内科学
内分泌学
臂旁核
刺激
生物
臂旁外侧核
肽YY
受体
降钙素基因相关肽
胰高血糖素
神经肽
下丘脑
细胞生物学
化学
神经肽Y受体
医学
激素
作者
Fredrik Anesten,Devesh Mishra,Adrià Dalmau Gasull,Linda Engström Ruud,Jakob Bellman,Vilborg Pálsdóttir,Fuping Zhang,Stefan Trapp,Karolina P. Skibicka,Matti Poutanen,John Olov Jansson
出处
期刊:Neuroendocrinology
[S. Karger AG]
日期:2019-01-01
卷期号:109 (4): 310-321
被引量:5
摘要
Interleukin (IL)-6 in the hypothalamus and hindbrain is an important downstream mediator of suppression of body weight and food intake by glucagon-like peptide-1 (GLP-1) receptor stimulation. CNS GLP-1 is produced almost exclusively in prepro-glucagon neurons in the nucleus of the solitary tract. These neurons innervate energy balance-regulating areas, such as the external lateral parabrachial nucleus (PBNel); essential for induction of anorexia. Using a validated novel IL-6-reporter mouse strain, we investigated the interactions in PBNel between GLP-1, IL-6, and calcitonin gene-related peptide (CGRP, a well-known mediator of anorexia). We show that PBNel GLP-1R-containing cells highly (to about 80%) overlap with IL-6-containing cells on both protein and mRNA level. Intraperitoneal administration of a GLP-1 analogue exendin-4 to mice increased the proportion of IL-6-containing cells in PBNel 3-fold, while there was no effect in the rest of the lateral parabrachial nucleus. In contrast, injections of an anorexigenic peptide growth and differentiation factor 15 (GDF15) markedly increased the proportion of CGRP-containing cells, while IL-6-containing cells were not affected. In summary, GLP-1R are found on IL-6-producing cells in PBNel, and GLP-1R stimulation leads to an increase in the proportion of cells with IL-6-reporter fluorescence, supporting IL-6 mediation of GLP-1 effects on energy balance.
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