PMID- 21262246 OWN - NLM STAT- MEDLINE DCOM- 20110715 LR - 20131121 IS - 1873-507X (Electronic) IS - 0031-9384 (Linking) VI - 103 IP - 2 DP - 2011 May 3 TI - Regulation by chronic-mild stress of glucocorticoids, monocyte chemoattractant protein-1 and adiposity in rats fed on a high-fat diet. PG - 173-80 LID - 10.1016/j.physbeh.2011.01.017 [doi] AB - Stress has been reported as a widespread problem and several studies have linked obesity and inflammation-related diseases. Moreover, the combination of suffering from chronic stress and high energy intake might be related to the onset of some metabolic diseases. To study the possible relationships between stress, inflammatory status and obesity, a chronic-mild stress (CMS) paradigm with a high-fat dietary intake model (Cafeteria diet) was implemented on male Wistar rats for 11 weeks. Stress and dietary intake effects on animal adiposity, serum biochemical as well as glucocorticoids and inflammation markers were all analyzed. As expected, consuming a high-fat diet increased body weight, adiposity and insulin resistance in non-stressed animals. A decrease of total white adipose tissue (WAT) and an increase of fecal glucocorticoids, as well as angiotensinogen, and monocyte chemoattractant protein-1 (MCP-1) expression level in retroperitoneal WAT were found only on control-stressed rats. Regarding the serum MCP-1, a decrease was observed on animals under CMS while being fed Cafeteria diet. Furthermore, 11beta-hydroxysteroid dehydrogenase activity, a glucocorticoid and obesity biomarker in the liver, was influenced by high-fat diet intake but not by stress. Finally, statistical analysis showed a strong relation between MCP-1 expression levels in retroperitoneal WAT, fecal corticosterone and total WAT. This trial proved that CMS induced a glucocorticoid-mediated response, which was reduced by the intake of a Cafeteria diet. These findings suggest that a high-fat diet could protect against a stress condition and revealed a different behavior to a stressful environment depending on the nutritional status. CI - Copyright (c) 2011 Elsevier Inc. All rights reserved. FAU - Paternain, L AU - Paternain L AD - Department of Nutrition and Food Sciences, Physiology and Toxicology, University of Navarra, c/Irunlarrea 1, 31008 Pamplona, Spain. FAU - Garcia-Diaz, D F AU - Garcia-Diaz DF FAU - Milagro, F I AU - Milagro FI FAU - Gonzalez-Muniesa, P AU - Gonzalez-Muniesa P FAU - Martinez, J A AU - Martinez JA FAU - Campion, J AU - Campion J LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20110122 PL - United States TA - Physiol Behav JT - Physiology & behavior JID - 0151504 RN - 0 (Chemokine CCL2) RN - 0 (Dietary Fats) RN - 11002-13-4 (Angiotensinogen) RN - EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases) RN - W980KJ009P (Corticosterone) SB - IM MH - 11-beta-Hydroxysteroid Dehydrogenases/metabolism MH - Adipose Tissue, White/drug effects/metabolism MH - Adiposity/drug effects/*physiology MH - Angiotensinogen/metabolism MH - Animals MH - Chemokine CCL2/blood/*metabolism MH - Corticosterone/*analysis MH - Dietary Fats/*pharmacology MH - Feces/chemistry MH - Insulin Resistance/physiology MH - Liver/drug effects/metabolism MH - Male MH - Rats MH - Rats, Wistar MH - Stress, Psychological/*metabolism EDAT- 2011/01/26 06:00 MHDA- 2011/07/16 06:00 CRDT- 2011/01/26 06:00 PHST- 2010/08/13 00:00 [received] PHST- 2011/01/11 00:00 [revised] PHST- 2011/01/16 00:00 [accepted] PHST- 2011/01/26 06:00 [entrez] PHST- 2011/01/26 06:00 [pubmed] PHST- 2011/07/16 06:00 [medline] AID - S0031-9384(11)00032-1 [pii] AID - 10.1016/j.physbeh.2011.01.017 [doi] PST - ppublish SO - Physiol Behav. 2011 May 3;103(2):173-80. doi: 10.1016/j.physbeh.2011.01.017. Epub 2011 Jan 22.