Is insulin a satiety signal? Insulin treatment antagonises starvation-induced increases in neuropeptide Y concentrations in the arcuate nucleus of the rat

Malabu, U.H., McCarthy, H.D., McKibbin, P.E., Burrows, C., and Williams, G. (1992) Is insulin a satiety signal? Insulin treatment antagonises starvation-induced increases in neuropeptide Y concentrations in the arcuate nucleus of the rat. Clinical Science, 83 (Supplement No. 27). p. 3.

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Abstract

Neuropeptide Y (NPY), the most powerful appetite stimulant known, is synthesised in hypothalamic arcuate nucleus (ARC). NPY levels rise in the ARC and in appetite-regulating hypothalamic nuclei in food-deprived rats, and may drive compensatory hyperphagia in starvation. Circulating insulin levels fall in starvation and insulin deficiency has been postulated to stimulate hypothalamic NPY; this supports the suggestion that insulin acts on the brain to inhibit feeding. We tested this hypothesis by determining whether the increase in NPY in the ARC of starved rats was suppressed by insulin treatment.

Adult male Wistar rats were studied. Controls (n=8) were freely-fed and two other groups were food-deprived for 72 hours, both losing 20% of initial weight (p<O.OOI vs controls). One food·deprived group n=10) received insulin (5 U/kg/day) injected subcutaneously twice daily and both other groups recieved saline. Mean blood glucose values (measured in tail-prick samples) were 5.9± 0.1 mmoVI in controls, 4.6± 0.3 mmol/l in food-deprived (p<O.OOI. vs controls) and in insulin·treated 4.4± 0.3 mmol/I (p<O.OOI vs controls; NS vs food-deprived group). Final plasma insulin levels in insulin·treated rats were higher than in saline-treated food-deprived rats (46.6± 8.9 vs 28.9± 4.5 pmol/l; p<O.OOI) and comparable with controls (52.6± 16.2 pmol/l; p=NS). ARC NPY concentrations rose significantly above controls in food·deprived rats (14.18± 1.79 vs 8.4± 2.16 fmol/ug protein; p<O.OOI) and were intermediate in the insulin-treated food-deprived group (11.19± 1.36 fmol/ug protein: p<O.OI vs controls and p<O.OOI vs saline-treated, food deprived). Other hypothalamic regions showed no differences between groups.

Insulin therefore antagonises fasting·induced increases in NPY concentrations in the ARC. This is consistent with the hypotheses that insulin deficiency stimulates hypothalamic NPY synthesis, and that peripheral insulin acts as a satiety factor by inhibiting hypothalamic NPY.

Item ID: 29859
Item Type: Article (Abstract)
ISSN: 1470-8736
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This special issue of Clinical Science contains communications of the Medical Research Society Meeting held on 8 and 9 April 1992.

Date Deposited: 31 Mar 2014 07:48
FoR Codes: 11 MEDICAL AND HEALTH SCIENCES > 1103 Clinical Sciences > 110306 Endocrinology @ 100%
SEO Codes: 92 HEALTH > 9201 Clinical Health (Organs, Diseases and Abnormal Conditions) > 920104 Diabetes @ 100%
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