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Palatable High‐Energy Diet Decreases the Expression of Cannabinoid Type 1 Receptor Messenger RNA in Specific Brain Regions in the Rat
Author(s) -
Timofeeva E.,
Baraboi E.D.,
Poulin A.M.,
Richard D.
Publication year - 2009
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.2009.01921.x
Subject(s) - medicine , endocrinology , parvocellular cell , hypothalamus , biology , leptin , receptor , arc (geometry) , appetite , obesity , geometry , mathematics
In laboratory rodents, a palatable high‐energy diet (PHED) is usually consumed in a higher quantity than a standard laboratory diet, leading to the development of an obese phenotype. The central effects of PHED are not fully understood. Nonetheless, the long‐term consumption of PHED can decrease cannabinoid type 1 receptor (CB1R) protein density in particular brain regions. However, little is known about the diet‐dependent regulation of the brain expression of CB1R mRNA. The present study aimed to investigate the effects of the long‐term consumption of PHED and short‐term (12 h) food deprivation on the brain expression of CB1R mRNA. For 13 weeks, rats were fed a standard laboratory chow or PHED presented as a free choice of chow, shortcake biscuits and pork spread. In total, the food intake of PHED rats was higher than that of chow‐fed animals. Expectedly, PHED rats demonstrated higher body weight than chow‐fed animals. The difference in body weight between PHED‐ and chow‐fed rats was as result of the fat but not the lean mass. PHED‐fed rats had significantly higher plasma levels of leptin and insulin and significantly higher levels of expression of suppressor of cytokine signalling 3 (SOCS‐3) in the arcuate hypothalamic nucleus. The long‐term consumption of PHED significantly decreased the levels of CB1R mRNA expression in the cingulate (Cg) cortex, ventromedial hypothalamic nucleus and the descending/autonomic divisions of the parvocellular hypothalamic nucleus (PVH), the ventrolateral parvocellular PVH and, to a lesser extent, the dorsomedial parvocellular PVH. Acute food deprivation decreased the levels of CB1R transcript in the Cg and ventrolateral parvocellular PVH. Altogether, the present results demonstrate that long‐term PHED leads to an increase in the hypothalamic expression of SOCS‐3 mRNA and a decrease in expression of CB1R mRNA in the Cg cortex and specific hypothalamic regions.