title: Energy metabolism of adipose tissue--physiological aspects and target in obesity treatment.
abstract: Body fat content is controlled, at least in part, by energy charge of adipocytes. In vitro studies indicated that lipogenesis as well as lipolysis depend on cellular ATP levels. Respiratory uncoupling may, through the depression of ATP synthesis, control lipid metabolism of adipose cells. Expression of some uncoupling proteins (UCP2 and UCP5) as well as other protonophoric transporters can be detected in the adipose tissue. Expression of other UCPs (UCP1 and UCP3) can be induced by pharmacological treatments that reduce adiposity. A negative correlation between the accumulation of fat and the expression of UCP2 in adipocytes was also found. Ectopic expression of UCP1 in the white fat of aP2-Ucp1 transgenic mice mitigated obesity induced by genetic or dietary factors. In these mice, changes in lipid metabolism of adipocytes were associated with the depression of intracellular energy charge. Recent data show that AMP-activated protein kinase may be involved in the complex changes elicited by respiratory uncoupling in adipocytes. Changes in energy metabolism of adipose tissue may mediate effects of treatments directed against adiposity, dyslipidemia, and insulin resistance.
authors.affiliation: Department of Adipose Tissue Biology, Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic. kopecky@biomed.cas.cz
authors.forename: J
authors.initials: J
authors.lastname: Kopecký
authors.forename: M
authors.initials: M
authors.lastname: Rossmeisl
authors.forename: P
authors.initials: P
authors.lastname: Flachs
authors.forename: P
authors.initials: P
authors.lastname: Brauner
authors.forename: J
authors.initials: J
authors.lastname: Sponarová
authors.forename: O
authors.initials: O
authors.lastname: Matejková
authors.forename: T
authors.initials: T
authors.lastname: Prazák
authors.forename: J
authors.initials: J
authors.lastname: Růzicková
authors.forename: K
authors.initials: K
authors.lastname: Bardová
authors.forename: O
authors.initials: O
authors.lastname: Kuda
mesh_terms: D055372:AMP-Activated Protein Kinases; D017667:Adipocytes / Q000378:metabolism*; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism; D004734:Energy Metabolism; D007473:Ion Channels; D050356:Lipid Metabolism; D008565:Membrane Proteins / Q000378:metabolism; D024821:Metabolic Syndrome / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D051379:Mice; D008822:Mice, Transgenic; D024101:Mitochondrial Proteins; D009097:Multienzyme Complexes / Q000378:metabolism; D009765:Obesity / Q000378:metabolism / Q000503:physiopathology* / Q000517:prevention & control; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D000071256:Uncoupling Protein 1
chemical_list: D002352:Carrier Proteins; D007473:Ion Channels; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D009097:Multienzyme Complexes; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1; D017346:Protein Serine-Threonine Kinases; D055372:AMP-Activated Protein Kinases