Effects of acute dietary restriction on gut motor, hormone and energy intake responses to duodenal fat in obese men.
Summary of "Effects of acute dietary restriction on gut motor, hormone and energy intake responses to duodenal fat in obese men."
Background:Previous patterns of energy intake influence gastrointestinal function and appetite, probably reflecting changes in small-intestinal nutrient-mediated feedback. Obese individuals consume more fat and may be less sensitive to its gastrointestinal and appetite-suppressant effects than lean individuals.Objective:To evaluate the hypothesis that, in obese individuals, the effects of duodenal fat on gastrointestinal motor and hormone function, and appetite would be enhanced by a short period on a very-low-calorie diet (VLCD).Methods:Eight obese men (body mass index 34+/-0.6 kg m(-2)) were studied on two occasions, before (V1), and immediately after (V2), a 4-day VLCD. On both occasions, antropyloroduodenal motility, plasma cholecystokinin (CCK), peptide-YY (PYY) and ghrelin concentrations, and appetite perceptions were measured during a 120-min intraduodenal fat infusion (2.86 kcal min(-1)). Immediately afterwards, energy intake was quantified.Results:During V2, basal pyloric pressure and the number and amplitude of isolated pyloric pressure waves (PWs) were greater, whereas the number of antral and duodenal PWs was less, compared with V1 (all P<0.05). Moreover, during V2, baseline ghrelin concentration was higher; the stimulation of PYY and suppression of ghrelin by lipid were greater, with no difference in CCK concentration; and hunger and energy intake (kJ; V1: 4378+/-691, V2: 3634+/-700) were less (all P<0.05), compared with V1.Conclusions:In obese males, the effects of small-intestinal lipid on gastrointestinal motility and some hormone responses and appetite are enhanced after a 4-day VLCD.International Journal of Obesity advance online publication, 3 August 2010; doi:10.1038/ijo.2010.153.
Affiliation
[1] University of Adelaide Discipline of Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia [2] NHMRC Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, University of Adelaide, Adelaide, Sout
Journal Details
This article was published in the following journal.
Name: International journal of obesity (2005)
ISSN: 1476-5497
Pages:
Links
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/20680017
- DOI: http://dx.doi.org/10.1038/ijo.2010.153
Medical and Biotech [MESH] Definitions
Protein-energy Malnutrition
The lack of sufficient energy or protein to meet the body's metabolic demands, as a result of either an inadequate dietary intake of protein, intake of poor quality dietary protein, increased demands due to disease, or increased nutrient losses.
Ghrelin
A 28-amino acid, acylated, orexigenic peptide that is a ligand for GROWTH HORMONE SECRETAGOGUE RECEPTORS. Ghrelin is widely expressed but primarily in the stomach in the adults. Ghrelin acts centrally to stimulate growth hormone secretion and food intake, and peripherally to regulate energy homeostasis. Its large precursor protein, known as appetite-regulating hormone or motilin-related peptide, contains ghrelin and obestatin.
Caloric Restriction
Reduction in caloric intake without reduction in adequate nutrition. In experimental animals, caloric restriction has been shown to extend lifespan and enhance other physiological variables.
Leptin
A 16-kDa peptide hormone secreted from WHITE ADIPOCYTES. Leptin serves as a feedback signal from fat cells to the CENTRAL NERVOUS SYSTEM in regulation of food intake, energy balance, and fat storage.
Receptors, Leptin
Cell surface receptors for obesity factor (LEPTIN), a hormone secreted by the WHITE ADIPOCYTES. Upon leptin-receptor interaction, the signal is mediated through the JAK2/STAT3 pathway to regulate food intake, energy balance and fat storage.
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