Publications by authors named "D Cota"

Objective: Steroidogenic factor-1 (SF1) neurons of the ventromedial hypothalamus play key roles in the regulation of food intake, body weight and glucose metabolism. The bile acid receptor Takeda G protein-coupled receptor 5 (TGR5) is expressed in the hypothalamus, where it determines some of the actions of bile acids on food intake and body weight through still poorly defined neuronal mechanisms. Here, we examined the role of TGR5 in SF1 neurons in the regulation of energy balance and glucose metabolism.

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Glucagon-like peptide 1 (GLP-1) stimulates insulin secretion and holds significant pharmacological potential. Nevertheless, the regulation of energy homeostasis by centrally-produced GLP-1 remains partially understood. Preproglucagon cells, known to release GLP-1, are found in the olfactory bulb (OB).

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Article Synopsis
  • The hypothalamus has lots of different neurons that control behavior and metabolism, and these neurons can change over time.
  • Researchers found special 'Ghost' neurons, which don't act like regular ones and were previously unnoticed by other methods.
  • The number of Ghost neurons increases in mice that gain weight from unhealthy diets, but they can change back when the mice lose weight, showing that neurons can adapt based on diet.
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The brain-gut neurocircuitry is proving to be finely involved in a wide range of physiological functions. In this issue of Neuron, Ren et al. show that adrenergic signaling suppresses postprandial glucagon-like peptide 1 (GLP-1) secretion.

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Objective: Intestinal gluconeogenesis (IGN), via the initiation of a gut-brain nervous circuit, accounts for the metabolic benefits linked to dietary proteins or fermentable fiber in rodents and has been positively correlated with the rapid amelioration of body weight after gastric bypass surgery in humans with obesity. In particular, the activation of IGN moderates the development of hepatic steatosis accompanying obesity. In this study, we investigated the specific effects of IGN on adipose tissue metabolism, independent of its induction by nutritional manipulation.

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