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Comment
. 2009 May;58(5):1037-9.
doi: 10.2337/db09-0290.

Adipose tissue plasticity in catch-up-growth trajectories to metabolic syndrome: hyperplastic versus hypertrophic catch-up fat

Abdul G Dulloo  1
Affiliations
Comment

Adipose tissue plasticity in catch-up-growth trajectories to metabolic syndrome: hyperplastic versus hypertrophic catch-up fat

Abdul G Dulloo. Diabetes. 2009 May.
No abstract available

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Figures

FIG. 1.
FIG. 1.
Conceptual model depicting mechanisms by which the thrifty catch-up–fat phenotype, driven by suppressed thermogenesis, may cross-link with the development of insulin resistance and glucose intolerance. The depletion (or delayed growth/development) of the adipose tissue fat stores suppresses skeletal muscle thermogenesis, which during refeeding leads to concomitant glucose sparing and muscle insulin resistance. The resulting compensatory hyperinsulinemia serves to redirect the glucose spared from oxidation in skeletal muscle toward de novo lipogenesis and fat storage in white adipose tissue. In hyperplastic catch-up fat, a greater number of smaller adipocytes, coupled with lipogenesis, provide an efficient buffering capacity against the spared glucose and, hence, help to achieve normal glucose tolerance. By contrast, in hypertrophic catch-up fat, the low capacity for adipogenesis, coupled with lipogenesis, generates enlarged adipocytes, which are more prone to release proinflammatory cytokines and/or to spillover of lipids to nonadipocytes (with consequential ectopic lipotoxicity). This further exacerbates insulin resistance in skeletal muscle and other insulin-sensitive tissues, thereby resulting in more pronounced systemic insulin resistance and impaired glucose tolerance. The outcome of catch-up growth toward a hyperplastic or a hypertrophic catch-up–fat phenotype is determined by interactions among genetics, epigenetics, and environment.
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