Summary
The aim of this work was to determine the possible inter-relationship between neuropeptide Y (NPY, a hypothalamic stimulator of feeding) and adipose tissue expression of the ob protein (a novel potent inhibitor of feeding). Such a relationship could be of importance in the maintenance of normal body weight. To this end, normal rats were intracerebro-ventricularly (i.c.v.) infused for 6 days with NPY. NPY infusion resulted in hyperphagia and a marked increase in adipose tissue ob mRNA levels. The effect of NPY on ob expression persisted when hyperphagia was prevented by pair-feeding, and was reversed following cessation of NPY infusion. Basal and glucose-stimulated insulinaemia were increased by i. c. v. NPY infusion compared to control values, regardless of whether animals were ad libitum-fed or pair-fed. Cessation of NPY infusion was accompanied by normalisation of insulinaemia. These changes in insulinaemia produced by i. c. v. NPY infusion paralleled the observed changes in ob expression. When normal rats were made hyperinsulinaemic-euglycaemic for 24 h, such hyperinsulinaemia also resulted in increased ob mRNA levels in white adipose tissue. This suggested that NPY-induced hyperinsulinaemia could be responsible for the upregulation of ob mRNA levels of NPY-infused rats. It is concluded that central (i. c. v.) NPY infusion increases adipose tissue ob expression, a functional relationship that is linked, at least in part, via NPY-induced hyperinsulinaemia.
Similar content being viewed by others
Abbreviations
- NPY:
-
Neuropeptide Y
- i. c. v.:
-
intracerebroventricular
References
Dryden S, Frankish H, Wang Q, Williams G (1994) Neuropeptide Y and energy balance: one way ahead for the treatment of obesity? Eur J Clin Invest 24: 293–308
Vettor R, Zarjevski N, Cusin I, Rohner-Jeanrenaud F, Jean-Jeanrenaud B (1994) Induction and reversibility of an obesity syndrome by intracerebroventricular neuropeptide Y administration to normal rats. Diabetologia 37: 1202–1208
Stephens TW, Basinski M, Bristow PK, et al (1995) The role of neuropeptide Y in the antiobesity action of the obese gene product. Nature 377: 530–532
Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM (1994) Positional cloning of the mouse obese gene and its human homologue. Nature 372: 425–432
Pelleymounter MA, Cullen MJ, Baker MB, et al. (1995) Effects of the obese gene product on body weight regulation in ob/ob mice. Science 269: 540–543
Halaas JL, Gajiwala KS, Maffei M, et al (1995) Weight-reducing effects of the plasma protein encoded by the obese gene. Science 269: 543–546
Campfield LA, Smith FJ, Guisez Y, Devos R, Burn P (1995) Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks. Science 269: 546–548
Maffei M, Halaas J, Ravussin E, et al. (1995) Leptin levels in human and rodent: measurement of plasma leptin and ob RNA in obese and weight-reduced subjects. Nature Medicine 1: 1155–1161
Saladin R, De Vos P, Guerre-Millo M, et al. (1995) Transient increase in obese gene expression after food intake or insulin administration. Nature 377: 527–529
Cusin I, Sainsbury A, Doyle P, Rohner-Jeanrenaud F, Jean-renaud B (1995) The ob gene and insulin. A relationship leading to clues to the understanding of obesity. Diabetes 44: 1467–1470
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Sainsbury, A., Cusin, I., Doyle, P. et al. Intracerebroventricular administration of neuropeptide Y to normal rats increases obese gene expression in white adipose tissue. Diabetologia 39, 353–356 (1996). https://doi.org/10.1007/BF00418353
Received:
Revised:
Issue Date:
DOI: https://doi.org/10.1007/BF00418353