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Glucagon-like peptide 1 receptor induced suppression of food intake, and body weight is mediated by central IL-1 and IL-6

Artikel i vetenskaplig tidskrift
Författare Rozita H. Shirazi
Vilborg Palsdottir
Jim Collander
Fredrik Anesten
Heike Vogel
F. Langlet
A. Jaschke
A. Schurmann
V. Prevot
Linus Ruijin Shao
John-Olov Jansson
Karolina P Skibicka
Publicerad i Proceedings of the National Academy of Sciences of the United States of America
Volym 110
Nummer/häfte 40
Sidor 16199-16204
ISSN 0027-8424
Publiceringsår 2013
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Sidor 16199-16204
Språk en
Länkar dx.doi.org/10.1073/pnas.1306799110
Ämnesord POMC, DVC, hypothermia, CENTRAL-NERVOUS-SYSTEM, MATURE-ONSET OBESITY, CAUDAL BRAIN-STEM, ARCUATE, NUCLEUS, GLUCAGON-LIKE-PEPTIDE-1 RECEPTOR, INSULIN-RESISTANCE, ENERGY-BALANCE, MESSENGER-RNAS, GLP-1 RECEPTOR, INFLAMMATION
Ämneskategorier Klinisk medicin

Sammanfattning

Glucagon-like peptide 1 (GLP-1), produced in the intestine and the brain, can stimulate insulin secretion from the pancreas and alleviate type 2 diabetes. The cytokine interleukin-6 (IL-6) may enhance insulin secretion from beta-cells by stimulating peripheral GLP-1 production. GLP-1 and its analogs also reduce food intake and body weight, clinically beneficial actions that are likely exerted at the level of the CNS, but otherwise are poorly understood. The cytokines IL-6 and interleukin 1 beta (IL-1 beta) may exert an anti-obesity effect in the CNS during health. Here we found that central injection of a clinically used GLP-1 receptor agonist, exendin-4, potently increased the expression of IL-6 in the hypothalamus (11-fold) and the hindbrain (4-fold) and of IL-1 beta in the hypothalamus, without changing the expression of other inflammation-associated genes. Furthermore, hypothalamic and hindbrain interleukin-associated intracellular signals [phosphorylated signal transducer and activator of transcription-3 (pSTAT3) and suppressor of cytokine signaling-1 (SOCS1)] were also elevated by exendin-4. Pharmacologic disruption of CNS IL-1 receptor or IL-6 biological activity attenuated anorexia and body weight loss induced by central exendin-4 administration in a rat. Simultaneous blockade of IL-1 and IL-6 activity led to a more potent attenuation of exendin-4 effects on food intake. Mice with global IL-1 receptor gene knockout or central IL-6 receptor knockdown showed attenuated decrease in food intake and body weight in response to peripheral exendin-4 treatment. GLP-1 receptor activation in the mouse neuronal Neuro2A cell line also resulted in increased IL-6 expression. These data outline a previously unidentified role of the central IL-1 and IL-6 in mediating the anorexic and body weight loss effects of GLP-1 receptor activation.

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