scholarly journals Effects of Taurocholic Acid on Glycemic, Glucagon-like Peptide-1, and Insulin Responses to Small Intestinal Glucose Infusion in Healthy Humans

2013 ◽  
Vol 98 (4) ◽  
pp. E718-E722 ◽  
Author(s):  
Tongzhi Wu ◽  
Michelle J. Bound ◽  
Scott D. Standfield ◽  
Karen L. Jones ◽  
Michael Horowitz ◽  
...  
2012 ◽  
Vol 15 (5) ◽  
pp. 474-477 ◽  
Author(s):  
T. Wu ◽  
M. J. Bound ◽  
S. D. Standfield ◽  
B. Gedulin ◽  
K. L. Jones ◽  
...  

1997 ◽  
Vol 273 (5) ◽  
pp. E981-E988 ◽  
Author(s):  
Michael A. Nauck ◽  
Ulrich Niedereichholz ◽  
Rainer Ettler ◽  
Jens Juul Holst ◽  
Cathrine Ørskov ◽  
...  

Glucagon-like peptide 1 (GLP-1) has been shown to inhibit gastric emptying of liquid meals in type 2 diabetic patients. It was the aim of the present study to compare the action of physiological and pharmacological doses of intravenous GLP-1-(7—36) amide and GLP-1-(7—37) on gastric emptying in normal volunteers. Nine healthy subjects participated (26 ± 3 yr; body mass index 22.9 ± 1.6 kg/m2; hemoglobin A1C 5.0 ± 0.2%) in five experiments on separate occasions after an overnight fast. A nasogastric tube was positioned for the determination of gastric volume by use of a dye-dilution technique (phenol red). GLP-1-(7—36) amide (0.4, 0.8, or 1.2 pmol ⋅ kg−1 ⋅ min−1), GLP-1-(7—37) (1.2 pmol ⋅ kg−1 ⋅ min−1), or placebo was infused intravenously from −30 to 240 min. A liquid meal (50 g sucrose, 8% amino acids, 440 ml, 327 kcal) was administered at 0 min. Glucose, insulin, and C-peptide were measured over 240 min. Gastric emptying was dose dependently slowed by GLP-1-(7—36) amide ( P < 0.0001). Effects of GLP-1-(7—37) at 1.2 pmol ⋅ kg−1 ⋅ min−1were virtually identical. GLP-1 dose dependently stimulated fasting insulin secretion (−30 to 0 min) and slightly reduced glucose concentrations. After the meal (0–240 min), integrated incremental glucose ( P < 0.0001) and insulin responses ( P = 0.01) were reduced (dose dependently) rather than enhanced. In conclusion, 1) GLP-1-(7—36) amide or -(7—37) inhibits gastric emptying also in normal subjects, 2) physiological doses (0.4 pmol ⋅ kg−1 ⋅ min−1) still have a significant effect, 3) despite the known insulinotropic actions of GLP-1-(7—36) amide and -(7—37), the net effect of administering GLP-1 with a meal is no change or a reduction in meal-related insulin responses. These findings suggest a primarily inhibitory function for GLP-1 (ileal brake mechanisms).


2013 ◽  
Vol 3 ◽  
Author(s):  
Kiyoshi Ebihara ◽  
Makoto Tachibe ◽  
Natsumi Kaneko ◽  
Taro Kishida

AbstractIt was examined whether the physiological effects of high-amylose maize starch (HAMS) are influenced by hydroxypropylation. Rats were fed one of the following three diets: an AIN-93-based diet with waxy maize starch (WMS) as a starch source, or this diet with 150 g of WMS replaced by either HAMS or hydroxypropylated HAMS (HP-HAMS). The activities of amylase in bile-pancreatic juice and sucrose, maltase and isomaltase of the jejunum and ileum were not affected by diet, but the digestibility of HAMS was decreased by hydroxypropylation. The amounts of SCFA in caecal content and H2 excreted in the breath and flatus for HAMS were decreased by hydroxypropylation. Plasma glucagon-like peptide-1 (GLP-1), glucose and insulin concentrations were not affected by diet. On the basis of PCR-denaturing gradient gel electrophoresis (DGGE) profiles, the similarity in caecal bacteria population of the HP-HAMS group and HAMS group was low, but that of the HP-HAMS and WMS groups was high. The amount of caecal IgA was not affected by hydroxypropylation, but those in the HAMS and HP-HAMS groups were greater than that in the WMS group. Plasma and liver concentrations of TAG and cholesterol for HAMS were not affected by hydroxypropylation. These results show that the small intestinal digestibility and fermentation-dependent parameters such as caecal SCFA and H2 productions and caecal bacterial profile of HAMS were affected by hydroxypropylation, but parameters of glucose metabolism such as GLP-1 and insulin, those of lipid metabolism such as plasma TAG and cholesterol and the amount of caecal IgA were not.


2017 ◽  
Vol 97 (1) ◽  
pp. 411-463 ◽  
Author(s):  
Robert E. Steinert ◽  
Christine Feinle-Bisset ◽  
Lori Asarian ◽  
Michael Horowitz ◽  
Christoph Beglinger ◽  
...  

The efficacy of Roux-en-Y gastric-bypass (RYGB) and other bariatric surgeries in the management of obesity and type 2 diabetes mellitus and novel developments in gastrointestinal (GI) endocrinology have renewed interest in the roles of GI hormones in the control of eating, meal-related glycemia, and obesity. Here we review the nutrient-sensing mechanisms that control the secretion of four of these hormones, ghrelin, cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), and peptide tyrosine tyrosine [PYY(3–36)], and their contributions to the controls of GI motor function, food intake, and meal-related increases in glycemia in healthy-weight and obese persons, as well as in RYGB patients. Their physiological roles as classical endocrine and as locally acting signals are discussed. Gastric emptying, the detection of specific digestive products by small intestinal enteroendocrine cells, and synergistic interactions among different GI loci all contribute to the secretion of ghrelin, CCK, GLP-1, and PYY(3–36). While CCK has been fully established as an endogenous endocrine control of eating in healthy-weight persons, the roles of all four hormones in eating in obese persons and following RYGB are uncertain. Similarly, only GLP-1 clearly contributes to the endocrine control of meal-related glycemia. It is likely that local signaling is involved in these hormones' actions, but methods to determine the physiological status of local signaling effects are lacking. Further research and fresh approaches are required to better understand ghrelin, CCK, GLP-1, and PYY(3–36) physiology; their roles in obesity and bariatric surgery; and their therapeutic potentials.


Diabetes ◽  
1996 ◽  
Vol 45 (11) ◽  
pp. 1524-1530 ◽  
Author(s):  
J. Rachman ◽  
F. M. Gribble ◽  
B. A. Barrow ◽  
J. C. Levy ◽  
K. D. Buchanan ◽  
...  

2008 ◽  
Vol 33 (5) ◽  
pp. 929-935 ◽  
Author(s):  
Eric M. Snyder ◽  
Richard D. Carr ◽  
Carolyn F. Deacon ◽  
Bruce D. Johnson

Altitude exposure has been associated with loss of appetite and weight loss in healthy humans; however, the endocrine factors that contribute to these changes remain unclear. Leptin and glucagon-like peptide-1 (GLP-1) are peptide hormones that contribute to the regulation of appetite. Leptin increases with hypoxia; however, the influence of hypoxia on GLP-1 has not been studied in animals or humans to date. We sought to determine the influence of normobaric hypoxia on plasma leptin and GLP-1 levels in 25 healthy humans. Subjects ingested a control meal during normoxia and after 17 h of exposure to normobaric hypoxia (fraction of inspired oxygen of 12.5%, simulating approximately 4100 m). Plasma leptin was assessed before the meal, and GLP-1 was assessed premeal, at 20 min postmeal, and at 40 min postmeal. We found that hypoxia caused a significant elevation in plasma leptin levels (normoxia, 4.9 ± 0.8 pg·mL–1; hypoxia, 7.7 ± 1.5 pg·mL–1; p < 0.05; range, –16% to 190%), no change in the average GLP-1 response to hypoxia, and only a small trend toward an increase in GLP-1 levels 40 min postmeal (fasting, 15.7 ± 0.9 vs 15.9 ± 0.7 pmol·L–1; 20 min postmeal, 21.7 ± 0.9 vs 21.8 ± 1.2 pmol·L–1; 40 min postmeal, 19.5 ± 1.2 vs. 21.0 ± 1.2 pmol·L–1 for normoxia and hypoxia, respectively; p > 0.05 normoxia vs hypoxia). There was a correlation between SaO2 and leptin after the 17 h exposure (r = 0.45; p < 0.05), but no relation between SaO2 and GLP-1. These data confirm that leptin increases with hypoxic exposure in humans. Further study is needed to determine the influence of hypoxia and altitude on GLP-1 levels.


2014 ◽  
Vol 111 (9) ◽  
pp. 1564-1576 ◽  
Author(s):  
Anne Krog Ingerslev ◽  
Peter Kappel Theil ◽  
Mette Skou Hedemann ◽  
Helle Nygaard Lærke ◽  
Knud Erik Bach Knudsen

The effects of increased colonic fermentation of dietary fibres (DF) on the net portal flux (NPF) of carbohydrate-derived metabolites (glucose, SCFA and, especially, butyrate), hormones (insulin, C-peptide, glucagon-like peptide 1 and glucose-dependent insulinotropic peptide) and NEFA were studied in a healthy catheterised pig model. A total of six pigs weighing 59 (sem1·6) kg were fitted with catheters in the mesenteric artery and in the portal and hepatic veins, and a flow probe around the portal vein, and included in a double 3 × 3 cross-over design with three daily feedings (at 09.00, 14.00 and 19.00 hours). Fasting and 5 h postprandial blood samples were collected after 7 d adaptation to each diet. The pigs were fed a low-DF Western-style control diet (WSD) and two high-DF diets (an arabinoxylan-enriched diet (AXD) and a resistant starch-enriched diet (RSD)). The NPF of insulin was lower (P= 0·04) in AXD-fed pigs (4·6 nmol/h) than in RSD-fed pigs (10·5 nmol/h), despite the lowest NPF of glucose being observed in RSD-fed pigs (203 mmol/h,P= 0·02). The NPF of total SCFA, acetate, propionate and butyrate were high, intermediate and low (P< 0·01) in AXD-, RSD- and WSD-fed pigs, respectively, with the largest relative increase being observed for butyrate in response to arabinoxylan supplementation. In conclusion, the RSD and AXD had different effects on the NPF of insulin and glucose, suggesting different impacts of arabinoxylan and resistant starch on human health.


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