A carbohydrate-restricted diet alters gut peptides and adiposity signals in men and women with metabolic syndrome.
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/m(2) vs. 32.0 +/- 1.3 kg/m(2)), 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 microg/L, respectively) by the end of Phase I (98.6 +/- 2.6 pmol/L and 33.3 +/- 4.1 microg/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.
Hayes
Matthew R
MR
Department of Nutritional Sciences, College of Health and Human Development, The Pennsylvania State University, University Park, PA 16802, USA.
Miller
Carla K
CK
Ulbrecht
Jan S
JS
Mauger
Joanna L
JL
Parker-Klees
Lynn
L
Gutschall
Melissa Davis
MD
Mitchell
Diane C
DC
Smiciklas-Wright
Helen
H
Covasa
Mihai
M
D050154:Adiposity / Q000502:physiology*; D000328:Adult; D004032:Diet; D004040:Dietary Carbohydrates / Q000494:pharmacology*; D004044:Dietary Proteins; D004435:Eating / Q000502:physiology; D005260:Female; D041981:Gastrointestinal Tract / Q000378:metabolism*; D054439:Ghrelin; D006801:Humans; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D008875:Middle Aged; D009747:Nutritional Physiological Phenomena; D036361:Peptide Hormones / Q000097:blood; D010455:Peptides / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology; D015431:Weight Loss
D004040:Dietary Carbohydrates; D004044:Dietary Proteins; D054439:Ghrelin; D007328:Insulin; D020738:Leptin; D036361:Peptide Hormones; D010455:Peptides