep restriction is associated with changes in energy homeostasis, insulin resistance and β-cell function. Epidemiological cohort studies established short sleep duration as a risk factor for developing obesity and T2DM. In addition, small studies suggested that short sleep duration was associated less weight loss following lifestyle interventions or bariatric surgery. In this article, we review the epidemiological evidence linking sleep duration to obesity and T2DM and plausible mechanisms. In addition, we review the impact of changes in sleep duration on obesity and T2DM.

Obesity is a disorder that develops from the interaction between genotype and environment involving social, behavioral, cultural, and physiological factors. Obesity increases the risk for type 2 diabetes mellitus, hypertension, cardiovascular disease, cancer, musculoskeletal disorders, chronic kidney and pulmonary disease. Although obesity is clearly associated with an increased prevalence of hypertension, many obese individuals may not develop hypertension. Protecting factors may exist and it is important to understand why obesity is not always related to hypertension. The aim of this review is to highlight the knowledge gap for the association between obesity, hypertension, and potential genetic and racial differences or environmental factors that may protect obese patients against the development of hypertension and other co-morbidities. Specific mutations in the leptin and the melaninocortin receptor genes in animal models of obesity without hypertension, the actions of α-melanocyte stimulating hormone, and SNS activity in obesity-related hypertension may promote recognition of protective and promoting factors for hypertension in obesity. Furthermore, gene-environment interactions may have the potential to modify gene expression and epigenetic mechanisms could also contribute to the heritability of obesity-induced hypertension. Finally, differences in nutrition, gut microbiota, exposure to sun light and exercise may play an important role in the presence or absence of hypertension in obesity.

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Background and Objective Type 1 diabetes is an important risk factor for the development of cardiovascular disease. Pulse wave velocity (PWV) and carotid intima‐media thickness (cIMT) measurements are well recognized as independent predictors for future cardiovascular disease. The aim of the present study was to systematically review the literature and conduct a meta‐analysis assessing measures of subclinical arterial damage in children and adolescents with type 1 diabetes in comparison to healthy controls. Methods PubMed and Cochrane Library were searched to identify studies comparing cIMT and carotid‐femoral PWV levels between children with type 1 diabetes and healthy controls. Meta‐analysis was performed to compare the difference of overall mean cIMT and carotid‐femoral PWV levels between the two groups. New Castle Ottawa quality assessment scale for case‐control studies was used to assess study quality. Results Twenty‐three studies were finally included in the meta‐analysis (20 studies for cIMT and 4 studies for carotid‐femoral PWV). Youth with type 1 diabetes had significantly higher cIMT levels than controls (mean difference [d] = 0.03, 95% confidence interval [CI] = 0.02‐0.04), as well as higher carotid‐femoral PWV levels (d = 0.26, 95% CI = 0.18‐0.34). Heterogeneity was present only in the cIMT analysis (I2 > 90%). Conclusions Youth with type 1 diabetes showed signs of subclinical arterial damage, as suggested by higher levels of cIMT and carotid‐femoral PWV compared to healthy controls at childhood and adolescence. Preventive and therapeutic interventions early in course of disease may be further studied to decrease morbidity in this high‐risk young patient group. PROSPERO registration number: 2018 CRD42018094354.

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Background and Aim Νon‐alcoholic fatty liver disease (NAFLD) is estimated to be the most common cause of end‐stage liver disease in the next years. Vitamin E has shown beneficial effects as a possible “scavenger” of oxidative stress products, which play a major role in pathogenesis of the disease. The purpose of the present meta‐analysis is to investigate the effects of vitamin E supplementation in biochemical and histological parameters in adult patients with NAFLD. Methods Literature search was performed in major electronic databases (MEDLINE, CENTRAL, and Embase) up to June 2020 for randomized clinical trials, which examined vitamin E versus placebo treatment in adults with NAFLD. Changes in liver enzymes were considered as primary outcomes while changes in histological, biochemical, and metabolic parameters as secondary. Quality of evidence was assessed through risk of bias according to the Cochrane risk of bias tool. Results Eight studies were included in qualitative analysis and seven in quantitative analysis. Vitamin E reduced the values of liver enzymes compared with placebo (−7.37 IU/L, 95% confidence interval: −10.11 to −4.64 for alanine aminotransferase, and −5.71 IU/L, 95% confidence interval: −9.49 to −1.93 for aspartate aminotransferase). Additionally, vitamin E improved statistically significantly liver pathology in every individual histological parameter as well as low‐density lipoprotein cholesterol, fasting blood glucose, and serum leptin values. Conclusions Vitamin E can improve biochemical and histological characteristics of NAFLD patients, especially of non‐alcoholic steatohepatitis patients. The results indicate that vitamin E could be a promising choice and be considered as a treatment option in patients with NAFLD.