135246 - Serotonin improves high fat diet induced obesity in mice.pdf (1.12 MB)
Serotonin improves high fat diet induced obesity in mice
journal contribution
posted on 2023-05-20, 07:32 authored by Watanabe, H, Nakano, T, Saito, R, Akasaka, D, Saito, K, Ogasawara, H, Minashima, T, Miyazawa, K, Kanaya, T, Takakura, I, Inoue, N, Ikeda, I, Chen, X, Miyake, M, Kitazawa, H, Shirakawa, H, Sato, K, Tahara, K, Nagasawa, Y, Michael RoseMichael Rose, Ohwada, S, Watanabe, K, Aso, HThere are two independent serotonin (5-HT) systems of organization: one in the central nervous system and the other in the periphery. 5-HT affects feeding behavior and obesity in the central nervous system. On the other hand, peripheral 5-HT also may play an important role in obesity, as it has been reported that 5-HT regulates glucose and lipid metabolism. Here we show that the intraperitoneal injection of 5-HT to mice inhibits weight gain, hyperglycemia and insulin resistance and completely prevented the enlargement of intra-abdominal adipocytes without having any effect on food intake when on a high fat diet, but not on a chow diet. 5-HT increased energy expenditure, O2 consumption and CO2 production. This novel metabolic effect of peripheral 5-HT is critically related to a shift in the profile of muscle fiber type from fast/glycolytic to slow/oxidative in soleus muscle. Additionally, 5-HT dramatically induced an increase in the mRNA expression of peroxisome proliferator-activated receptor coactivator 1α (PGC-1α)-b and PGC-1α-c in soleus muscle. The elevation of these gene mRNA expressions by 5-HT injection was inhibited by treatment with 5-HT receptor (5HTR) 2A or 7 antagonists. Our results demonstrate that peripheral 5-HT may play an important role in the relief of obesity and other metabolic disorders by accelerating energy consumption in skeletal muscle.
History
Publication title
PLoS ONEVolume
11Article number
e0147143Number
e0147143Pagination
1-14ISSN
1932-6203Department/School
Tasmanian Institute of Agriculture (TIA)Publisher
Public Library of SciencePlace of publication
United StatesRights statement
Copyright 2016 Watanabe et al. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/Repository Status
- Open