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Titolo:
New insights into sympathetic regulation of glucose and fat metabolism
Autore:
Nonogaki, K;
Indirizzi:
Univ Calif San Francisco, Dept Psychiat, Nina Ireland Lab Dev Neurobiol, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA
Titolo Testata:
DIABETOLOGIA
fascicolo: 5, volume: 43, anno: 2000,
pagine: 533 - 549
SICI:
0012-186X(200005)43:5<533:NIISRO>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
BETA(3)-ADRENERGIC RECEPTOR GENE; AGOUTI OBESITY SYNDROME; CENTRAL-NERVOUS-SYSTEM; BROWN ADIPOSE-TISSUE; SKELETAL-MUSCLE; VENTROMEDIAL HYPOTHALAMUS; NEUROPEPTIDE-Y; BETA-3-ADRENERGIC RECEPTOR; MOLECULAR-CLONING; OB/OB MICE;
Keywords:
leptin; sympathetic; adrenergic; glucose; obesity; diabetes;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
125
Recensione:
Indirizzi per estratti:
Indirizzo: Nonogaki, K Univ Calif San Francisco, Dept Psychiat, Nina Ireland Lab Dev Neurobiol, 401 Parnassus Ave, San Francisco, CA 94143 USA Univ Calif San Francisco 401 Parnassus Ave San Francisco CA USA 94143
Citazione:
K. Nonogaki, "New insights into sympathetic regulation of glucose and fat metabolism", DIABETOLOG, 43(5), 2000, pp. 533-549

Abstract

The autonomic nervous system modulates glucose and fat metabolism through both direct neural effects and hormonal effects. This review presents recent concepts on the sympathetic regulation of glucose and fat metabolism. Focally released norepinephrine from sympathetic nerves is likely to increase glucose uptake in skeletal muscle and adipose tissues independent of insulin but norepinephrine does not contribute so much as epinephrine to hepatic glucose production. Epinephrine increases hepatic glucose production and inhibits insulin secretion and the glucose uptake by tissues that is induced by insulin. Additionally, catecholamines can increase thermogenesis and lipolysis, leading to increased energy expenditure and decreased fat stores. It is likely that beta-(beta 3)-adrenergic receptors mediate these responses. Alterations of central neurotransmission and environmental factors can change the relative contribution of sympathetic outflow to the pancreas, liver, adrenal medulla and adipose tissues, leading to the modulation of glucose and fat metabolism. Recent studies have proposed that leptin, an adipocyte hormone, affects the central nervous system to increase sympathetic outflow independent of feeding. The effects of leptin on glucose and fat metabolism could be in part mediated by the sympathetic nervous system. Studies using mice with a genetic disruption of serotonin 5-HT2c receptor indicate that central neural mechanisms in the regulation of sympathetic outflow and satiety could be dissociated. Abnormalities of sympathetic effects, including disturbances of leptin and beta 3-adrenergic receptor signalling, are likely to cause obesity and impaired glucose tolerance in rodents and humans. These findings indicate that dysfunction of the sympathetic nervous system could predispose to obesity and Type II (non-insulin-dependent) diabetes mellitus.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 10:17:46