Key result
Loss of the insulin receptor in fat is sufficient to disrupt white fat formation and brown fat thermogenic function, leading to severe lipoatrophic diabetes, whereas the IGF-1 receptor has only a modest contribution.
Loss of the insulin receptor is sufficient to disrupt white fat formation but not brown fat formation, while IGF1R has only a modest contribution to adipose tissue development.
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Hypothesis-generating in mice; human relevance of insulin vs IGF-1 receptor contributions to adipose dysfunction remains open.
Boucher et al. (2016) studied Lipodystrophy and Diabetes. Fat-specific knockout of insulin receptor (IR) and/or IGF-1 receptor (IGF1R) vs. Control (Adipo-Cre negative floxed) mice was evaluated on White and brown adipose tissue mass and metabolic function. Loss of the insulin receptor in fat is sufficient to disrupt white fat formation and brown fat thermogenic function, leading to severe lipoatrophic diabetes, whereas the IGF-1 receptor has only a modest contribution.
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