期刊
SEMINARS IN REPRODUCTIVE MEDICINE
卷 29, 期 3, 页码 237-245出版社
THIEME MEDICAL PUBL INC
DOI: 10.1055/s-0031-1275517
关键词
Adipogenesis; lipogenesis; PPAR gamma; obesity
资金
- American Heart Association [0865125F]
- National Institute of Child Health and Human Development [R03HD060241, R01HD054751]
- National Institute of Diabetes and Digestive and Kidney [R56DK081756]
- UCLA-UCSD DERC (Diabetes and Endocrinology Research Center) to Mina Desai
A newly recognized primary cause of obesity epidemic is the developmental programming effects of (1) intrauterine growth-restricted (IUGR) newborns exposed in utero to undernutrition, and (2) normal or excessive weight newborns exposed to maternal obesity and high-fat (HF) diets. The mechanisms contributing to offspring obesity have been extensively studied in animal models with adipose tissue identified as one of the principal targets of programming. IUGR and HF offspring exhibit programmed adipocytes, such that an intrinsic enhanced lipogenesis and adipocyte proliferation contribute to the development of obesity. This is attributed to early induction of adipogenic transcription factor peroxisome proliferator-activated receptor (PPAR)gamma, whose activity is enhanced under limited or excess nutrient availability. Nonetheless, this occurs via different mechanisms involving PPAR gamma coregulators: In IUGR, it is upregulation of coactivators, whereas in HF newborns, it is downregulation of compressors. Thus preventive therapeutic interventions will require target-specific modalities that depend on the primary etiology.
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