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Clin Sci (Lond). 2006 Jan;110(1):1-9.

The adipocyte life cycle hypothesis.

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The Mike Rosenbloom Laboratory for Cardiovascular Research, McGill University Health Centre, Royal Victoria Hospital, 687 Pine Avenue West, Montreal, Quebec H3A 1A1, Canada.


The adipocyte life cycle hypothesis states that the metabolic properties of an adipocyte vary predictably during its life cycle: that as an adipocyte matures, it accumulates triacylglycerol (triglyceride) and becomes larger; that the rates of triacylglycerol synthesis and lipolysis are matched within adipocytes and that larger adipocytes, in general, have greater rates of triacylglycerol synthesis and, concurrently, greater rates of lipolysis and, therefore, larger adipocytes have greater rates of transmembrane fatty acid flux; and that the secretion of cytokines can also be related to adipocyte size with larger adipocytes having a more unfavourable profile of cytokine secretion than smaller adipocytes. Adipocyte location is an important modifier of this relationship and the favoured sites of adipocyte proliferation are a function of gender and the position within the life cycle of the organism at which proliferation occurs. The adipocyte life cycle hypothesis posits that the metabolic consequences of obesity depend on whether expansion of adipose tissue is achieved primarily by an increase in adipocyte number or adipocyte size. This hypothesis may explain a variety of previously unanswered clinical puzzles such as the vulnerability of many peoples from South East Asia to the adverse metabolic consequences of obesity.

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