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Titolo:
IMPAIRED FATTY-ACID METABOLISM IN FAMILIAL COMBINED HYPERLIPIDEMIA - A MECHANISM ASSOCIATING HEPATIC APOLIPOPROTEIN-B OVERPRODUCTION AND INSULIN-RESISTANCE
Autore:
CABEZAS MC; DEBRUIN TWA; DEVALK HW; SHOULDERS CC; JANSEN H; ERKELENS DW;
Indirizzi:
UNIV HOSP UTRECHT G02 228,DEPT INTERNAL MED,POB 85500 3508 GA UTRECHTNETHERLANDS UNIV HOSP UTRECHT,DEPT ENDOCRINOL 3508 GA UTRECHT NETHERLANDS HAMMERSMITH HOSP,DIV MOLEC MED LONDON W12 0HS ENGLAND UNIV HOSP ROTTERDAM,DEPT BIOCHEM 3000 DR ROTTERDAM NETHERLANDS UNIV HOSP ROTTERDAM,DEPT MED 3000 DR ROTTERDAM NETHERLANDS
Titolo Testata:
The Journal of clinical investigation
fascicolo: 1, volume: 92, anno: 1993,
pagine: 160 - 168
SICI:
0021-9738(1993)92:1<160:IFMIFC>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT DIABETES-MELLITUS; CORONARY HEART-DISEASE; LIPOPROTEIN-LIPASE; DYSLIPIDEMIC HYPERTENSION; COMBINED HYPERLIPEMIA; PLASMA-LIPOPROTEINS; RAT HEPATOCYTES; A-I; HYPERTRIGLYCERIDEMIA; SECRETION;
Keywords:
APOLIPOPROTEIN-B; FATTY ACIDS; HYPERINSULINEMIA; INSULIN RESISTANCE; PREMATURE ATHEROSCLEROSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
50
Recensione:
Indirizzi per estratti:
Citazione:
M.C. Cabezas et al., "IMPAIRED FATTY-ACID METABOLISM IN FAMILIAL COMBINED HYPERLIPIDEMIA - A MECHANISM ASSOCIATING HEPATIC APOLIPOPROTEIN-B OVERPRODUCTION AND INSULIN-RESISTANCE", The Journal of clinical investigation, 92(1), 1993, pp. 160-168

Abstract

To establish whether insulin resistance and/or postprandial fatty acid metabolism might contribute to familial combined hyperlipidemia (FCH) we have examined parameters of insulin resistance and lipid metabolism in six FCH kindreds. Probands and relatives (n = 56) were divided into three tertiles on the basis of fasting plasma triglycerides (TG). Individuals in the highest tertile (TG > 2.5 mM; n = 14) were older and had increased body mass index, systolic blood pressure, and fasting plasma insulin concentrations compared with individuals in the lowest tertile (n = 24). The former also presented with decreased HDL cholesterol and increased total plasma cholesterol, HDL-TG, and apoprotein B,E, and CIII concentrations. Insulin concentrations were positively correlated with plasma apo B, apo CIII, apo E, and TG, and inversely with HDL cholesterol. Fasting nonesterified fatty acids (NEFA) were elevated in FCH subjects compared to six unrelated controls and five subjects with familial hypertriglyceridemia. Prolonged and exaggerated postprandial plasma NEFA concentrations were found in five hypertriglyceridemic FCH probands. In FCH the X2 minor allele of the AI-CIII-AIV gene cluster was associated with increased fasting plasma TG, apo CIII, apoAl, and NEFA concentrations and decreased postheparin lipolytic activities. The clustering of risk factors associated with insulin resistance in FCH indicates a common metabolic basis for the FCH phenotype andthe syndrome of insulin resistance probably mediated by an impaired fatty acid metabolism.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/09/20 alle ore 00:32:39