Literature DB >> 20031131

Postprandial metabolic and hormonal responses of obese dyslipidemic subjects with metabolic syndrome to test meals, rich in carbohydrate, fat or protein.

Dalia El Khoury1, Nahla Hwalla, Vincent Frochot, Jean-Marc Lacorte, Michèle Chabert, Athina D Kalopissis.   

Abstract

BACKGROUND: The metabolic syndrome (MS) is a cluster of heterogeneous abnormalities conferring increased risk of cardiovascular diseases. Few postprandial studies have been conducted in MS individuals.
OBJECTIVES: We aimed to study MS subjects with the same abnormalities: abdominal obesity, hypertriglyceridemia and low plasma HDL. We assessed postprandial variations of metabolic parameters related to obesity, dyslipidemia and glucose homeostasis.
METHODS: In this randomized, double-blind, cross-over study, male MS and control subjects consumed, at separate occasions, a high carbohydrate (HC), high fat (HF) or high protein (HP) breakfast meal providing 30% of each subject's resting energy expenditure.
RESULTS: Appetite hormones peptide YY and ghrelin did not differ between-subject groups. Interleukin-6 was two-fold higher in MS compared with control subjects, consistently with an inflammatory state. Hypertriglyceridemia of MS subjects was aggravated postprandially with the HF and HP meals and was lowest after the HC meal, arguing against increased hepatic VLDL production. HDL-cholesterol of MS subjects remained low postprandially, whereas apolipoprotein (apo) A-II was higher than in control subjects. Unexpectedly, postprandial insulin and glucose responses were higher in MS compared with control subjects, with the HP meal inducing the greater effects.
CONCLUSIONS: The sustained postprandial hypertriglyceridemia of MS subjects after all meals suggests defective catabolism of triglyceride-rich lipoproteins. The greater postprandial increases in plasma insulin and glucose in MS relatively to control subjects indicate decreased insulin sensitivity, not revealed in the fasted state. Copyright 2009. Published by Elsevier Ireland Ltd.

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Year:  2009        PMID: 20031131     DOI: 10.1016/j.atherosclerosis.2009.11.017

Source DB:  PubMed          Journal:  Atherosclerosis        ISSN: 0021-9150            Impact factor:   5.162


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