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Obesity

Ankyrin-B in susceptibility to obesity

Nature Reviews Endocrinology volume 14, page 65 (2018)Cite this article

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Overeating and lack of physical activity are the leading causes of obesity; however, genetics might also be involved. Strong evidence has linked many genetic loci to obesity, but the mechanism remains elusive. A new study has shown that dysfunction of ankyrin-B (a protein expressed by the proposed obesity susceptibility gene ANK2) in adipose tissue results in cell-autonomous adiposity by increasing glucose uptake and lipogenesis.

Previous studies by Damaris Lorenzo, Vann Bennett and colleagues found that ankyrin-B mutant mice consumed more glucose and exhibited increased levels of GLUT4 in adipose tissue and striated muscle. Mice deficient in ankyrin-B in only adipocytes showed the same results, suggesting that the observed effects were due to fat cells.

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References

  1. Lorenzo, D. N. & Bennett, V. Cell-autonomous adiposity through increased cell surface GLUT4 due to ankyrin-B deficiency. Proc. Natl Acad. Sci USA http://dx.doi.org/10.1073/pnas.1708865114 (2017)

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  1. Ivone Leong
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Lorenzo, D. N. et al. Ankyrin-B metabolic syndrome combines age-dependent adiposity with pancreatic B cell insufficiency. J. Clin. Invest. 125, 3087–3102 (2015)

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Leong, I. Ankyrin-B in susceptibility to obesity. Nat Rev Endocrinol 14, 65 (2018). https://doi.org/10.1038/nrendo.2017.163

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