Evaluating obesityrelated hypotheses for progression of type diabetes

Although the portal hypothesis is associated with obesity, insulin resistance and the pathogenesis of type 2 diabetes associations between subcutaneous fat on the trunk and insulin resistance have been shown in obese non-diabetic men (Abate et al., 1995; Goodpaster et al., 1997) and in men with type 2 diabetes Abate et al., 1996; Kelley and Mandarino, 2000; Smith et al., 2001. As the present data suggests that subcutaneous fat, which accounts for 80 per cent of total adipose tissue, is a cause of insulin resistance this must occur via a non-portal mechanism as this fat depot does not drain into the portal vein. Furthermore, insulin resistance appears independently by an increased truncal subcutaneous adipose tissue and an increased visceral fat store (Albu et al., 2000; Marcus et al., 1999; Bavenholm et al., 2003). Because of growing evidence that subcutaneous fat may play an important role in obesity-related type 2 diabetes with conflicting evidence for the role of the portal fat, changes in the model for the understanding of adipose tissue in the pathogenesis of type 2 diabetes have been proposed (Kuhn, 1962). The two emerging models are 'the ectopic fat storage syndrome' and to view the adipocyte as an endocrine organ (Ravussin and Smith, 2002).

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