Regulation of adipocyte differentiation and function by polyunsaturated fatty acids.
A diet enriched in PUFAs, in particular of the n-3 family, decreases adipose tissue mass and suppresses development of obesity in rodents. Although several nuclear hormone receptors are identified as PUFA targets, the precise molecular mechanisms underlying the effects of PUFAs still remain to be elucidated. Here we review research aimed at elucidating molecular mechanisms governing the effects of PUFAs on the differentiation and function of white fat cells. This review focuses on dietary PUFAs as signaling molecules, with special emphasis on agonistic and antagonistic effects on transcription factors currently implicated as key players in adipocyte differentiation and function, including peroxisome proliferator activated receptors (PPARs) (alpha, beta and gamma), sterol regulatory element binding proteins (SREBPs) and liver X receptors (LXRs). We review evidence that dietary n-3 PUFAs decrease adipose tissue mass and suppress the development of obesity in rodents by targeting a set of key regulatory transcription factors involved in both adipogensis and lipid homeostasis in mature adipocytes. The same set of factors are targeted by PUFAs of the n-6 family, but the cellular/physiological responses are dependent on the experimental setting as n-6 PUFAs may exert either an anti- or a proadipogenic effect. Feeding status and hormonal background may therefore be of particular importance in determining the physiological effects of PUFAs of the n-6 family.
Madsen
Lise
L
Department of Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark.
Petersen
Rasmus Koefoed
RK
Kristiansen
Karsten
K
D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D022762:CCAAT-Enhancer-Binding Proteins / Q000037:antagonists & inhibitors; D002454:Cell Differentiation / Q000187:drug effects; D004268:DNA-Binding Proteins / Q000037:antagonists & inhibitors; D003907:Dexamethasone; D005231:Fatty Acids, Unsaturated / Q000096:biosynthesis / Q000494:pharmacology*; D006801:Humans; D007328:Insulin; D000071518:Liver X Receptors; D051379:Mice; D057093:Orphan Nuclear Receptors; D047493:PPAR alpha / Q000819:agonists*; D047494:PPAR delta / Q000819:agonists*; D018160:Receptors, Cytoplasmic and Nuclear / Q000037:antagonists & inhibitors; D051780:Sterol Regulatory Element Binding Protein 1; D014157:Transcription Factors / Q000037:antagonists & inhibitors
D022762:CCAAT-Enhancer-Binding Proteins; D004268:DNA-Binding Proteins; D005231:Fatty Acids, Unsaturated; D007328:Insulin; D000071518:Liver X Receptors; D057093:Orphan Nuclear Receptors; D047493:PPAR alpha; D047494:PPAR delta; D018160:Receptors, Cytoplasmic and Nuclear; C497387:SREBF1 protein, human; C497388:Srebf1 protein, mouse; D051780:Sterol Regulatory Element Binding Protein 1; D014157:Transcription Factors; D003907:Dexamethasone