Role of glucocorticoids in the physiopathology of excessive fat deposition and insulin resistance

Asensio, Cédric S.; Muzzin, Patrick; Rohner‐Jeanrenaud, Françoise

doi:10.1038/sj.ijo.0802856

Cited by 110 publications

(95 citation statements)

References 97 publications

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“…This increase cannot be explained by the physiological understanding of resistin action derived from mice experiments, where a strong relationship between adiposity, insulin resistance and resistin was observed. 9,13,27 Similar to other human and rodent studies 4,7,28-31 our findings indicate that resistin levels were slightly higher in females than in males and decreased with age. Resistin concentrations were not significantly different between lean and overweight subjects.…”

Section: Discussionsupporting

confidence: 90%

Increase in serum resistin during weight loss in overweight subjects is related to lipid metabolism

et al. 2006

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Objective: Human resistin has been stated to influence preadipocyte cell numbers and to stimulate adipocyte triglyceride lipolysis in vivo and in vitro. However, its role in human obesity remains unclear. Design: Cross-sectional study for comparisons of lean and obese subjects, and subsequent longitudinal 4-month weight loss intervention study in obese subjects. Subjects: Healthy subjects, lean (n ¼ 20, BMIo25) and overweight (n ¼ 43, BMIX25). Measurements: Serum resistin, body weight, body fat, waist-to-hip ratio, as well as markers of insulin resistance and lipid metabolism at baseline and after 4 months of intervention. Results: Serum resistin was positively correlated to HOMA-IR (partial r ¼ 0.288; P ¼ 0.055), serum fructosamines (partial r ¼ 0.280; P ¼ 0.062), serum NEFA (partial r ¼ 0.276; P ¼ 0.066) and negatively to age (partial r ¼ À0.349; P ¼ 0.019) and serum apolipoprotein A-1 (partial r ¼ À0.363; P ¼ 0.014). During the intervention, serum resistin increased significantly (Po0.001). The increase was inversely related to changes in waist-to-hip ratio (P ¼ 0.025) and positively to serum apolipoprotein B (P ¼ 0.011). In males only, the increase in resistin during weight loss was predicted by total serum cholesterol at baseline (r ¼ 0.703, P ¼ 0.007). No relation was observed between changes in resistin and changes in HOMA-IR. Conclusion: The present study indicates an association between serum resistin and markers of abdominal fat distribution as well as the regulation of lipid metabolism. However, human resistin is unlikely to play an independent role in the regulation of glucose metabolism.

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Section: Discussionsupporting

confidence: 90%

Increase in serum resistin during weight loss in overweight subjects is related to lipid metabolism

et al. 2006

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“…The effect of the group formation process on serum insulin followed that of the changes in body weight, as concentrations were significantly lower in subordinate compared with dominant females at week 7, regardless of SERT genotype. However, concentrations fell from baseline in l/l females but rose in s-variant females, indicating more studies are needed to determine whether social status-5HTTLPR differences in insulin secretion are due to differences in food intake or glucocorticoid-induced decreases in insulin sensitivity [72].…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms in the serotonin reuptake transporter gene modify the consequences of social status on metabolic health in female rhesus monkeys

Jarrell¹,

Hoffman²,

Kaplan³

et al. 2008

Physiology & Behavior

109

163

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Individuals vary substantially in their vulnerability to physical and psychosocial stressors. The causes of such variation in susceptibility to stress are poorly understood, but are thought to relate in part to genetic factors. The present study evaluated the extent to which polymorphisms in the gene encoding the serotonin reuptake transporter (5HTTLPR or SERT) modulated physiologic responses to the imposition of psychosocial stress (social reorganization and subordinate social status) in female rhesus monkeys. Forty females, drawn from the middle ranking genealogies of several large social groups, were reorganized into eight groups containing 5 monkeys each; four groups were comprised entirely of animals homogeneous for the long promoter variant in the SERT gene (l/l), while the other four groups had monkeys with at least one allele of the short promoter variant (l/s or s/s). Females were sequentially introduced into these new groups in random order and dominance ranks were established within several days. During the ensuing 6 weeks, dominant monkeys exhibited elevated rates of aggression while subordinates displayed high rates of submission. Notably, females with the s-variant SERT genotype, collapsed across social status positions, exhibited the highest overall rates of both aggression and submission. Although neither social status nor SERT genotype influenced morning cortisol concentrations, glucocorticoid negative feedback was reduced significantly in subordinate compared to dominant females irrespective of genotype. All animals lost weight and abdominal fat across the experiment. However, decreases were greatest in subordinates, regardless of genotype, and least in dominant females with the l/l genotype. Serum concentrations of insulin, glucose, and ghrelin decreased significantly during the group formation process, effects that were independent of genotype or social status. In contrast, social status and genotype interacted to influence changes in serum concentrations of leptin and triiodothyronine (T3), as dominant, l/l females had the highest levels while subordinate s-variant females had the lowest levels. The order in which a female was introduced to her group generally predicted her eventual social rank. However, rank was additionally predicted by pre-experimental T3 and abdominal fat values, but only in the l/l animals. While these findings must be replicated with a larger sample size, the data suggest that the s-variant SERT genotype confers increased vulnerability to the adverse effects of psychosocial stress associated with subordinate status while the l/l genotype benefits the most from the absence of stress conferred by dominant social status. These findings suggest that genetic factors modify the responses of monkeys to social subordination and perhaps other psychosocial stressors.

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“…Previous studies have shown that obesity is associated with HPA axis dysregulation that may originate from increased forward drive, decreased sensitivity to negative feedback regulation, or altered sensitivity of peripheral tissues such as fat and skeletal muscle tissue to glucocorticoids [15,16]. Obese humans show a hypersensitive response to stimulation of the HPA axis, the magnitude of this exaggerated response being dependent on fat distribution [17,18].…”

Section: Obesity Is Associated With Dysregulation Of the Hpa Axismentioning

confidence: 99%

Effects of energy restriction on activity of the hypothalamo-pituitary-adrenal axis in obese humans and rodents: implications for diet-induced changes in body composition

Seimon

Hostland

Silveira

et al. 2013

Hormone Molecular Biology and Clinical Investigation

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Background: Obesity treatments aim to maximize fat loss, particularly abdominal or visceral fat, without compromising lean or bone mass. However, the literature contains numerous examples of obesity treatments that -in addition to fat loss -result in loss of lean mass and/or bone mass. Materials and methods: Because of the known effects of energy restriction to increase activity of the hypothalamopitutiary adrenal (HPA) axis in lean humans and animals, and because increases in circulating glucocorticoid levels could potentially contribute to adverse body compositional changes with obesity treatments, we conducted a systematic PubMed search to determine whether HPA axis activation also occurs in response to energy restriction in obese humans and animals. Results and conclusions:In most studies in obese humans, short-term severe energy restriction increased circulating cortisol levels, and this response was also seen in two longer-term human studies involving severe or moderate energy restriction. These fi ndings parallel studies on short-or long-term energy restriction in obese rodents, with most studies showing increases in circulating corticosterone concentrations, and no change or actual increases in hypothalamic expression of corticotropin-releasing hormone, urocortin 3 or their receptors. However, a signifi cant proportion of studies involving longer-term severe or moderate energy restriction in obese humans showed no change or decreases in HPA axis function. There was variability among human studies in the duration of energy restriction and timing of the HPA axis investigations (i.e., during energy restriction, or aft er a period of post-restriction weight maintenance). In order to unambiguously determine changes in HPA axis function with energy restriction in obese humans, it will be important to assess HPA axis function at multiple time points during energy restriction, given that obese individuals may spend many

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Role of glucocorticoids in the physiopathology of excessive fat deposition and insulin resistance

Cited by 110 publications

References 97 publications

Increase in serum resistin during weight loss in overweight subjects is related to lipid metabolism

Increase in serum resistin during weight loss in overweight subjects is related to lipid metabolism

Polymorphisms in the serotonin reuptake transporter gene modify the consequences of social status on metabolic health in female rhesus monkeys

Effects of energy restriction on activity of the hypothalamo-pituitary-adrenal axis in obese humans and rodents: implications for diet-induced changes in body composition

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