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The Amplifying Pathway of the β-Cell Contributes to Diet-induced Obesity

Published in The Journal of biological chemistry. 2016, vol. 291, no. 25, p. 13063-13075
Abstract Efficient energy storage in adipose tissues requires optimal function of the insulin-producing β-cell, whereas its dysfunction promotes diabetes. The associated paradox related to β-cell efficiency is that excessive accumulation of fat in adipose tissue predisposes for type 2 diabetes. Insulin exocytosis is regulated by intracellular metabolic signal transduction, with glutamate dehydrogenase playing a key role in the amplification of the secretory response. Here, we used mice with β-cell-selective glutamate dehydrogenase deletion (βGlud1(-/-)), lacking an amplifying pathway of insulin secretion. As opposed to control mice, βGlud1(-/-) animals fed a high calorie diet maintained glucose tolerance and did not develop diet-induced obesity. Islets of βGlud1(-/-) mice did not increase their secretory response upon high calorie feeding, as did islets of control mice. Inhibited adipose tissue expansion observed in knock-out mice correlated with lower expression of genes responsible for adipogenesis. Rather than being efficiently stored, lipids were consumed at a higher rate in βGlud1(-/-) mice compared with controls, in particular during food intake periods. These results show that reduced β-cell function prior to high calorie feeding prevented diet-induced obesity.
Keywords diabetesinsulinpancreatic islets
PMID: 27137930
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Article (Published version) (2.8 MB) - public document Free access
Research group Mitochondries et métabolisme énergétique (671)
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VETTERLI, Laurene Marine et al. The Amplifying Pathway of the β-Cell Contributes to Diet-induced Obesity. In: The Journal of biological chemistry, 2016, vol. 291, n° 25, p. 13063-13075. doi: 10.1074/jbc.M115.707448 https://archive-ouverte.unige.ch/unige:89721

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Deposited on : 2016-12-02

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