Search

Your search keyword '"I Cusin"' showing total 2 results
Start Over Author "I Cusin" Journal comptes rendus des seances de la societe de biologie et de ses filiales
2 results on '"I Cusin"'

1. [From Claude Bernard to the regulatory system between the hypothalamus and the periphery: implications for homeostasis of body weight and obesity]

Author

B, Jeanrenaud, I, Cusin, and F, Rohner-Jeanrenaud

Subjects
Leptin, Physiology, Body Weight, Hypothalamus, Proteins, History, 19th Century, Receptors, Cell Surface, History, 20th Century, Models, Biological, Rats, Adipose Tissue, Animals, Homeostasis, Humans, Receptors, Leptin, Neuropeptide Y, France, Obesity, Carrier Proteins
Abstract

The concept of interrelationships between the central nervous system and the periphery aimed at maintaining normal body weight homeostasis has been strengthened by the discovery of hypothalamic neuropeptide Y (NPY) and adipose tissue leptin. NPY, when infused intracerebroventricularly in normal animals produces hyperphagia and hormono-metabolic changes (hyperinsulinemia, hypercorticism) channeling nutrients preferentially toward lipogenesis and storage in adipose tissue and away from their utilization by muscles (muscle insulin resistance). Storage in NPY-infused rats is further favored by the observed decrease in the expression of uncoupling proteins. NPY-induced hyperinsulinemia and hypercorticosteronemia also promote leptin over-secretion. Released leptin, acting within the hypothalamus, decreases hypothalamic NPY levels (probably those of other hypothalamic neuropeptides as well), food intake, insulinemia, insulin sensitivity of white adipose tissue, while increasing that of muscles. Leptin acting centrally additionally favors the expression of uncoupling protein 1, 2, and 3, in keeping with an eflect on energy dissipating mechanisms. The respective hormono-metabolic eflects of NPY and leptin maintain a normal body homeostasis. In most obesity syndromes, the functional relationships between NPY and leptin are altered. Due to hypothalamic leptin receptor mutations or dysfunctions, leptin cannot exert its eflects: NPY levels (possibly those of other neuropeptides) remain elevated, maintaining excess storage, insulin as well as leptin resistance.

Published
1999

2. [From Claude Bernard to the regulatory system between the hypothalamus and the periphery: implications for homeostasis of body weight and obesity].

Author

Jeanrenaud B, Cusin I, and Rohner-Jeanrenaud F

Subjects
Animals, Carrier Proteins genetics, Carrier Proteins physiology, France, History, 19th Century, History, 20th Century, Homeostasis, Humans, Hypothalamus physiopathology, Leptin, Models, Biological, Obesity genetics, Physiology history, Rats, Receptors, Leptin, Adipose Tissue physiology, Body Weight, Hypothalamus physiology, Neuropeptide Y physiology, Obesity physiopathology, Proteins physiology, Receptors, Cell Surface
Abstract

The concept of interrelationships between the central nervous system and the periphery aimed at maintaining normal body weight homeostasis has been strengthened by the discovery of hypothalamic neuropeptide Y (NPY) and adipose tissue leptin. NPY, when infused intracerebroventricularly in normal animals produces hyperphagia and hormono-metabolic changes (hyperinsulinemia, hypercorticism) channeling nutrients preferentially toward lipogenesis and storage in adipose tissue and away from their utilization by muscles (muscle insulin resistance). Storage in NPY-infused rats is further favored by the observed decrease in the expression of uncoupling proteins. NPY-induced hyperinsulinemia and hypercorticosteronemia also promote leptin over-secretion. Released leptin, acting within the hypothalamus, decreases hypothalamic NPY levels (probably those of other hypothalamic neuropeptides as well), food intake, insulinemia, insulin sensitivity of white adipose tissue, while increasing that of muscles. Leptin acting centrally additionally favors the expression of uncoupling protein 1, 2, and 3, in keeping with an eflect on energy dissipating mechanisms. The respective hormono-metabolic eflects of NPY and leptin maintain a normal body homeostasis. In most obesity syndromes, the functional relationships between NPY and leptin are altered. Due to hypothalamic leptin receptor mutations or dysfunctions, leptin cannot exert its eflects: NPY levels (possibly those of other neuropeptides) remain elevated, maintaining excess storage, insulin as well as leptin resistance.

Published
1998

Catalog

Books, media, physical & digital resources
See catalog results