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An enriched environment re-establishes metabolic homeostasis by reducing obesity-induced inflammation
- Source :
- Disease Models & Mechanisms, Vol 15, Iss 6 (2022)
- Publication Year :
- 2022
- Publisher :
- The Company of Biologists, 2022.
-
Abstract
- Obesity can lead to chronic inflammation in different tissues, generating insulin and leptin resistance and alterations in glucose and lipid metabolism, favoring the development of degenerative diseases, including type II diabetes. Congruently, the inflammatory signaling inhibition prevents the development of obesity and restores insulin sensitivity. Via the enhancement of central nervous system activity, an enriched environment (EE) has beneficial effects on learning and memory as well as on immune cell functions and inflammation in different disease models. Here, we explored whether an EE can restore energy balance in obese mice that previously presented metabolic alterations. We discovered that an EE improved glucose metabolism, increased insulin signaling in liver, and reduced hepatic steatosis and inflammation, and increased lipolysis and browning in the white adipose tissue of high-fat diet (HFD)-fed mice. Finally, we found reduced inflammatory signaling and increased anorexigenic signaling in the hypothalamus of HFD-fed mice exposed to an EE. These data indicate that an EE is able to restore the metabolic imbalance caused by HFD feeding. Thus, we propose EE as a novel therapeutic approach for treating obesity-related metabolic alterations. This article has an associated First Person interview with the first author of the paper.
- Subjects :
- obesity
enriched environment
inflammation
metabolism
Medicine
Pathology
RB1-214
Subjects
Details
- Language :
- English
- ISSN :
- 17548403 and 17548411
- Volume :
- 15
- Issue :
- 6
- Database :
- Directory of Open Access Journals
- Journal :
- Disease Models & Mechanisms
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.141ede2316644e986d54401b8bda206
- Document Type :
- article
- Full Text :
- https://doi.org/10.1242/dmm.048936