Direct effect of incretin hormones on glucose and glycerol metabolism and hemodynamics
| Autor: | Thomas P. J. Solomon, Kristian Karstoft, Stefan P. Mortensen, Sine H. Knudsen |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Blood Glucose
Glycerol Male Physiology Endocrinology Diabetes and Metabolism Hemodynamics Incretins/pharmacology Blood Pressure Regional Blood Flow/drug effects chemistry.chemical_compound Heart Rate Glucose/metabolism Medicine Glucose kinetics Glucose disposal Heart Rate/drug effects Glucose clamp technique Glucagon-like peptide-1 Somatostatin Hyperglycemia/metabolism hormones hormone substitutes and hormone antagonists Adult endocrine system medicine.medical_specialty Glucose-dependent insulinotropic polypeptide Adolescent Carotid Artery Common Incretin Carbohydrate metabolism Incretins Blood Pressure/drug effects Young Adult Blood Glucose/drug effects Physiology (medical) Internal medicine Humans Pancreas business.industry Pancreas/drug effects Carotid Artery Common/drug effects Pancreatic clamp Hemodynamics/drug effects Glucose Endocrinology Glycerol/metabolism chemistry Regional Blood Flow Hyperglycemia Glucose Clamp Technique Glucose effectiveness business Hormone |
| Zdroj: | Karstoft, K, Mortensen, S, Knudsen, S H & Solomon, T P J 2015, ' Direct effect of incretin hormones on glucose and glycerol metabolism and hemodynamics ', American Journal of Physiology: Endocrinology and Metabolism, vol. 308, no. 5, ajpendo.00520.2014, pp. E426-E433 . https://doi.org/10.1152/ajpendo.00520.2014 |
| ISSN: | 1522-1555 0193-1849 |
| Popis: | The objective of this study was to assess the insulin-independent effects of incretin hormones on glucose and glycerol metabolism and hemodynamics under euglycemic and hyperglycemic conditions. Young, healthy men ( n = 10) underwent three trials in a randomized, controlled, crossover study. Each trial consisted of a two-stage (euglycemia and hyperglycemia) pancreatic clamp (using somatostatin to prevent endogenous insulin secretion). Glucose and lipid metabolism was measured via infusion of stable glucose and glycerol isotopic tracers. Hemodynamic variables (femoral, brachial, and common carotid artery blood flow and flow-mediated dilation of the brachial artery) were also measured. The three trials differed as follows: 1) saline [control (CON)], 2) glucagon-like peptide (GLP-1, 0.5 pmol·kg−1·min−1), and 3) glucose-dependent insulinotropic polypeptide (GIP, 1.5 pmol·kg−1·min−1). No between-trial differences in glucose infusion rates (GIR) or glucose or glycerol kinetics were seen during euglycemia, whereas hyperglycemia resulted in increased GIR and glucose rate of disappearance during GLP-1 compared with CON and GIP ( P < 0.01 for all). However, when normalized to insulin levels, no differences between trials were seen for GIR or glucose rate of disappearance. Besides a higher femoral blood flow during hyperglycemia with GIP (vs. CON and GLP-1, P < 0.001), no between-trial differences were seen for the hemodynamic variables. In conclusion, GLP-1 and GIP have no direct effect on whole body glucose metabolism or hemodynamics during euglycemia. On the contrary, during hyperglycemia, GIP increases femoral artery blood flow with no effect on glucose metabolism, whereas GLP-1 increases glucose disposal, potentially due to increased insulin levels. |
| Databáze: | OpenAIRE |
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