![]() ![]() In adipose tissue, an excess in energy intake generates cellular stress, which induces the expression of cytokines and chemokines, leading to the recruitment and activation of different immune cells, mainly macrophages ( Gregor and Hotamisligil, 2011). Different studies have shown that obesity is accompanied by a low-grade chronic inflammatory state that has been described in different tissues and organs, including pancreas, skeletal muscle, adipose tissue, liver and brain ( Lumeng and Saltiel, 2011). Obesity is of clinical interest as it is linked with an increased risk of developing other pathologies, such as cardiovascular and neurodegenerative diseases, cancer and type II diabetes ( Hotamisligil, 2006). Obesity has become an increasing worldwide health issue over the past years in some countries it accounts for over 20% of the adult population ( OECD, 2017). ![]() This article has an associated First Person interview with the first author of the paper. Thus, we propose EE as a novel therapeutic approach for treating obesity-related metabolic alterations. These data indicate that an EE is able to restore the metabolic imbalance caused by HFD feeding. Finally, we found reduced inflammatory signaling and increased anorexigenic signaling in the hypothalamus of HFD-fed mice exposed to an EE. ![]() 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. Here, we explored whether an EE can restore energy balance in obese mice that previously presented metabolic alterations. 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. Congruently, the inflammatory signaling inhibition prevents the development of obesity and restores insulin sensitivity. 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. ![]()
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