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Titolo:
Mechanisms of hepatic very low-density lipoprotein overproduction in insulin resistance
Autore:
Adeli, K; Taghibiglou, C; Van Iderstine, SC; Lewis, GF;
Indirizzi:
Univ Toronto, Hosp Sick Children, DIv Clin Biochem, Dept Lab Med & Pathobiol,DPLM, Toronto, ON M5G 1X8, Canada Univ Toronto Toronto ON Canada M5G 1X8 ,DPLM, Toronto, ON M5G 1X8, Canada Univ Toronto, Dept Endocrinol & Metab, Toronto, ON M5G 1X8, Canada Univ Toronto Toronto ON Canada M5G 1X8 Metab, Toronto, ON M5G 1X8, Canada
Titolo Testata:
TRENDS IN CARDIOVASCULAR MEDICINE
fascicolo: 5, volume: 11, anno: 2001,
pagine: 170 - 176
SICI:
1050-1738(200107)11:5<170:MOHVLL>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRIGLYCERIDE TRANSFER PROTEIN; APOLIPOPROTEIN-B SECRETION; PHOSPHATIDYLINOSITOL 3-KINASE ACTIVATION; FREE FATTY-ACIDS; APO-B; RAT HEPATOCYTES; HEPG2 CELLS; TYROSINE PHOSPHATASES; ENDOPLASMIC-RETICULUM; RECEPTOR SUBSTRATE-1;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
73
Recensione:
Indirizzi per estratti:
Indirizzo: Adeli, K Univ Toronto, Hosp Sick Children, DIv Clin Biochem, Dept Lab Med & Pathobiol,DPLM, Toronto, ON M5G 1X8, Canada Univ Toronto Toronto ON Canada M5G 1X8 ronto, ON M5G 1X8, Canada
Citazione:
K. Adeli et al., "Mechanisms of hepatic very low-density lipoprotein overproduction in insulin resistance", TREND CARD, 11(5), 2001, pp. 170-176

Abstract

An important complication of insulin-resistant states, such as obesity andtype 2 diabetes, is an atherogenic dyslipidemia profile characterized by hypertriglyceridemia, low plasma high-density lipoproteins (HDL) cholesteroland a small, dense low-density lipoprotein (LDL) particle profile. The physiological basis of this metabolic dyslipidemia appears to be hepatic overproduction of apoB-containing very low-density lipoprotein (VLDL) particles. This has focused attention on the mechanisms that regulate VLDL secretion in insulin-resistant states. Recent studies in animal models of insulin resistance, particularly the fructose-fed hamster, have enhanced our understanding of these mechanisms, and certain key factors have recently been identified that play important roles in hepatic insulin resistance and dysregulation of the VLDL secretory process. This review focuses on these recent developments as well as on the hypothesis that an interaction between enhanced flux of free fatty acids from peripheral tissues to liver, chronic up-regulation of de novo lipogenesis by hyperinsulinemia and attenuated insulin signaling in the liver may be critical to the VLDL overproduction state observed in insulin resistance. It should be noted that the focus of this review is on molecular mechanisms of the hypertriglyceridemic state associated with insulin resistance and not that observed in association with insulin deficiency (e.g., in streptozotocin-treated animals), which appears to have a different etiology and is related to a catabolic defect rather than secretory overproduction of triglyceride-rich lipoproteins. (C) 2001, Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 02:37:39