Acute Effect on Satiety, Resting Energy Expenditure, Respiratory Quotient, Glucagon-Like Peptide-1, Free Fatty Acids, and Glycerol Following Consumption of a Combination of Bioactive Food Ingredients in Overweight Subjects

Abstract Purpose Impaired glucose tolerance (IGT) is a pathophysiological condition characterized by insulin resistance with known metabolic consequences such as postprandial hyperglycemia and hypertriglyceridemia. We hypothesized that fortifying a meal with mushrooms rich in β-glucans may diminish glucose and triglyceride responses by improving postprandial gastrointestinal hormone release. Methods In a randomized controlled crossover study, 22 subjects with IGT ingested a meal either enriched with 20 g powder (8.1 g β-glucans) of oven-dried Pleurotus ostreatus (enriched meal, EN) or without enrichment (control meal, CON). Blood was collected before and repeatedly within 4 h after the meal to determine AUC of glucose (primary outcome), insulin, triglycerides, non-esterified free fatty acids (NEFAs), glucagon-like peptide-1 (GLP-1), gastric inhibitory polypeptide (GIP) and ghrelin. Appetite sensations (hunger, satiety, fullness, and desire to eat) were assessed before and after meal consumption by visual analog scales. Results Postprandial glucose, insulin, triglycerides, GIP and ghrelin concentrations as well as the corresponding AUCs did not differ between EN and CON. NEFAs-AUC was 14% lower (P = 0.026) and GLP-1-AUC 17% higher (P = 0.001) after EN compared to CON. Appetite ratings did not differ between treatments, except for hunger (AUC 22% lower after EN vs. CON; P = 0.031). Conclusion The observed immediate postprandial metabolic changes indicate that an easily manageable fortification of a single meal with powder from dried oyster mushrooms as β-glucan source may improve postprandial metabolism. If the effect is preserved long term, this measure can diminish the risk for further development of overweight/obesity and type 2 diabetes in subjects with IGT. Clinical trial registration German Clinical Trial Register on 09/08/2018; trial-ID: DRKS00015244.

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Glucagon-like peptide-1 production in the GLUTag cell line is impaired by free fatty acids via endoplasmic reticulum stress

Metabolism ◽

10.1016/j.metabol.2014.02.012 ◽

2014 ◽

Vol 63 (6) ◽

pp. 800-811 ◽

Cited By ~ 29

Author(s):

Hiroto Hayashi ◽

Ren Yamada ◽

Siddhartha Shankar Das ◽

Taiki Sato ◽

Aki Takahashi ◽

...

Keyword(s):

Fatty Acids ◽

Endoplasmic Reticulum ◽

Endoplasmic Reticulum Stress ◽

Free Fatty Acids ◽

Cell Line ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1

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Effect of large bowel fermentation on insulin, glucose, free fatty acids, and glucagon-like peptide 1 (7-36) amide in patients with coronary heart disease

Nutrition ◽

10.1016/s0899-9007(98)00177-4 ◽

1999 ◽

Vol 15 (3) ◽

pp. 183-188 ◽

Cited By ~ 14

Author(s):

Gary Frost ◽

Audrey Brynes ◽

Anthony Leeds

Keyword(s):

Fatty Acids ◽

Coronary Heart Disease ◽

Heart Disease ◽

Free Fatty Acids ◽

Large Bowel ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1

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Higher fasting plasma concentrations of glucagon-like peptide 1 are associated with higher resting energy expenditure and fat oxidation rates in humans

American Journal of Clinical Nutrition ◽

10.1093/ajcn/84.3.556 ◽

2006 ◽

Vol 84 (3) ◽

pp. 556-560 ◽

Cited By ~ 57

Author(s):

Nicola Pannacciulli ◽

Joy C Bunt ◽

Juraj Koska ◽

Clifton Bogardus ◽

Jonathan Krakoff

Keyword(s):

Energy Expenditure ◽

Plasma Concentrations ◽

Resting Energy Expenditure ◽

Fat Oxidation ◽

Oxidation Rates ◽

Fasting Plasma ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1 ◽

Resting Energy

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Comparison of effects of diabetic enteral nutrition and standard enteral nutrition on postprandial level of glycemia, free fatty acids and glucagon-like peptide-1.

Atherosclerosis ◽

10.1016/j.atherosclerosis.2016.07.545 ◽

2016 ◽

Vol 252 ◽

pp. e93

Author(s):

J. Visek ◽

A. Ticha ◽

L. Sobotka ◽

V. Blaha

Keyword(s):

Fatty Acids ◽

Enteral Nutrition ◽

Free Fatty Acids ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1

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Metabolic, gastrointestinal, and CNS neuropeptide effects of brain leptin administration in the rat

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.276.5.r1425 ◽

1999 ◽

Vol 276 (5) ◽

pp. R1425-R1433 ◽

Cited By ~ 4

Author(s):

Gertjan van Dijk ◽

Randy J. Seeley ◽

Todd E. Thiele ◽

Mark I. Friedman ◽

Hong Ji ◽

...

Keyword(s):

Fatty Acids ◽

Body Weight ◽

Energy Expenditure ◽

Neuropeptide Y ◽

Caloric Restriction ◽

Resting Energy Expenditure ◽

Corticotropin Releasing Hormone ◽

Plasma Fatty Acids ◽

The Third ◽

Ad Libitum

To investigate whether brain leptin involves neuropeptidergic pathways influencing ingestion, metabolism, and gastrointestinal functioning, leptin (3.5 μg) was infused daily into the third cerebral ventricular of rats for 3 days. To distinguish between direct leptin effects and those secondary to leptin-induced anorexia, we studied vehicle-infused rats with food available ad libitum and those that were pair-fed to leptin-treated animals. Although body weight was comparably reduced (−8%) and plasma glycerol was comparably increased (142 and 17%, respectively) in leptin-treated and pair-fed animals relative to controls, increases in plasma fatty acids and ketones were only detected (132 and 234%, respectively) in pair-fed rats. Resting energy expenditure (−15%) and gastrointestinal fill (−50%) were reduced by pair-feeding relative to the ad libitum group, but they were not reduced by leptin treatment. Relative to controls, leptin increased hypothalamic mRNA for corticotropin-releasing hormone (CRH; 61%) and for proopiomelanocortin (POMC; 31%) but did not reduce mRNA for neuropeptide Y. These results suggest that CNS leptin prevents metabolic/gastrointestinal responses to caloric restriction by activating hypothalamic CRH- and POMC-containing pathways and raise the possibility that these peripheral responses to CNS leptin administration contribute to leptin’s anorexigenic action.

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Changes in 24-h substrate oxidation in older and younger men in response to exercise

Journal of Applied Physiology ◽

10.1152/japplphysiol.01455.2006 ◽

2007 ◽

Vol 103 (5) ◽

pp. 1576-1582 ◽

Cited By ~ 18

Author(s):

Edward L. Melanson ◽

William T. Donahoo ◽

Gary K. Grunwald ◽

Robert Schwartz

Keyword(s):

Fatty Acids ◽

Energy Expenditure ◽

Free Fatty Acids ◽

Plasma Free Fatty Acid ◽

Fat Oxidation ◽

Substrate Oxidation ◽

Net Energy ◽

Younger Men ◽

Response To Exercise ◽

Time Point

The purpose of this study was to compare 24-h substrate oxidation in older (OM; 60–75 yr, n = 7) and younger (YM; 20–30 yr, n = 7) men studied on sedentary day (Con) and on a day with exercise (Ex; net energy expenditure = 300 kcal). Plasma glucose and free fatty acids were also measured at several time points during the 24-h measurement. Weight was not different in OM and YM (means ± SD; 84.8 ± 16.9 vs. 81.4 ± 10.4 kg, respectively), although percent body fat was slightly higher in OM (25.9 ± 3.5 vs. 21.9 ± 9.7%; P = 0.17).Values of 24-h energy expenditure did not differ in OM and YM on the Con (means ± SE; 2,449 ± 162 vs. 2,484 ± 104 kcal/day, respectively) or Ex (2,902 ± 154 vs. 2,978 ± 122 kcal/day) days. Under both conditions, 24-h respiratory quotient was significantly lower and fat oxidation significantly higher in OM. Glucose concentrations were not different at any time point, but plasma free fatty acid concentrations were higher in OM, particularly following meals. Thus, under these controlled conditions, 24-h fat oxidation was not reduced and was in fact greater in OM. We speculate that differences in the availability of circulating free fatty acids in the postprandial state contributed to the observed differences in 24-h fat oxidation in OM and YM.

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