Palatable high-energy diet decreases the expression of cannabinoid type 1 receptor messenger RNA in specific brain regions in the rat.
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.
Timofeeva
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E
Centre de Recherche de l'Institut Universitaire de Cardiologie et de Pneumologie de Québec, l'Université Laval, Québec, Canada. elena.timofeeva@ap.ulaval.ca
Baraboi
E-D
ED
Poulin
A-M
AM
Richard
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D
D000273:Adipose Tissue; D000818:Animals; D001823:Body Composition; D001835:Body Weight; D001921:Brain / Q000378:metabolism*; D004032:Diet; D004435:Eating / Q000502:physiology*; D002149:Energy Intake; D005508:Food Deprivation; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D043884:Receptor, Cannabinoid, CB1 / Q000235:genetics / Q000378:metabolism*; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000378:metabolism; D013997:Time Factors
C543264:Cnr1 protein, rat; D007328:Insulin; D020738:Leptin; D012333:RNA, Messenger; D043884:Receptor, Cannabinoid, CB1; C491410:Socs3 protein, rat; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins