Dynamic differences in oxidative stress and the regulation of metabolism with age in visceral versus subcutaneous adipose.
Once thought only as storage for excess nutrients, adipose tissue has been shown to be a dynamic organ implicated in the regulation of many physiological processes. There is emerging evidence supporting differential roles for visceral and subcutaneous white adipose tissue in maintaining health, although how these roles are modulated by the aging process is not clear. However, the proposed beneficial effects of subcutaneous fat suggest that targeting maintenance of this tissue could lead to healthier aging. In this study, we tested whether alterations in adipose function with age might be associated with changes in oxidative stress. Using visceral and subcutaneous adipose from C57BL/6 mice, we discovered effects of both age and depot location on markers of lipolysis and adipogenesis. Conversely, accumulation of oxidative damage and changes in enzymatic antioxidant expression with age were largely similar between these two depots. The activation of each of the stress signaling pathways JNK and MAPK/ERK was relatively suppressed in subcutaneous adipose tissue suggesting reduced sensitivity to oxidative stress. Similarly, pre-adipocytes from subcutaneous adipose were significantly more resistant than visceral-derived cells to cell death caused by oxidative stress. Cellular respiration in visceral-derived cells was dramatically higher than in cells derived from subcutaneous adipose despite little evidence for differences in mitochondrial density. Together, our data identify molecular mechanisms by which visceral and subcutaneous adipose differ with age and suggest potential targetable means to preserve healthy adipose aging.
The Sam and Ann Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Roy
R
Liu
The Sam and Ann Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA; Departments of Cellular & Structural Biology, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Daniel A
DA
Pulliam
The Sam and Ann Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Yuhong
Y
Liu
The Sam and Ann Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA; Molecular Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA; Geriatric Research, Education and Clinical Center, South Texas Veterans Health Care System, San Antonio, TX, USA. Electronic address: salmona@uthscsa.edu.
Adam B
AB
Salmon
D017667:Adipocytes / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D050156:Adipogenesis / Q000187:drug effects; D000375:Aging / Q000378:metabolism*; D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D019069:Cell Respiration / Q000187:drug effects; D048049:Extracellular Signal-Regulated MAP Kinases / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation; D050152:Intra-Abdominal Fat / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D008066:Lipolysis / Q000187:drug effects; D048670:MAP Kinase Kinase 4 / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D018384:Oxidative Stress; D010269:Paraquat / Q000494:pharmacology; D010545:Peroxides / Q000494:pharmacology; D061251:Primary Cell Culture; D015398:Signal Transduction; D050151:Subcutaneous Fat / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*
D000447:Aldehydes; D010545:Peroxides; D048049:Extracellular Signal-Regulated MAP Kinases; D048670:MAP Kinase Kinase 4; C027576:4-hydroxy-2-nonenal; C000602361:tert-butyl peroxide; D010269:Paraquat
Fat; JNK; MAPK/ERK; Mitochondria; Pre-adipocytes; Seahorse