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Titolo:
Postprandial dyslipidemia in men with visceral obesity: an effect of reduced LDL receptor expression?
Autore:
Mamo, JCL; Watts, GF; Barrett, PHR; Smith, D; James, AP; Pal, S;
Indirizzi:
Curtin Univ Technol, Dept Nutr Dietet & Food Sci, Bentley, WA 6102, Australia Curtin Univ Technol Bentley WA Australia 6102 Bentley, WA 6102, Australia
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
fascicolo: 3, volume: 281, anno: 2001,
pagine: E626 - E632
SICI:
0193-1849(200109)281:3<E626:PDIMWV>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRIGLYCERIDE-RICH LIPOPROTEINS; CHYLOMICRON REMNANTS; INSULIN-RESISTANCE; BODY-FAT; METABOLISM; LIPEMIA; RATS; HYPERTRIGLYCERIDEMIA; HYPERCHOLESTEROLEMIA; HYPERINSULINEMIA;
Keywords:
postprandial lipemia; insulin resistance;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Mamo, JCL Curtin Univ Technol, Sch Publ Hlth, Dept Nutr Dietet & Food Sci,GPO Box 41987, Perth, WA 6845, Australia Curtin Univ Technol GPO Box 41987Perth WA Australia 6845 tralia
Citazione:
J.C.L. Mamo et al., "Postprandial dyslipidemia in men with visceral obesity: an effect of reduced LDL receptor expression?", AM J P-ENDO, 281(3), 2001, pp. E626-E632

Abstract

Postprandial lipemia after an oral fat challenge was studied in middle-aged men with visceral obesity. The two groups had similar plasma cholesterol levels, but obese subjects had higher levels of plasma triglyceride and reduced amounts of high-density cholesterol. Fasting plasma insulin was fourfold greater in obese subjects because of concomitant insulin resistance, with a calculated HOMA score of 3.1 +/- 0.6 vs. 0.8 +/- 0.2, respectively. Plasma apolipoprotein B-48 (apoB(48)) and retinyl palmitate (RP) after an oralfat challenge were used to monitor chylomicron metabolism. Compared with lean subjects, the fasting concentration of apoB48 was more than twofold greater in obese individuals, suggestive of an accumulation of posthydrolyzed particles. After the oral lipid load, the incremental areas under the apoB(48) and RP curves (IAUC) were both significantly greater in obese subjects (apoB48: 97 +/- 17 vs. 44 +/- 12 mug.ml(-1).h; RP: 3,120 +/- 511 vs. 1,308 /- 177 U.ml(-1).h, respectively). A delay in the conversion of chylomicrons to remnants probably contributed to postprandial dyslipidemia in viscerally obese subjects. The triglyceride IAUC was 68% greater in obese subjects (4.7 +/- 0.6 vs. 2.8 +/- 0.8 mM.h, P < 0.06). Moreover, peak postprandial triglyceride was delayed by <similar to>2 h in obese subjects. The reductionin triglyceride lipolysis in vivo did not appear to reflect changes in hydrolytic enzyme activities. Postheparin plasma lipase rates were found to besimilar for lean and obese subjects. In this study, low-density lipoprotein (LDL) receptor expression on mononuclear cells was used as a surrogate marker of hepatic activity. We found that, in obese subjects, the binding of LDL was reduced by one-half compared with lean controls (70.9 +/- 15.07 vs.38.9 +/- 4.6 ng LDL bound/mug cell protein, P = 0.02). Because the LDL receptor is involved in the removal of proatherogenic chylomicron remnants, wesuggest that the hepatic clearance of these particles might be compromisedin insulin-resistant obese subjects. Premature and accelerated atherogenesis in viscerally obese, insulin-resistant subjects may in part reflect delayed clearance of postprandial lipoprotein remnants.

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Documento generato il 19/01/20 alle ore 01:13:09