Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion

Item Type:Article
Title:Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion
Creators Name:Gregnani, M.F. and Budu, A. and Batista, R.O. and Ornellas, F.H. and Estrela, G.R. and Arruda, A.C. and Freitas-Lima, L.C. and Kremer, J.L. and Favaroni Mendes, L.A. and Casarini, D.E. and Lotfi, C.F.P. and Oyama, L.M. and Bader, M. and Araujo, R.C.
Abstract:Our group has shown in several papers that kinin B1 receptor (B1R) is involved in metabolic adaptations, mediating glucose homeostasis and interfering in leptin and insulin signaling. Since catecholamines are involved with metabolism management, we sought to evaluate B1R role in catecholamine synthesis/secretion. Using B1R global knockout mice, we observed increased basal epinephrine content, accompanied by decreased hepatic glycogen content and increased glucosuria. When these mice were challenged with maximal intensity exercise, they showed decreased epinephrine and norepinephrine response, accompanied by disturbed glycemic responses to effort and poor performance. This phenotype was related to alterations in adrenal catecholamine synthesis: increased basal epinephrine concentration and reduced norepinephrine content in response to exercise, as well decreased gene expression and protein content of tyrosine hydroxylase and decreased gene expression of dopamine beta hydroxylase and kinin B2 receptor. We conclude that the global absence of B1R impairs catecholamine synthesis, interfering with glucose metabolism at rest and during maximal exercise.
Keywords:Catecholamines, Kinin Receptors, Physical Exercise, Glucose Homeostasis, Animals, Mice
Source:Molecular and Cellular Endocrinology
ISSN:0303-7207
Publisher:Elsevier
Volume:579
Page Range:112085
Date:1 January 2024
Official Publication:https://doi.org/10.1016/j.mce.2023.112085
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library