Cell Metabolism . . . The calCR neurons in the hind brain are involved in regulating non-anorexic indentation.

In developed countries, obesity accounts for one-third of the population. Diabetes and cardiovascular diseases caused by obesity aggravate the mortality rate. At the same time, the current treatment of obesity is not effective.January 16, 2020, Martin g. Myers, University of Michigan, USA, The Jr. team and Clemence blouet team of Cambridge University (the first author is Dr. Wenwen Cheng) jointly published an article in the journal cell metabolism: calcium receptor neurons in the mouse nucleus tractus solitarius control energy balance via the non adverse suppression of Feeding revealed that the activation of CALCR neurons in the hindbrain can inhibit food intake without causing anorexia.in order to study the regulation of the hindbrain on food intake, the authors studied the neurons expressing calcitonin receptor (CALCR) in the hindbrain, and found that knockout of CALCR gene in the hindbrain significantly reduced the inhibition of diet and weight loss by agonist (agonist) of CALCR.in addition, more importantly, the activation of CALCR neurons in the hindbrain significantly inhibited food intake and weight loss in mice, without the side effect of anorexia (conditional taste aversion). The researchers further found that the CALCR neurons in the posterior brain projected to the non CGRP neurons of paraspinal nucleus and led to the decrease of appetite.in addition, silencing of CALCR neurons in the hindbrain can change the feeding pattern of mice, and high-energy food can lead to significant obesity in mice whose CALCR neurons are silenced.finally, silencing of CALCR neurons significantly attenuated the effects of other appetite reducing hormones, such as CCK and exendin-4, and dietary inhibiting amino acids such as leucine.original link: