PALATABILITY-INDUCED HYPERPHAGIA INCREASES HYPOTHALAMIC DYNORPHIN PEPTIDE AND MESSENGER-RNA LEVELS

Opioid involvement in regulating the intake of highly palatable diets was studied by examining the effect of feeding either a cornstarch-bas ed diet (CHO) or a high fat diet containing sucrose (Fat/Sucrose) on h ypothalamic opioid levels. Rats received either CHO ad libitum, Fat/Su crose ad libitum, Fat/Sucrose pair-fed to the caloric intake of CHO or Fat/Sucrose at 60% of ad libitum Fat/Sucrose intake. Animals recievin g Fat/Sucrose ad libitum consumed more calories and gained more weight than animals receiving CHO (P < 0.001). Relative to CHO, ad libitum i ntake 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 pro Opiomelanocortin (POMC), or PVN levels of Met-Enkephalin or beta-Endor phin. 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-Enkeph alin beta-Endorphin were not affected by dietary treatment. Feeding Fa t/Sucrose at 60% of ad limitum intake resulted in mRNA levels of proDy norphin, proEnkephalin and POMC, and Dynorphin A(1-17) levels that wer e similar to those observed in CHO group. Hypothalamic Dynorphin A(1-1 7) and proDynorphin mRNA levels are stimulated by feeding a highly pal atable diet rich in fat and sucrose. The increased synthesis may be du e in part to a palatability-induced overconsumption of calories. Calor ic restriction of the same diet decreases mRNA levels of proDynorphin, proEnkephalin and POMC, as well as levels of Dynorphin A(1-17).