Abstract | BACKGROUND: METHODS: RESULTS: Our results revealed that RYGB efficiently improved both glucose tolerance and insulin resistance in GK diabetic rats by upregulating GLP-1/GLP-1R expression. In addition, GLP-1R agonist exendin-4 dose-dependently increased insulin secretion in RIN-m5F cells and regulated the proliferation and apoptosis of these cells. CONCLUSIONS: RYGB provides a valuable therapeutic option for patients with type 2 diabetes. GLP-1 may contribute to the regulation of pancreatic β-cell function through its receptor following RYGB.
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Authors | Yuan Liu, Yong Zhou, Yong Wang, Donghua Geng, Jingang Liu |
Journal | Obesity surgery
(Obes Surg)
Vol. 21
Issue 9
Pg. 1424-31
(Sep 2011)
ISSN: 1708-0428 [Electronic] United States |
PMID | 21479766
(Publication Type: Journal Article)
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Chemical References |
- Blood Glucose
- Glp1r protein, rat
- Glucagon-Like Peptide-1 Receptor
- Insulin
- Peptides
- Receptors, Glucagon
- Venoms
- Glucagon-Like Peptide 1
- Exenatide
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Topics |
- Animals
- Blood Glucose
(metabolism)
- Blotting, Western
- Body Weight
- Cell Line
- Diabetes Mellitus, Type 2
(blood, metabolism, surgery)
- Eating
- Enzyme-Linked Immunosorbent Assay
- Exenatide
- Gastric Bypass
- Glucagon-Like Peptide 1
(blood)
- Glucagon-Like Peptide-1 Receptor
- Glucose Tolerance Test
- Insulin
(blood, metabolism)
- Insulin Resistance
- Insulin-Secreting Cells
(drug effects, metabolism)
- Male
- Peptides
(pharmacology)
- Random Allocation
- Rats
- Rats, Wistar
- Receptors, Glucagon
(agonists, metabolism)
- Venoms
(pharmacology)
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