Sexual-Dimorphism in Exercise-Induced Beiging and Altered Mitochondrial Function in Inguinal White Adipose Tissue (iWAT) from the Mouse

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 758-P
Author(s):  
PASQUALE NIGRO ◽  
ROELAND MIDDELBEEK ◽  
CHRISTIANO R. ALVES ◽  
BRENT G. ALBERTSON ◽  
LESLIE A. ROWLAND ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Sexual Dimorphism ◽  
White Adipose Tissue ◽  
Mitochondrial Function ◽  
Exercise Induced

scholarly journals Fndc5 loss‐of‐function attenuates exercise‐induced browning of white adipose tissue in mice

2019 ◽  
Vol 33 (5) ◽  
pp. 5876-5886 ◽  
Author(s):  
Yan Xiong ◽  
Zihuan Wu ◽  
Bin Zhang ◽  
Chao Wang ◽  
Fengyi Mao ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Loss Of Function ◽  
Exercise Induced

scholarly journals The role of sex steroids in white adipose tissue adipocyte function

Reproduction ◽  
2017 ◽  
Vol 153 (4) ◽  
pp. R133-R149 ◽  
Author(s):  
A E Newell-Fugate
Keyword(s):  
Adipose Tissue ◽  
Sexual Dimorphism ◽  
White Adipose Tissue ◽  
Hormonal Factors ◽  
Obesity Epidemic ◽  
Health And Disease ◽  
Males And Females ◽  
Hormonal Milieu ◽  
Gender Influences

With the increasing knowledge that gender influences normal physiology, much biomedical research has begun to focus on the differential effects of sex on tissue function. Sexual dimorphism in mammals is due to the combined effects of both genetic and hormonal factors. Hormonal factors are mutable particularly in females in whom the estrous cycle dominates the hormonal milieu. Given the severity of the obesity epidemic and the fact that there are differences in the obesity rates in men and women, the role of sex in white adipose tissue function is being recognized as increasingly important. Although sex differences in white adipose tissue distribution are well established, the mechanisms affecting differential function of adipocytes within white adipose tissue in males and females remain largely understudied and poorly understood. One of the largest differences in the endocrine environment in males and females is the concentration of circulating androgens and estrogens. This review examines the effects of androgens and estrogens on lipolysis/lipogenesis, adipocyte differentiation, insulin sensitivity and adipokine production in adipocytes from white adipose tissue with a specific emphasis on the sexual dimorphism of adipocyte function in white adipose tissue during both health and disease.

scholarly journals Diurnal Regulation Of Exercise-induced Anabolic And Catabolic Signaling In White Adipose Tissue

2020 ◽  
Vol 52 (7S) ◽  
pp. 920-920
Author(s):  
Elias Maurice Malek ◽  
Caitlin K. Reynolds ◽  
Charli D. Aguilar ◽  
Graham R. McGinnis
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Exercise Induced ◽  
Diurnal Regulation

Sex differences in the effect of high-fat diet feeding on rat white adipose tissue mitochondrial function and insulin sensitivity

Metabolism ◽  
2012 ◽  
Vol 61 (8) ◽  
pp. 1108-1117 ◽  
Author(s):  
Emilia Amengual-Cladera ◽  
Isabel Lladó ◽  
Magdalena Gianotti ◽  
Ana M. Proenza
Keyword(s):  
Sex Differences ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
White Adipose Tissue ◽  
Mitochondrial Function ◽  
High Fat Diet ◽  
High Fat

Mitochondrial function/dysfunction in white adipose tissue

2014 ◽  
Vol 99 (9) ◽  
pp. 1168-1178 ◽  
Author(s):  
Sihem Boudina ◽  
Timothy E. Graham
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Mitochondrial Function

Melatonin improves mitochondrial function in inguinal white adipose tissue of Zücker diabetic fatty rats

2014 ◽  
Vol 57 (1) ◽  
pp. 103-109 ◽  
Author(s):  
Aroa Jimenéz-Aranda ◽  
Gumersindo Fernández-Vázquez ◽  
María Mohammad A-Serrano ◽  
Russel J. Reiter ◽  
Ahmad Agil
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Mitochondrial Function ◽  
Zucker Diabetic Fatty Rats

scholarly journals Sexual dimorphism in adipose tissue mitochondrial function and metabolic flexibility in obesity

2021 ◽  
Author(s):  
Amanda D. V. MacCannell ◽  
T. Simon Futers ◽  
Anna Whitehead ◽  
Amy Moran ◽  
Klaus K. Witte ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Sexual Dimorphism ◽  
Energy Expenditure ◽  
Body Mass ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Metabolic Flexibility ◽  
Female Mice

Abstract Objective The prevalence of obesity is growing globally. Adiposity increases the risk for metabolic syndrome, type 2 diabetes and cardiovascular disease. Adipose tissue distribution influences systemic metabolism and impacts metabolic disease risk. The link between sexual dimorphisms of adiposity and metabolism is poorly defined. We hypothesise that depot-specific adipose tissue mitochondrial function contributes to the sexual dimorphism of metabolic flexibility in obesity. Methods Male and female mice fed high fat diet (HFD) or standard diet (STD) from 8–18 weeks of age underwent whole animal calorimetry and high-resolution mitochondrial respirometry analysis on adipose tissue depots. To determine translatability we used RT-qPCR to examine key brown adipocyte-associated gene expression: peroxisome proliferator-activated receptor co-activator 1α, Uncoupling protein 1 and cell death inducing DFFA like effector a in brown adipose tissue (BAT) and subcutaneous adipose tissue (sWAT) of 18-week-old mice and sWAT from human volunteers. Results Male mice exhibited greater weight gain compared to female mice when challenged with HFD. Relative to increased body mass, the adipose to body weight ratio for BAT and sWAT depots was increased in HFD-fed males compared to female HFD-fed mice. Oxygen consumption, energy expenditure, respiratory exchange ratio and food consumption did not differ between males and females fed HFD. BAT mitochondria from obese females showed increased Complex I & II respiration and maximal respiration compared to lean females whereas obese males did not exhibit adaptive mitochondrial BAT respiration. Sexual dimorphism in BAT-associated gene expression in sWAT was also associated with Body Mass Index in humans. Conclusions We show that sexual dimorphism of weight gain is reflected in mitochondrial respiration analysis. Female mice have increased metabolic flexibility to adapt to changes in energy intake by regulating energy expenditure through increased complex II and maximal mitochondrial respiration within BAT when HFD challenged and increased proton leak in sWAT mitochondria.

Biochemical adaptations in white adipose tissue following aerobic exercise: from mitochondrial biogenesis to browning

2020 ◽  
Vol 477 (6) ◽  
pp. 1061-1081 ◽  
Author(s):  
Greg L. McKie ◽  
David C. Wright
Keyword(s):  
Adipose Tissue ◽  
Aerobic Exercise ◽  
White Adipose Tissue ◽  
Mitochondrial Biogenesis ◽  
Past Research ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Underlying Mechanisms ◽  
Exercise Induced ◽  
A Site

Our understanding of white adipose tissue (WAT) biochemistry has evolved over the last few decades and it is now clear that WAT is not simply a site of energy storage, but rather a pliable endocrine organ demonstrating dynamic responsiveness to the effects of aerobic exercise. Similar to its established effects in skeletal muscle, aerobic exercise induces many biochemical adaptations in WAT including mitochondrial biogenesis and browning. While past research has focused on the regulation of these biochemical processes, there has been renewed interest as of late given the potential of harnessing WAT mitochondrial biogenesis and browning to treat obesity and type II diabetes. Unfortunately, despite increasing evidence that innumerable factors, both exercise induced and pharmacological, can elicit these biochemical adaptations in WAT, the underlying mechanisms remain poorly defined. Here, we begin with a historical account of our understanding of WAT exercise biochemistry before presenting detailed evidence in favour of an up-to-date model by which aerobic exercise induces mitochondrial biogenesis and browning in WAT. Specifically, we discuss how aerobic exercise induces increases in WAT lipolysis and re-esterification and how this could be a trigger that activates the cellular energy sensor 5′ AMP-activated protein kinase to mediate the induction of mitochondrial biogenesis and browning via the transcriptional co-activator peroxisome proliferator-activated receptor gamma co-activator-1 alpha. While this review primarily focuses on mechanistic results from rodent studies special attention is given to the translation of these results, or lack thereof, to human physiology.

Ameliorating effects of lifelong physical activity on healthy aging and mitochondrial function in human white adipose tissue

2021 ◽  
Author(s):  
Anders Gudiksen ◽  
Albina Qoqaj ◽  
Stine Ringholm ◽  
Jørgen Wojtaszewski ◽  
Peter Plomgaard ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Exercise Training ◽  
White Adipose Tissue ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Healthy Aging ◽  
Venous Blood ◽  
Oxidative Capacity ◽  
Low Grade ◽  
Lifelong Exercise

Abstract Growing old is patently among the most prominent risk factors for lifestyle related diseases and deterioration in physical performance. Aging in particular affects mitochondrial homeostasis and maintaining a well-functioning mitochondrial pool is imperative in order to avoid age-associated metabolic decline. White adipose tissue (WAT) is a key organ in energy balance and impaired mitochondrial function in adipocytes has been associated with increased low-grade inflammation, altered metabolism, excessive ROS production and an accelerated aging phenotype. Exercise training improves mitochondrial health but whether lifelong exercise training can sufficiently maintain WAT mitochondrial function is currently unknown. Therefore, to dissect the role and dose-dependence of lifelong exercise training on aging WAT metabolic parameters and mitochondrial function, young and older untrained, as well as moderately and highly exercise trained older male subjects were recruited and abdominal subcutaneous (s)WAT biopsies and venous blood samples were obtained to measure mitochondrial function and key metabolic factors in WAT and plasma. Mitochondrial intrinsic respiratory capacity was lower in sWAT from older than in young subjects. In spite of this, maximal mitochondrial respiration per wet weight, markers of oxidative capacity, and mitophagic capacity were increased in sWAT from lifelong highly exercise trained than all other groups. Furthermore, ROS emission was generally lower in sWAT from lifelong highly exercise trained than older untrained subjects. Taken together, aging reduces intrinsic mitochondrial respiration in human sWAT, but lifelong high volume exercise training increases oxidative capacity by increasing mitochondrial volume likely contributing to healthy aging.

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