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Metabolic Syndrome - U.S. Department of Veterans Affairs

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Last Updated: 23 April 2022

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ErbB4 deletion predisposes to development of metabolic syndrome in mice.

A link between ErbB4 and type 2 diabetes and obesity has been found by genetic studies, but the role in metabolic syndrome has not been established. Increased subcutaneous and visceral fat in ErbB4 deletion mice, as well as elevated serum leptin levels, were also present in wild-type mice, although adiponectin levels were not significantly different, although adiponectin levels were not significantly different. During 3T3-L1 preadipocyte differentiation differentiation, ErbB4 expression decreased during ErbB4-mediated differentiation. Administration of neuroregulin 4, a specific ligand for ErbB4, failed lipogenesis and lipolysis, promoted browning, triggered GLUT4 redistribution to the cell membrane, and increased glucose uptake in 3T3-L1 adipocytes. These results were significantly reduced in adipocytes isolated from wild-type mice isolated from ErbB4 deletion mice, which was also increased glucose uptake in adipocytes isolated from wild-type mice. In conclusion, our results show that ErbB4 may play a vital role in glucose homeostasis and lipogenesis.

Source link: https://doi.org/10.1152/ajpendo.00166.2018

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions