Abstract

Ingestion of a high carbohydrate (HC) or high fat (HF) diet induces obesity in association or not with modifications of the feeding behaviour. Effects of diet composition on NPY, a powerful stimulant of weight gain and food intake (particularly carbohydrates), are not known. That is why we measured NPY in 10 microdissected brain nuclei of rats fed either a HC diet (69% of energy from carbohydrates), a HF diet (68% of energy from fat) or a control well-balanced diet (54% of energy from carbohydrates; 30% of energy from fat) during a 14-day period. Total caloric intake was significantly greater (+12%) in rats fed on the HF diet than in the control and HC rats. HF rats also gained more weight than the two other groups (47.5 ± 2.4 g vs 37.6 ± 2.6 g (control) and 29.1 ± 1.4 g (HC); p < 0.001). NPY variations were restricted to two hypothalamic areas. In the parvocellular part of the paraventricular nucleus, NPY was smaller with the HC diet than with the HF diet (42.1 ± 2.3 vs 49.5 ± 2.7 ng/mg protein; p < 0.05). A decrease was observed in the lateral hypothalamus with the HF diet when compared with the control diet (11.3 ± 0.7 vs 14.6 ± 1.1 ng/mg protein; p < 0.05). No variations were observed either in other hypothalamic nuclei such as arcuate, dorsomedian, ventromedian or suprachiasmatic nuclei or in extra-hypothalamic areas such as the ventral tegmental area or submamillary bodies. It appears therefore that diet composition can modulate NPY levels in specific nuclei involved in the regulation of food intake. NPY changes might be related to the carbohydrate-to-fat ratio in the paraventricular nucleus and to the caloric load ingested in the lateral hypothalamus.

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