1.
Melatonin Supplementation Lowers Oxidative Stress and Regulates Adipokines in Obese Patients on a Calorie-Restricted Diet.
Szewczyk-Golec, K, Rajewski, P, Gackowski, M, Mila-Kierzenkowska, C, Wesołowski, R, Sutkowy, P, Pawłowska, M, Woźniak, A
Oxidative medicine and cellular longevity. 2017;2017:8494107
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Obesity is one of the major global health problems. Melatonin is a hormone which regulates wakefulness, functions as an antioxidant and plays a role in the immune system. Previous research suggests that melatonin deficiency is associated with obesity. The aim of this study was to estimate the effect of melatonin on oxidative stress and levels of cell signalling proteins released by fat cells (adipokines) in obese patients on a calorie-restricted diet. Thirty obese patients were supplemented with a daily dose of 10 mg of melatonin or placebo for 30 days with a calorie-restricted diet. Blood levels of melatonin, adipokines and markers of oxidative stress were measured at baseline and after supplementation. Significant body weight reduction (7%) was observed only in the melatonin group. After melatonin supplementation, the adiponectin and omentin-1 levels and glutathione peroxidase activities statistically increased, whereas the malondialdehyde concentrations were reduced. In the placebo group, a significant rise in 4-hydroxynonenal and a drop in the melatonin concentrations were found. The results show evidence of increased oxidative stress accompanying calorie restriction. The authors concluded that melatonin supplementation facilitated body weight reduction, improved the antioxidant defence, and regulated adipokine secretion. The findings suggest that melatonin should be considered in the management of obesity.
Abstract
Obesity is one of the major global health problems. Melatonin deficiency has been demonstrated to correlate with obesity. The aim of the study was to estimate the effect of melatonin on oxidative stress and adipokine levels in obese patients on a calorie-restricted diet. Thirty obese patients were supplemented with a daily dose of 10 mg of melatonin (n = 15) or placebo (n = 15) for 30 days with a calorie-restricted diet. Serum levels of melatonin, 4-hydroxynonenal (HNE), adiponectin, omentin-1, leptin, and resistin, as well as erythrocytic malondialdehyde (MDA) concentration and Zn/Cu-superoxide dismutase, catalase, and glutathione peroxidase (GPx) activities, were measured at baseline and after supplementation. Significant body weight reduction was observed only in the melatonin group. After melatonin supplementation, the adiponectin and omentin-1 levels and GPx activities statistically increased, whereas the MDA concentrations were reduced. In the placebo group, a significant rise in the HNE and a drop in the melatonin concentrations were found. The results show evidence of increased oxidative stress accompanying calorie restriction. Melatonin supplementation facilitated body weight reduction, improved the antioxidant defense, and regulated adipokine secretion. The findings strongly suggest that melatonin should be considered in obesity management. This trial is registered with CTRI/2017/07/009093.
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Impact of five nights of sleep restriction on glucose metabolism, leptin and testosterone in young adult men.
Reynolds, AC, Dorrian, J, Liu, PY, Van Dongen, HP, Wittert, GA, Harmer, LJ, Banks, S
PloS one. 2012;7(7):e41218
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Chronic sleep deprivation is a feature of modern life. It may be due to social, lifestyle and/or occupational demands. It has been associated with metabolic disorders such as type 2 diabetes, metabolic syndrome, insulin resistance and obesity. This study aimed to examine the impact of sleep restriction on glucose metabolism, triglycerides and to explore the impact on testosterone, leptin and cortisol in healthy young men. The sample were 16 men aged between 22 and 36, who did not have any acute or chronic medical or psychological conditions. Subjects were studied in groups of 3 or 4 for 9 consecutive days, and had two baseline nights of 10 hours sleep followed by five nights of 4 hours sleep. Food intake was controlled during the laboratory phase. The study found evidence of impaired glucose metabolism following sleep restriction (elevated glucose and insulin). Researchers suggested this may be due to a rise in afternoon cortisol reflecting adrenal axis activation. Leptin levels also increased, but did not lead to appetite changes. Testosterone levels did not change but SHBG did decrease, possibly due to increases in insulin that could have down-regulated SHBG. There were also alterations in cortisol levels, with elevated levels in the afternoon and evening. The researchers concluded that short term sleep restriction may lead to an increased risk of type 2 diabetes.
Abstract
BACKGROUND Sleep restriction is associated with development of metabolic ill-health, and hormonal mechanisms may underlie these effects. The aim of this study was to determine the impact of short term sleep restriction on male health, particularly glucose metabolism, by examining adrenocorticotropic hormone (ACTH), cortisol, glucose, insulin, triglycerides, leptin, testosterone, and sex hormone binding globulin (SHBG). METHODOLOGY/PRINCIPAL FINDINGS N = 14 healthy men (aged 27.4±3.8, BMI 23.5±2.9) underwent a laboratory-based sleep restriction protocol consisting of 2 baseline nights of 10 h time in bed (TIB) (B1, B2; 22:00-08:00), followed by 5 nights of 4 h TIB (SR1-SR5; 04:00-08:00) and a recovery night of 10 h TIB (R1; 22:00-08:00). Subjects were allowed to move freely inside the laboratory; no strenuous activity was permitted during the study. Food intake was controlled, with subjects consuming an average 2000 kcal/day. Blood was sampled through an indwelling catheter on B1 and SR5, at 09:00 (fasting) and then every 2 hours from 10:00-20:00. On SR5 relative to B1, glucose (F(1,168) = 25.3, p<0.001) and insulin (F(1,168) = 12.2, p<0.001) were increased, triglycerides (F(1,168) = 7.5, p = 0.007) fell and there was no significant change in fasting homeostatic model assessment (HOMA) determined insulin resistance (F(1,168) = 1.3, p = 0.18). Also, cortisol (F(1,168) = 10.2, p = 0.002) and leptin (F(1,168) = 10.7, p = 0.001) increased, sex hormone binding globulin (F(1,167) = 12.1, p<0.001) fell and there were no significant changes in ACTH (F(1,168) = 0.3, p = 0.59) or total testosterone (F(1,168) = 2.8, p = 0.089). CONCLUSIONS/SIGNIFICANCE Sleep restriction impaired glucose, but improved lipid metabolism. This was associated with an increase in afternoon cortisol, without significant changes in ACTH, suggesting enhanced adrenal reactivity. Increased cortisol and reduced sex hormone binding globulin (SHBG) are both consistent with development of insulin resistance, although hepatic insulin resistance calculated from fasting HOMA did not change significantly. Short term sleep curtailment leads to changes in glucose metabolism and adrenal reactivity, which when experienced repeatedly may increase the risk for type 2 diabetes.