Considerations of the pathophysiology of non-insulin dependent diabete
s mellitus (NIDDM) usually focus on the respective roles of the so-cal
led triumvirate-beta cell, muscle and liver [1]. Often overlooked in t
his context is the role of the adipose tissue, and attention is usuall
y addressed to consideration of studies in which isolated adipocytes w
ere used as a surrogate for muscle in studies of insulin action. The g
oal of this presentation will be to develop a radically different hypo
thesis, and marshal evidence that it is the loss of normal regulation
of adipose tissue that plays the central role in both the hyperglycaem
ia and the dyslipidaemia that characterizes patients with NIDDM.