Inherited stress resiliency prevents the development of metabolic alterations in diet‐induced obese mice
Objective Chronic stress promotes obesity and metabolic comorbidities. The ability of individuals to cope with stress may serve as an important parameter in the development of obesity‐related metabolic outcomes. The aim of this study was to clarify whether differences in stress response affect metab...
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Published in | Obesity (Silver Spring, Md.) Vol. 31; no. 8; pp. 2043 - 2056 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Blackwell Publishing Ltd
01.08.2023
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Subjects | |
Online Access | Get full text |
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Abstract | Objective
Chronic stress promotes obesity and metabolic comorbidities. The ability of individuals to cope with stress may serve as an important parameter in the development of obesity‐related metabolic outcomes. The aim of this study was to clarify whether differences in stress response affect metabolic health under obesity.
Methods
The study was performed in a selectively bred mouse model of social dominance (Dom) and submissiveness (Sub), which exhibit stress resilience or vulnerability, respectively. Mice were given a high‐fat diet (HFD) or standard diet, followed by physiological, histological, and molecular analyses.
Results
The HFD caused hyperleptinemia, glucose intolerance, insulin resistance, steatosis of the liver and pancreas, and brown adipose tissue whitening in Sub mice, whereas Dom mice were protected from these consequences of the HFD. The HFD increased circulating levels of interleukin (IL)‐1β and induced the expression of proinflammatory genes in the liver and in epididymal white adipose tissue of Sub mice, with no changes in Dom mice. The Cox2 inhibitor celecoxib (15 mg/kg/d) reduced serum IL‐1β, improved glucose tolerance and insulin sensitivity, and prevented hepatic and brown adipose tissue whitening in HFD‐fed Sub mice.
Conclusions
The extent of stress resiliency is associated with inflammation and contributes to population heterogeneity in the development of healthy or unhealthy obesity. |
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AbstractList | Objective: Chronic stress promotes obesity and metabolic comorbidities. The ability of individuals to cope with stress may serve as an important parameter in the development of obesity-related metabolic outcomes. The aim of this study was to clarify whether differences in stress response affect metabolic health under obesity. Methods: The study was performed in a selectively bred mouse model of social dominance (Dorn) and submissiveness (Sub), which exhibit stress resilience or vulnerability, respectively. Mice were given a high-fat diet (HFD) or standard diet, followed by physiological, histological, and molecular analyses. Results: The HFD caused hyperleptinemia, glucose intolerance, insulin resistance, steatosis of the liver and pancreas, and brown adipose tissue whitening in Sub mice, whereas Dom mice were protected from these consequences of the HFD. The HFD increased circulating levels of interleukin (IL)-lß and induced the expression of proinflammatory genes in the liver and in epididymal white adipose tissue of Sub mice, with no changes in Dom mice. The Cox2 inhibitor celecoxib (15 mg/kg/d) reduced serum IL-lß, improved glucose tolerance and insulin sensitivity, and prevented hepatic and brown adipose tissue whitening in HFD-fed Sub mice. Conclusions: The extent of stress resiliency is associated with inflammation and contributes to population heterogeneity in the development of healthy or unhealthy obesity. OBJECTIVEChronic stress promotes obesity and metabolic comorbidities. The ability of individuals to cope with stress may serve as an important parameter in the development of obesity-related metabolic outcomes. The aim of this study was to clarify whether differences in stress response affect metabolic health under obesity. METHODSThe study was performed in a selectively bred mouse model of social dominance (Dom) and submissiveness (Sub), which exhibit stress resilience or vulnerability, respectively. Mice were given a high-fat diet (HFD) or standard diet, followed by physiological, histological, and molecular analyses. RESULTSThe HFD caused hyperleptinemia, glucose intolerance, insulin resistance, steatosis of the liver and pancreas, and brown adipose tissue whitening in Sub mice, whereas Dom mice were protected from these consequences of the HFD. The HFD increased circulating levels of interleukin (IL)-1β and induced the expression of proinflammatory genes in the liver and in epididymal white adipose tissue of Sub mice, with no changes in Dom mice. The Cox2 inhibitor celecoxib (15 mg/kg/d) reduced serum IL-1β, improved glucose tolerance and insulin sensitivity, and prevented hepatic and brown adipose tissue whitening in HFD-fed Sub mice. CONCLUSIONSThe extent of stress resiliency is associated with inflammation and contributes to population heterogeneity in the development of healthy or unhealthy obesity. Objective Chronic stress promotes obesity and metabolic comorbidities. The ability of individuals to cope with stress may serve as an important parameter in the development of obesity‐related metabolic outcomes. The aim of this study was to clarify whether differences in stress response affect metabolic health under obesity. Methods The study was performed in a selectively bred mouse model of social dominance (Dom) and submissiveness (Sub), which exhibit stress resilience or vulnerability, respectively. Mice were given a high‐fat diet (HFD) or standard diet, followed by physiological, histological, and molecular analyses. Results The HFD caused hyperleptinemia, glucose intolerance, insulin resistance, steatosis of the liver and pancreas, and brown adipose tissue whitening in Sub mice, whereas Dom mice were protected from these consequences of the HFD. The HFD increased circulating levels of interleukin (IL)‐1β and induced the expression of proinflammatory genes in the liver and in epididymal white adipose tissue of Sub mice, with no changes in Dom mice. The Cox2 inhibitor celecoxib (15 mg/kg/d) reduced serum IL‐1β, improved glucose tolerance and insulin sensitivity, and prevented hepatic and brown adipose tissue whitening in HFD‐fed Sub mice. Conclusions The extent of stress resiliency is associated with inflammation and contributes to population heterogeneity in the development of healthy or unhealthy obesity. Chronic stress promotes obesity and metabolic comorbidities. The ability of individuals to cope with stress may serve as an important parameter in the development of obesity-related metabolic outcomes. The aim of this study was to clarify whether differences in stress response affect metabolic health under obesity. The study was performed in a selectively bred mouse model of social dominance (Dom) and submissiveness (Sub), which exhibit stress resilience or vulnerability, respectively. Mice were given a high-fat diet (HFD) or standard diet, followed by physiological, histological, and molecular analyses. The HFD caused hyperleptinemia, glucose intolerance, insulin resistance, steatosis of the liver and pancreas, and brown adipose tissue whitening in Sub mice, whereas Dom mice were protected from these consequences of the HFD. The HFD increased circulating levels of interleukin (IL)-1β and induced the expression of proinflammatory genes in the liver and in epididymal white adipose tissue of Sub mice, with no changes in Dom mice. The Cox2 inhibitor celecoxib (15 mg/kg/d) reduced serum IL-1β, improved glucose tolerance and insulin sensitivity, and prevented hepatic and brown adipose tissue whitening in HFD-fed Sub mice. The extent of stress resiliency is associated with inflammation and contributes to population heterogeneity in the development of healthy or unhealthy obesity. Abstract Objective Chronic stress promotes obesity and metabolic comorbidities. The ability of individuals to cope with stress may serve as an important parameter in the development of obesity‐related metabolic outcomes. The aim of this study was to clarify whether differences in stress response affect metabolic health under obesity. Methods The study was performed in a selectively bred mouse model of social dominance (Dom) and submissiveness (Sub), which exhibit stress resilience or vulnerability, respectively. Mice were given a high‐fat diet (HFD) or standard diet, followed by physiological, histological, and molecular analyses. Results The HFD caused hyperleptinemia, glucose intolerance, insulin resistance, steatosis of the liver and pancreas, and brown adipose tissue whitening in Sub mice, whereas Dom mice were protected from these consequences of the HFD. The HFD increased circulating levels of interleukin (IL)‐1β and induced the expression of proinflammatory genes in the liver and in epididymal white adipose tissue of Sub mice, with no changes in Dom mice. The Cox2 inhibitor celecoxib (15 mg/kg/d) reduced serum IL‐1β, improved glucose tolerance and insulin sensitivity, and prevented hepatic and brown adipose tissue whitening in HFD‐fed Sub mice. Conclusions The extent of stress resiliency is associated with inflammation and contributes to population heterogeneity in the development of healthy or unhealthy obesity. image |
Author | Pinhasov, Albert Ben‐Shachar, Michaella Wollman, Ayala Daniel, Tehila Rosenzweig, Tovit Govindaraj, Sharmila Aviel‐Ronen, Sarit |
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Chronic stress promotes obesity and metabolic comorbidities. The ability of individuals to cope with stress may serve as an important parameter in... Chronic stress promotes obesity and metabolic comorbidities. The ability of individuals to cope with stress may serve as an important parameter in the... Abstract Objective Chronic stress promotes obesity and metabolic comorbidities. The ability of individuals to cope with stress may serve as an important... Objective: Chronic stress promotes obesity and metabolic comorbidities. The ability of individuals to cope with stress may serve as an important parameter in... OBJECTIVEChronic stress promotes obesity and metabolic comorbidities. The ability of individuals to cope with stress may serve as an important parameter in the... |
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SubjectTerms | Body fat Cognition & reasoning Cytokines Genotype & phenotype Glucose Hypotheses Insulin resistance Laboratory animals Metabolism Mortality Obesity Physiology Polymerase chain reaction Proteins |
Title | Inherited stress resiliency prevents the development of metabolic alterations in diet‐induced obese mice |
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