Palatability-induced hyperphagia increases hypothalamic Dynorphin peptide and mRNA levels

Opioid involvement in regulating the intake of highly palatable diets was studied by examining the effect of feeding either a cornstarch-based diet (CHO) or a high fat diet containing sucrose (Fat/Sucrose) on hypothalamic opioid levels. Rats received either CHO ad libitum, Fat/Sucrose ad libitum, Fat/Sucrose pair-fed to the caloric intake of CHO or Fat/Sucrose at 60% of ad libitum Fat/Sucrose intake. Animals recieving Fat/Sucrose ad libitum consumed more calories and gained more weight than animals receiving CHO (P < 0.001). Relative to CHO, ad libitum intake of Fat/Sucrose elevated proDynorphin mRNA levels in the arcuate and Dynorphin A(1-17) levels in the paraventricular nucleus (PVN) (P < 0.05), but did not affect arcuate mRNA levels of proEnkephalin or proOpiomelanocortin (POMC), or PVN levels of Met-Enkephalin or beta-Endorphin. Pair-feeding the Fat/Sucrose diet to the level of intake of the CHO diet resulted in levels of proDynorphin and Dynorphin A(1-17) that were similar in the two diet groups. Pair-feeding Fat/Sucrose reduced mRNA levels of proDynorpin, proEnkephalin and POMC, and Dynorphin A(1-17) levels, relative to ad libitum feeding of Fat/Sucrose. Met-Enkephalin beta-Endorphin were not affected by dietary treatment. Feeding Fat/Sucrose at 60% of ad limitum intake resulted in mRNA levels of proDynorphin, proEnkephalin and POMC, and Dynorphin A(1-17) levels that were similar to those observed in CHO group. Hypothalamic Dynorphin A(1-17) and proDynorphin mRNA levels are stimulated by feeding a highly palatable diet rich in fat and sucrose. The increased synthesis may be due in part to a palatability-induced overconsumption of calories. Caloric restriction of the same diet decreases mRNA levels of proDynorphin, proEnkephalin and POMC, as well as levels of Dynorphin A(1-17).