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Hypothalamic MC4R regulates glucose homeostasis through adrenaline-mediated control of glucose reabsorption via renal GLUT2 in mice – published online 14/10/2020

de Souza Cordeiro GA

Leticia Maria de Souza Cordeiro, Arwa Elsheikh, Nagavardhini Devisetty, Donald A. Morgan, Steven N. Ebert, Kamal Rahmouni, Kavaljit H. Chhabra

Obesity and increased plasma insulin levels (insulin resistance) are major risk factors for type 2 diabetes in the general population. Yet, individuals with melanocortin 4 receptor (MC4R) deficiency either do not develop, or are at a relatively lower risk of developing, diabetes. To understand why MC4R deficiency prevents diabetes despite obesity and insulin resistance, de Souza Cordeiro et al (https://doi.org/10.1007/s00125-020-05289-z) investigated the function of this protein in glucose regulation using mouse models. The authors observed that lack of MC4R in mice increased glucosuria, thereby keeping blood glucose levels normal. The increase in urinary glucose excretion was due to reduced plasma adrenaline and expression of the glucose transporter GLUT2 in the kidneys. These findings demonstrate that elevated glucosuria may be one of the reasons why MC4R deficiency prevents diabetes. Based on the study findings, the authors propose that blocking kidney-specific GLUT2 has the potential to treat diabetes.

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