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Nutrition and Disease

A Carbohydrate-Restricted Diet Alters Gut Peptides and Adiposity Signals in Men and Women with Metabolic Syndrome^1,2

³ Department of Nutritional Sciences, College of Health and Human Development, ⁴ Penn State Diabetes Center, ⁵ Departments of Biobehavioral Health and Medicine, Colleges of Health and Human Development and Medicine, and ⁶ General Clinical Research Center, The Pennsylvania State University, University Park, PA 16802; and ⁷ Center Medical Surgical Associates, State College, PA 16803

^* To whom correspondence should be addressed. E-mail: mzc13{at}psu.edu.

Carbohydrate-restricted diets have been shown to enhance satiation- and other homeostatic-signaling pathways controlling food intake and energy balance, which may serve to reduce the incidence of obesity and metabolic syndrome. This study was designed as a correlational, observational investigation of the effects of a carbohydrate-restricted diet on weight loss and body fat reduction and associated changes in circulating leptin, insulin, ghrelin, and cholecystokinin (CCK) concentrations in overweight/obese patients (4 men and 16 women) with metabolic syndrome. Subjects received clinical instruction on the initiation and maintenance of the commercial South Beach Diet, consisting of 2 phases: Phase I (initial 2 wk of the study) and Phase II (remaining 10 wk). Participants showed a decrease (P < 0.05) in body weight (93.5 ± 3.6 kg vs. 88.3 ± 3.4 kg), BMI (33.9 ± 1.3 kg/m² vs. 32.0 ± 1.3 kg/m²), waist circumference (112.8 ± 2.8 cm vs. 107.7 ± 3.0 cm), and total percent body fat (40.2 ± 1.5% vs. 39.2 ± 1.5%) by study completion. Plasma fasting insulin and leptin concentrations decreased significantly from baseline concentrations (139.1 ± 12.2 pmol/L and 44.1 ± 4.5 µg/L, respectively) by the end of Phase I (98.6 ± 2.6 pmol/L and 33.3 ± 4.1 µg/L, respectively). Plasma fasting ghrelin concentrations significantly increased from baseline (836.7 ± 66.7 ng/L) by Phase II (939.9 ± 56.8 ng/L). The postprandial increase in plasma CCK concentrations (difference in plasma CCK concentrations from fasting to postprandial) after Phase I (2.4 ± 0.3 pmol/L) and Phase II (2.5 ± 0.4 pmol/L) was significantly greater than the postprandial increase at baseline (1.1 ± 0.5 pmol/L). Collectively, these results suggest that in patients with metabolic syndrome, improved adiposity signaling and increased postprandial CCK concentrations may act together as a possible compensatory control mechanism to maintain low intakes and facilitate weight loss, despite an increase in fasting ghrelin concentrations and subjective measures of hunger.

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