RGD Reference Report - Hyperglycemia acutely lowers the postprandial excursions of glucagon-like Peptide-1 and gastric inhibitory polypeptide in humans. - Rat Genome Database

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Hyperglycemia acutely lowers the postprandial excursions of glucagon-like Peptide-1 and gastric inhibitory polypeptide in humans.

Authors: Vollmer, K  Gardiwal, H  Menge, BA  Goetze, O  Deacon, CF  Schmidt, WE  Holst, JJ  Meier, JJ 
Citation: Vollmer K, etal., J Clin Endocrinol Metab. 2009 Apr;94(4):1379-85. Epub 2009 Jan 27.
RGD ID: 2312590
Pubmed: PMID:19174495   (View Abstract at PubMed)
DOI: DOI:10.1210/jc.2008-2197   (Journal Full-text)

INTRODUCTION: Impaired secretion of glucagon-like peptide 1 (GLP-1) has been suggested to contribute to the deficient incretin effect in patients with type 2 diabetes. It is unclear whether this is a primary defect or a consequence of the hyperglycemia in type 2 diabetes. We examined whether acute hyperglycemia reduces the postprandial excursions of gastric inhibitory polypeptide (GIP) and GLP-1, and if so, whether this can be attributed to changes in gastric emptying. PATIENTS AND METHODS: Fifteen nondiabetic individuals participated in a euglycemic clamp and a hyperglycemic clamp experiment, carried out over 285 min. A mixed meal was ingested after 45 min. Plasma concentrations of glucose, insulin, C-peptide, glucagon, triglycerides, GIP, and GLP-1 were determined, and gastric emptying was assessed using a (13)C-octanoate breath test. RESULTS: Glucose levels were 160 +/- 1 mg/dl during the hyperglycemic clamp experiments and 83 +/- 3 mg/dl during the euglycemia (P < 0.0001). Glucose infusion rates were higher during hyperglycemia, but meal ingestion led to a decline in glucose requirements in both experiments (P < 0.0001). Insulin and C-peptide levels were higher during the hyperglycemic clamp experiments (P < 0.0001), whereas glucagon levels were higher during euglycemia (P < 0.0001). The postprandial increases in GIP and GLP-1 concentrations were 46 and 52% lower during the experiments with hyperglycemia (P = 0.0017 and P = 0.021). Hyperglycemia also elicited a significant delay in gastric emptying (P < 0.0001). CONCLUSIONS: Hyperglycemia acutely reduces the postprandial levels of GIP and GLP-1, possibly through a deceleration of gastric emptying. This supports the concept that reduced incretin levels in some patients with type 2 diabetes are a consequence rather than a cause of type 2 diabetes.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
GIPHumanhyperglycemia  IEP associated with Diabetes Mellitus more ...RGD 
GipRathyperglycemia  ISOGIP (Homo sapiens)associated with Diabetes Mellitus more ...RGD 
GipMousehyperglycemia  ISOGIP (Homo sapiens)associated with Diabetes Mellitus more ...RGD 

Objects Annotated

Genes (Rattus norvegicus)
Gip  (gastric inhibitory polypeptide)

Genes (Mus musculus)
Gip  (gastric inhibitory polypeptide)

Genes (Homo sapiens)
GIP  (gastric inhibitory polypeptide)


Additional Information