title: Exercise Effects on White Adipose Tissue: Beiging and Metabolic Adaptations.
abstract: Regular physical activity and exercise training have long been known to cause adaptations to white adipose tissue (WAT), including decreases in cell size and lipid content and increases in mitochondrial proteins. In this article, we discuss recent studies that have investigated the effects of exercise training on mitochondrial function, the "beiging" of WAT, regulation of adipokines, metabolic effects of trained adipose tissue on systemic metabolism, and depot-specific responses to exercise training. The major WAT depots in the body are found in the visceral cavity (vWAT) and subcutaneously (scWAT). In rodent models, exercise training increases mitochondrial biogenesis and activity in both these adipose tissue depots. Exercise training also increases expression of the brown adipocyte marker uncoupling protein 1 (UCP1) in both adipose tissue depots, although these effects are much more pronounced in scWAT. Consistent with the increase in UCP1, exercise training increases the presence of brown-like adipocytes in scWAT, also known as browning or beiging. Training results in changes in the gene expression of thousands of scWAT genes and an altered adipokine profile in both scWAT and vWAT. Transplantation of trained scWAT in sedentary recipient mice results in striking improvements in skeletal muscle glucose uptake and whole-body metabolic homeostasis. Human and rodent exercise studies have indicated that exercise training can alter circulating adipokine concentration as well as adipokine expression in adipose tissue. Thus, the profound changes to WAT in response to exercise training may be part of the mechanism by which exercise improves whole-body metabolic health.
authors.affiliation: Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Boston, MA Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
authors.forename: Kristin I
authors.initials: KI
authors.lastname: Stanford
authors.affiliation: Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Boston, MA Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Boston, MA.
authors.forename: Roeland J W
authors.initials: RJ
authors.lastname: Middelbeek
authors.affiliation: Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Boston, MA Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA laurie.goodyear@joslin.harvard.edu.
authors.forename: Laurie J
authors.initials: LJ
authors.lastname: Goodyear
mesh_terms: D000222:Adaptation, Physiological; D017667:Adipocytes / Q000502:physiology; D054392:Adipokines / Q000378:metabolism; D052436:Adipose Tissue, White / Q000502:physiology* / Q000637:transplantation; D000818:Animals; D015444:Exercise; D006801:Humans; D007473:Ion Channels / Q000378:metabolism / Q000502:physiology; D051379:Mice; D008928:Mitochondria / Q000502:physiology; D024101:Mitochondrial Proteins / Q000378:metabolism / Q000502:physiology; D018482:Muscle, Skeletal / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000502:physiology; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D010805:Physical Conditioning, Animal; D014157:Transcription Factors / Q000502:physiology; D000071256:Uncoupling Protein 1
chemical_list: D054392:Adipokines; D007473:Ion Channels; D024101:Mitochondrial Proteins; C486497:PPARGC1A protein, human; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D014157:Transcription Factors; C000604371:UCP1 protein, human; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1; D052250:Nitric Oxide Synthase Type III