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A Carbohydrate-Restricted Diet Alters Gut Peptides and Adiposity Signals in Men and Women with Metabolic Syndrome
The Journal of Nutrition, August 2007
Abstract of the Study
Matthew R. Hayes3, Carla K. Miller3,4, Jan S. Ulbrecht4,5, Joanna L. Mauger6, Lynn Parker-Klees7, Melissa Davis Gutschall3, Diane C. Mitchell3, Helen Smiciklas-Wright3 and Mihai Covasa3,*
3
  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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