title: Inverse regulation of basal lipolysis in perigonadal and mesenteric fat depots in mice.
abstract: Given the strong link between visceral adiposity and (hepatic) insulin resistance as well as liver steatosis, it is crucial to characterize obesity-associated alterations in adipocyte function, particularly in fat depots drained to the liver. Yet these adipose tissues are not easily accessible in humans, and the most frequently studied depot in rodents is the perigonadal, which is drained systemically. In the present study, we aimed to study alterations in lipolysis between mesenteric and perigonadal adipocytes in mice. Basal free fatty acid and glycerol release was significantly lower in perigonadal compared with mesenteric adipocytes isolated from chow-fed C57BL/6J mice. However, this difference completely vanished in high-fat diet-fed mice. Consistently, protein levels of the G(0)/G(1) switch gene 2 (G0S2), which were previously found to be inversely related to basal lipolysis, were significantly lower in mesenteric compared with perigonadal fat of chow-fed mice. Similarly, perilipin was differently expressed between the two depots. In addition, adipocyte-specific overexpression of G0S2 led to significantly decreased basal lipolysis in mesenteric adipose tissue of chow-fed mice. In conclusion, lipolysis is differently regulated between perigonadal and mesenteric adipocytes, and these depot-specific differences might be explained by altered regulation of G0S2 and/or perilipin.
authors: Dept. of Pediatric Endocrinology and Diabetology, University Children's Hospital, Steinwiesstrasse 75, Zurich, Switzerland. daniel.konrad@kispi.uzh.ch
authors: Stephan
authors: S
authors: Wueest
authors: Xingyuan
authors: X
authors: Yang
authors: Jun
authors: J
authors: Liu
authors: Eugen J
authors: EJ
authors: Schoenle
authors: Daniel
authors: D
authors: Konrad
mesh_terms: D017667:Adipocytes / Q000378:metabolism / Q000473:pathology; D050154:Adiposity; D000818:Animals; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism*; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism*; D002469:Cell Separation; D048429:Cell Size; D016207:Cytokines / Q000378:metabolism; D004041:Dietary Fats / Q000009:adverse effects; D005227:Fatty Acids / Q000097:blood; D005786:Gene Expression Regulation; D050152:Intra-Abdominal Fat / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology; D008066:Lipolysis; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009928:Organ Specificity; D050177:Overweight / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D000070778:Perilipin-1; D010750:Phosphoproteins / Q000235:genetics / Q000378:metabolism*; D011168:Portal System / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism
chemical_list: D002352:Carrier Proteins; D018797:Cell Cycle Proteins; D016207:Cytokines; D004041:Dietary Fats; D005227:Fatty Acids; C508072:G0S2 protein, mouse; D000070778:Perilipin-1; D010750:Phosphoproteins; D012333:RNA, Messenger