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Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets
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GIP contributes to islet trihormonal abnormalities in type 2 diabetes
Chee W Chia1, Juliana O Odetunde, Wook Kim
1Laboratory of Clinical Investigation (C.W.C., J.O.O., O.D.C., J.M.E.) and Translational Gerontology Branch (L.F.), National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21225; and Department of Molecular Science and Technology (W.K.), Ajou University, Suwon 443-749, South Korea.
The Journal of Clinical Endocrinology and Metabolism
|April 10, 2014
Summary
Glucose-dependent insulinotropic polypeptide (GIP) may cause multiislet hormone dysregulation in type 2 diabetes. This study found elevated GIP levels and GIP receptor interactions in pancreatic polypeptide cells, suggesting a new therapeutic target.
Area of Science:
- Endocrinology
- Metabolic Diseases
- Molecular Biology
Background:
- Type 2 diabetes research primarily targets insulin deficiency, neglecting other islet hormones.
- This study investigates the role of glucose-dependent insulinotropic polypeptide (GIP) in diabetes-associated multiislet hormone dysregulation.
Purpose of the Study:
- To test the hypothesis that GIP is involved in the multiislet hormone dysregulation observed in type 2 diabetes.
- To explore the potential interaction between GIP and other islet hormones, such as pancreatic polypeptide (PP).
Main Methods:
- A case-control study involving 92 volunteers (type 2 diabetes, prediabetes, normal glucose tolerance) from the Baltimore Longitudinal Study of Aging (BLSA).
- An intervention study with 13 type 2 diabetes patients receiving GIP infusion or placebo.
- Rodent and in vitro cell line studies to investigate GIP receptor expression and function.
Main Results:
- Individuals with type 2 diabetes showed significantly elevated levels of glucose, glucagon, pancreatic polypeptide (PP), glucagon-like peptide-1 (GLP-1), and GIP compared to normal and prediabetes groups.
- GIP infusion in type 2 diabetes patients led to significantly higher PP levels compared to placebo.
- GIP administration to mice increased PP levels, and GIP receptors were identified on human and mouse PP cells.
Conclusions:
- Up-regulation of GIP production is implicated in the multihormonal dysregulation characteristic of type 2 diabetes.
- GIP likely influences other islet hormones through interactions with GIP receptors found on pancreatic polypeptide cells.
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