Effect of protein, fat, carbohydrate and fibre on gastrointestinal peptide release in humans

Karhunen, Leila; Juvonen, Kristiina; Huotari, Anne; Purhonen, Anna-Kaisa; Herzig, Karl‐Heinz

doi:10.1016/j.regpep.2007.10.008

Cited by 210 publications

(191 citation statements)

References 185 publications

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“…However, relying on only a single food may have masked effects of eating rate on ad libitum intake due to influences on sensoryspecific satiety [37]. Our results might also be limited to mixedcomposition meals as several putative enteroendocrine hormones are sensitive to the type of carbohydrate in the meal as well as the macronutrient composition of the meal [5]. Inclusion of smokers in the trial may also affect outcomes.…”

Section: Discussionmentioning

confidence: 96%

“…In addition to factors such as macronutrient composition [5] and viscosity [6], how one eats may affect postprandial responses of the enteroendocrine hormones that mediate appetite. Eating fast has been associated with excess energy intake and overweight [7][8][9][10][11][12], while eating slowly is hypothesized to discourage excess energy intake by allowing time for peripheral satiation signals to be consciously recognized before overeating occurs.…”

Section: Introductionmentioning

confidence: 99%

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Eating rate during a fixed-portion meal does not affect postprandial appetite and gut peptides or energy intake during a subsequent meal

Karl

Young

Montain

2011

Physiology & Behavior

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, "Eating rate during a fixed-portion meal does not affect postprandial appetite and gut peptides or energy intake during a subsequent meal" (2011). US Army Research. 131. http://digitalcommons.unl.edu/usarmyresearch/131 Eating rate during a fixed-portion meal does not affect postprandial appetite and gut peptides or energy intake during a subsequent meal ☆ Eating rate has recently been shown to influence energy intake and appetite during an ad libitum meal, and alter postprandial secretion of glucagon-like peptide-1 (GLP-1) and peptide-YY (PYY) following a fixed-portion meal. Whether these effects influence satiety, as measured by energy intake at the subsequent meal, is unclear. We manipulated eating rate during a fixed-portion meal in order to examine how eating behavior and associated periprandial and postprandial responses of putative endocrine mediators of appetite would affect energy intake at the following meal in fifteen non-obese (BMIb 25 kg/m²) and ten obese (BMI≥ 30 kg/m²) healthy adult men and women. In random order, each participant consumed a standardized, fixed-portion meal in 7 (FM), 14 (MM) or 28 (SM) minutes. Fullness, measured by the Satiety Labeled Intensity Magnitude (SLIM) scale, serum insulin, glucose, leptin, pancreatic polypeptide (PP), PYY, GLP-1, neuropeptide-Y, and plasma cholecystokinin (CCK) were measured for 3 h following the fixed-portion meal. Ad libitum energy intake at the next meal was then measured. Eating slowly delayed time to peak fullness (P ≤ 0.05), but did not alter peak fullness. Peak PP concentrations were attenuated during FM compared to MM and SM (P ≤ 0.05) and were reached earlier during MM compared to SM (P ≤ 0.05). A meal-by-time interaction (P ≤ 0.05), but no differences in AUC, peak, or time to peak were observed for CCK. No additional between meal differences in AUC, peak or time to peak for any endocrine mediator of appetite was observed. Ad libitum energy intake was not different between trials. In conclusion, the rate at which a fixed-portion meal is consumed does not appear to alter satiety despite a small effect on PP and CCK responses.Published by Elsevier Inc.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Eating rate during a fixed-portion meal does not affect postprandial appetite and gut peptides or energy intake during a subsequent meal

Karl

Young

Montain

2011

Physiology & Behavior

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“…In order to determine directly the role of PYY in mediating the satiating effects of protein, Batterham et al (68) generated PYY-null mice that were selectively resistant to the satiating and weight-reducing effects of protein; these animals developed marked obesity that was reversed by exogenous PYY treatment. In addition to CCK and PYY, a wide range of intestinal mediators have been described to be linked to dietary protein intake, as reviewed by Karhunen et al (69) . Ghrelin, …”

Section: Detection Of Protein and Amino Acids During Digestion And Comentioning

confidence: 99%

Peripheral and central mechanisms involved in the control of food intake by dietary amino acids and proteins

et al. 2012

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The present review summarises current knowledge and recent findings on the modulation of appetite by dietary protein, via both peripheral and central mechanisms. Of the three macronutrients, proteins are recognised as the strongest inhibitor of food intake. The well-recognised poor palatability of proteins is not the principal mechanism explaining the decrease in high-protein (HP) diet intake. Consumption of a HP diet does not induce conditioned food aversion, but rather experience-enhanced satiety. Amino acid consumption is detected by multiple and redundant mechanisms originating from visceral (during digestion) and metabolic (inter-prandial period) sources, recorded both directly and indirectly (mainly vagus-mediated) by the central nervous system (CNS). Peripherally, the satiating effect of dietary proteins appears to be mediated by anorexigenic gut peptides, principally cholecystokinin, glucagon-like peptide-1 and peptide YY. In the CNS, HP diets trigger the activation of noradrenergic and adrenergic neurons in the nucleus of the solitary tract and melanocortin neurons in the arcuate nucleus. Additionally, there is evidence that circulating leucine levels may modulate food intake. Leucine is associated with neural mechanisms involving mammalian target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK), energy sensors active in the control of energy intake, at least in the arcuate nucleus of the hypothalamus. In addition, HP diets inhibit the activation of opioid and GABAergic neurons in the nucleus accumbens, and thus inhibit food intake by reducing the hedonic response to food, presumably because of their low palatability. Future studies should concentrate on studying the adaptation of different neural circuits following the ingestion of protein diets.

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“…Ingested foods evoke satiety signals in the gut by mechanical stimulation involving gastric expansion or by gut hormonal stimulation, and both of these mechanisms affect the satiety centre via afferent nerves. 4,5) The gut hormones with the most robust effects on appetite suppression include cholecystokinin (CCK), glucagonlike peptide 1 (GLP-1) and peptide YY (PYY). 6) Food components that specifically stimulate these satietyrelated gut hormones have recently been the focus of nutritional and clinical attempts to reduce over-eating.…”

mentioning

confidence: 99%

Suppressive Effect on Food Intake of a Potato Extract (Potein<sup>®</sup>) Involving Cholecystokinin Release in Rats

Chen

Hira

Nakajima

et al. 2012

Bioscience, Biotechnology, and Biochemistry

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Effect of protein, fat, carbohydrate and fibre on gastrointestinal peptide release in humans

Cited by 210 publications

References 185 publications

Eating rate during a fixed-portion meal does not affect postprandial appetite and gut peptides or energy intake during a subsequent meal

Eating rate during a fixed-portion meal does not affect postprandial appetite and gut peptides or energy intake during a subsequent meal

Peripheral and central mechanisms involved in the control of food intake by dietary amino acids and proteins

Suppressive Effect on Food Intake of a Potato Extract (Potein<sup>®</sup>) Involving Cholecystokinin Release in Rats

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Effect of protein, fat, carbohydrate and fibre on gastrointestinal peptide release in humans

Cited by 210 publications

References 185 publications

Eating rate during a fixed-portion meal does not affect postprandial appetite and gut peptides or energy intake during a subsequent meal

Eating rate during a fixed-portion meal does not affect postprandial appetite and gut peptides or energy intake during a subsequent meal

Peripheral and central mechanisms involved in the control of food intake by dietary amino acids and proteins

Suppressive Effect on Food Intake of a Potato Extract (Potein<sup>&reg;</sup>) Involving Cholecystokinin Release in Rats

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Suppressive Effect on Food Intake of a Potato Extract (Potein<sup>®</sup>) Involving Cholecystokinin Release in Rats