作者: Andrew J. Murphy , Laurent Yvan-Charvet
DOI: 10.2337/DB14-1553
关键词:
摘要: In the early 1980s, it was established that adipose tissue not only plays an important role in triglyceride storage but also accounts for approximately 25% of total body cholesterol humans (1). However, obese individuals this proportion can increase to well over half and could contribute adipocyte dysfunction obesity-mediated metabolic syndrome, including low levels plasma HDL (1–4). Consistent with view behaves as a sink, its accumulation is proportional triglycerides response nutritional changes maintain cellular integrity regulate hypertrophy, surprising adipocytes have developed unique ability deal It may be reason evolved extremely limited capacity perform de novo synthesis (1) possess multiple strategies extract from circulating lipoproteins (5,6). Despite being delivered cholesteryl ester adipocytes, 95% paradoxically exists free (FC) (7) resides membrane or cytosolic interface lipid droplets where readily available mobilization (8). Cholesterol involves ATP-binding cassette transporter A1 (ABCA1), which has recently been shown biogenesis vivo (9,10). These findings illustrate exquisite balance between concentration raise question about obesity associated complications. ATP-binding transporters ABCA1 ABCG1 primarily mediate efflux peripheral cells. promote unidirectional lipid-poor apolipoprotein A-I (apoA-I), apoE, particles, respectively, are under transcriptional control liver X receptors (LXRs), master intracellular sensors activated …