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Titolo:
Neuroendocrine perturbations as a cause of insulin resistance
Autore:
Bjorntorp, P;
Indirizzi:
Gothenburg Univ, Sahlgrens Hosp, Dept Heart & Lung Dis, S-41345 Gothenburg, Sweden Gothenburg Univ Gothenburg Sweden S-41345 is, S-41345 Gothenburg, Sweden
Titolo Testata:
DIABETES-METABOLISM RESEARCH AND REVIEWS
fascicolo: 6, volume: 15, anno: 1999,
pagine: 427 - 441
SICI:
1520-7552(199911/12)15:6<427:NPAACO>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
BODY-FAT DISTRIBUTION; FRAGMENT-LENGTH-POLYMORPHISM; DEPENDENT DIABETES-MELLITUS; ADIPOSE-TISSUE DISTRIBUTION; PITUITARY-ADRENAL AXIS; RAT SKELETAL-MUSCLE; MIDDLE-AGED MEN; CORTISOL SECRETION; BLOOD-PRESSURE; VISCERAL FAT;
Keywords:
insulin resistance; abdominal obesity; cortisol; sex steroids; glucocorticoid receptors; glycogen synthase;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
113
Recensione:
Indirizzi per estratti:
Indirizzo: Bjorntorp, P Gothenburg Univ, Sahlgrens Hosp, Dept Heart & Lung Dis, S-41345 Gothenburg, Sweden Gothenburg Univ Gothenburg Sweden S-41345 othenburg, Sweden
Citazione:
P. Bjorntorp, "Neuroendocrine perturbations as a cause of insulin resistance", DIABET M R, 15(6), 1999, pp. 427-441

Abstract

Insulin resistance is followed by several prevalent diseases. The most common condition with insulin resistance is obesity, particularly when localized to abdominal, visceral regions. A summary of recent reviews on the pathogenesis of systemic insulin resistance indicates that major factors are decreased insulin effects on muscularglycogen synthase or preceding steps in the insulin signalling cascade, onendogenous glucose production and on circulating free fatty acids (FFA) from adipose tissue lipolysis. Contributions of morphologic changes in muscleand other factors are considered more uncertain. Newly developed methodology has made it possible to determine more precisely the neuroendocrine abnormalities in abdominal obesity including increased cortisol and adrenal androgen secretions. This is probably due to a hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, amplified by inefficient feedback inhibition by central glucocorticoid receptors, associated with molecular genetic defects. Secondly, secretion of gender-specific sex steroid hormones becomes inhibited and the sympathetic nervous system activated. At this stage the HPA axis shows signs of a 'burned-out' condition,and cortisol secretion is no longer elevated. Cortisol counteracts the insulin activation of glycogen synthase in muscle, the insulin inhibition of hepatic glucose production and the insulin inhibition of lipolysis in adipose tissue, leading to the well-established systemic insulin resistance caused by excess cortisol. This is exaggerated by increased free fatty acid mobilization, particularly with a concomitant elevation of the activity of the sympathetic nervous system. Furthermore, capillarization and fiber composition in muscle are changed. These are the identical perturbations responsible for insulin resistance in recent reviews. The diminished sex steroid secretion in abdominal obesity has the same consequences. It is thus clear that insulin resistance may be induced by neuroendocrine abnormalities, such as those seen in abdominal obesity. These endocrine perturbations also direct excess fat to visceral fat depots via mechanisms that are largely known, indicating why abdominal obesity is commonly associated with insulin resistance. This possible background to the most prevalent condition of insulin resistance has been revealed by development of methodology that allows sufficiently sensitive measurements of HPA axis activity. These findings demonstrate the power of neuroendocrine regulations for somatic health. Copyright (C) 1999 John Wiley & Sons, Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 01:35:35