Glucagon-like peptide-1(7–36)amide and glucose-dependent insulinotropic polypeptide secretion in response to nutrient ingestion in man: acute post-prandial and 24-h secretion patterns

Elliott, Ruan; Morgan, LM; Tredger, J. Michael; Deacon, Steve; Wright, John W.; Marks, Vincent

doi:10.1677/joe.0.1380159

Cited by 607 publications

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“…We found that delivery of fat calories through the gastrointestinal tract compared with fat delivered directly into the systemic circulation is important for release of GIP, GLP-1, and PYY . Fat content in the diet has been found to be an important trigger for the secretion of these gastrointestinal peptides (14,32,36). However, whereas previous studies have found that dietary fat is a potent stimulus for gastrointestinal peptides secretion, we found a potent reduction in only GIP, with just a modest reduction in GLP-1 and PYY , when most of the fat was removed from the diet.…”

Section: Discussioncontrasting

confidence: 85%

“…However, many of the mechanisms governing gastrointestinal peptide secretion remain unclear. Fat content in the diet has been found to be a trigger for the secretion of these gastrointestinal peptides (14,32,36), but the impact of removing fat calories from the diet on the magnitude of change in the secretion of these peptides is not known.The primary goal of this study was to determine the acute glycemic and endocrine responses to the reduction of fat content from a meal. To better address the influence of ingested fat on postprandial glucose response, subjects ingested tracerlabeled carbohydrate ([ 13 C]glucose) to measure the delivery of the exogenous glucose to the systemic circulation.…”

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confidence: 99%

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confidence: 99%

“…Over the past several years, the gastrointestinal tract has been found to release important peptide hormones into the systemic circulation in response to the contents of the meal (1,14,21). These gastrointestinal peptides, such as glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and peptide YY ) have several important metabolic actions, including mediating pancreatic insulin secretion and effecting the sensation of hunger and satiety (3,27,36).…”

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Reducing dietary fat from a meal increases the bioavailability of exogenous carbohydrate without altering plasma glucose concentration

Knuth¹,

Shrivastava²,

Horowitz³

2009

Journal of Applied Physiology

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Knuth ND, Shrivastava CR, Horowitz JF. Reducing dietary fat from a meal increases the bioavailability of exogenous carbohydrate without altering plasma glucose concentration. J Appl Physiol 106: 122-129, 2009. First published November 13, 2008 doi:10.1152/japplphysiol.90404.2008.-The primary goal of this study was to determine the acute glycemic and endocrine responses to the reduction of fat content from a meal. On three separate occasions, nine overweight subjects (body mass index ϭ 30 Ϯ 1 kg/m 2 ; 5 men, 4 women) consumed 1) a control meal (ϳ800 kcal; 100 g of carbohydrate, 31 g of fat, and 30 g of protein), 2) a low-fat meal (ϳ530 kcal; 100 g of carbohydrate, 1 g of fat, and 30 g of protein), or 3) a low-fat meal plus lipid infusion [same meal as low-fat meal, but the total energy provided was the same as control (800 kcal), with the "missing" fat (ϳ30 g) provided via an intravenous lipid infusion]. All three meals contained [ 13 C]glucose (3 mg/kg body wt) to assess the bioavailability of ingested glucose. During the 5-h period after each meal, we measured the recovery of [ 13 C]glucose in plasma, plasma glucose, and insulin concentrations. We also measured plasma concentration of the gastrointestinal peptides: glucosedependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and peptide YY 3-36 (PYY3-36). The recovery of the ingested [ 13 C]glucose in the hour after ingestion was greater (P Ͻ 0.05) after the low-fat than after the control meal [area under the curve (AUC): 1,206 Ϯ 252 and 687 Ϯ 161 M ⅐ h, respectively]. However, removing dietary fat from the meal did not affect the plasma concentration of glucose or insulin. Importantly, [ 13 C]glucose recovery was not different during the low-fat and lipid infusion trials (AUC: 1,206 Ϯ 252 and 1,134 Ϯ 247 M ⅐ h, respectively), indicating that the accelerated delivery of exogenous glucose found after removing fat from the meal is due exclusively to the reduction of fat in the gastrointestinal tract. In parallel with these findings, the reduction in fat calories from the meal reduced plasma concentration of GIP, GLP-1, and PYY 3-36. In summary, these data suggest that removing fat from the diet expedited exogenous glucose delivery into the systemic circulation and reduced the concentration of key gastrointestinal peptides, yet maintained plasma glucose concentration at control levels. glucose metabolism; incretins; gastrointestinal peptides; low-fat diet; obesity METABOLIC ALTERATIONS after a single meal (e.g., hyperglycemia, hyperlipidemia) have been found to be important independent risk factors for development of obesity-related diseases (19,31,37). However, the impact of the acute response to meal ingestion often gets little attention. For example, despite the fact that low-fat diets have been advocated for weight loss for decades, surprisingly little is understood about the acute metabolic effects of reducing fat calories from the meals. Findings from studies evaluating the metabolic and endocrine responses to the removal of fat from ...

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Section: Discussioncontrasting

confidence: 85%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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Reducing dietary fat from a meal increases the bioavailability of exogenous carbohydrate without altering plasma glucose concentration

Knuth¹,

Shrivastava²,

Horowitz³

2009

Journal of Applied Physiology

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“…In rats, a greater hyperinsulinaemic response was seen after a 6-week diet enriched in monounsaturated and polyunsaturated fatty acids compared to a diet high in saturated fatty acids [46]. GLP-1 is secreted by the intestinal endocrine Lcells in response to a mixed meal [47], with both glucose and fatty acids being stimulants [48] but circulating and neural mediators could also be important [49]. Plasma active GLP-1 concentrations potentiate glucose-stimulated insulin secretion [50] in a dosedependent manner [49] via GLP-1 receptors on the beta cell.…”

Section: Discussionmentioning

confidence: 99%

Interaction between specific fatty acids, GLP-1 and insulin secretion in humans

et al. 2002

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Aims/hypothesis. Fatty acids affect insulin secretion in vivo, but little is known about the effects of specific fatty acids. Our aim was to investigate differential effects of acutely increased plasma monounsaturated, polyunsaturated and saturated fatty acids on glucosestimulated insulin secretion in healthy humans. Methods. A new experimental protocol was used to increase plasma monounsaturated (MUFA test), polyunsaturated (PUFA test) or saturated (SFA test) nonesterified fatty acids for 2 h by repeated oral fat feeding and continuous intravenous heparin infusion. This was followed by a hyperglycaemic clamp (10 mmol/l) to test insulin secretion in response to a prior plasma NEFA increase. Results. Total plasma NEFA concentrations were increased during the fat tests compared to the control visit (1.7-fold increase for MUFA and SFA tests and 1.4-fold increase for PUFA test; p<0.001). Exaggerated responses in plasma insulin, C-peptide and proinsulin concentrations were seen during the hyperglycaemic clamp after increasing plasma NEFA concentrations compared with the control (p<0.01). The effects were greatest for the MUFA test followed by the PUFA test and SFA test (p<0.01). Plasma GLP-1 concentrations increased during fat feeding, with a higher response during the MUFA test compared to PUFA and SFA tests (p<0.01). Conclusion/interpretation. Increasing plasma NEFA concentrations by oral fat feeding with heparin infusion augments glucose-stimulated insulin secretion with the greatest effect for monounsaturated fatty acids and the lowest effect for saturated fatty acids. Monounsaturated fatty acids also increase GLP-1 more than saturated fatty acids. Therefore, the exaggerated insulin concentrations could be due to both NEFA and GLP-1. [Diabetologia (2002[Diabetologia ( ) 45:1533[Diabetologia ( -1541 Keywords Monounsaturated fatty acids, polyunsaturated fatty acids, saturated fatty acids, insulin secretion, GLP-1. High fat diets lead to obesity, which in turn is one of the main causes of the development of Type II (noninsulin-dependent) diabetes mellitus. Both obesity and Type II diabetes are characterized by increased plasma non-esterified fatty acid concentrations [1] and raised fasting plasma NEFA concentrations are a risk marker for the development of Type II diabetes in Caucasian subjects [2] and in Pima Indians [3]. Increased plasma NEFA concentrations can have adverse effects on various tissues. Excess plasma NEFA concentrations can lead to a reduced skeletal muscle glucose uptake and oxidation [4,5,6], increased hepatic glucose output [7] and a decrease in hepatic insulin clearance [8,9]. These mechanisms could lead to glucose intolerance and insulin resistance leading to Type II diabetes.Inappropriately high concentrations of plasma NEFA have also been shown to alter glucose-stimulat-

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Effect of glucagon on carbohydrate-mediated secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-36 amide) (GLP-1)

Ranganath

Schäper

Gama

et al. 1999

Diabetes Metab. Res. Rev.

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Glucagon-like peptide-1(7–36)amide and glucose-dependent insulinotropic polypeptide secretion in response to nutrient ingestion in man: acute post-prandial and 24-h secretion patterns

Cited by 607 publications

References 0 publications

Reducing dietary fat from a meal increases the bioavailability of exogenous carbohydrate without altering plasma glucose concentration

Reducing dietary fat from a meal increases the bioavailability of exogenous carbohydrate without altering plasma glucose concentration

Interaction between specific fatty acids, GLP-1 and insulin secretion in humans

Effect of glucagon on carbohydrate-mediated secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-36 amide) (GLP-1)

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