Smith Steven R, Ravussin Eric
Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA 70808-4124, USA.
Curr Diab Rep. 2002 Jun;2(3):223-30. doi: 10.1007/s11892-002-0087-1.
It is widely accepted that increasing adiposity is associated with insulin resistance and increased risk of type 2 diabetes. The predominant paradigm used to explain this link is the portal/visceral hypothesis. This hypothesis proposes that increased adiposity, particularly in the visceral depots, leads to increased free fatty acid flux and inhibition of insulin action via Randle's effect in insulin-sensitive tissues. Recent data do not entirely support this hypothesis. As such, two new paradigms have emerged that may explain the established links between adiposity and disease.
人们普遍认为,肥胖程度增加与胰岛素抵抗及2型糖尿病风险增加有关。用于解释这种关联的主要范式是门静脉/内脏假说。该假说提出,肥胖程度增加,尤其是在内脏脂肪库中,会导致游离脂肪酸通量增加,并通过兰德尔效应在胰岛素敏感组织中抑制胰岛素作用。最近的数据并不完全支持这一假说。因此,出现了两种新的范式,它们可能解释肥胖与疾病之间已确立的联系。