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Year : 2013  |  Volume : 3  |  Issue : 4  |  Page : 347-351

Association of amylin in the development of impaired fasting glucose and impaired glucose tolerance

1 Department of Biochemistry and Cell Biology, Biomedical Research Group, BIRDEM, Dhaka 1000, Bangladesh
2 Department of Pharmacy, Southeast University, Dhaka 1213, Bangladesh
3 Department of Biochemistry and Molecular Biology, Rajshahi University, Rajshahi 6205, Bangladesh

Correspondence Address:
Md Abdur Rashid
Lab of Molecular Signaling, National Institute on Alcohol Abuse and Alcoholism, 5625 Fisher Lane, Room # 3S-O2, MD 20852, USA

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2231-0738.119842

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Objective: The present study was planned to explore the role of amylin in the pathogenesis of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) subjects. Subjects and Methods: In this study, 20 IFG and 25 IGT subjects along with 30 healthy subjects were included. Plasma glucose (fasting and 2 h after 75 g glucose) was measured by glucose oxidase method, serum triglyceride and total cholesterol, high density lipoprotein (HDL) and low density lipoprotein (LDL) by enzymatic method. Serum insulin and amylin were measured by the enzyme-linked immunosorbent assay method. B-cell secretory capacity (Homeostasis model assessment [HOMA] %B) and insulin sensitivity (HOMA %S) were estimated by HOMA-CIGMA software. Results: Age and body mass index were matched among control and the hyperglycemic groups (IFG, IGT). Fasting total cholesterol, HDL and LDL was significantly higher in IGT subjects compared with control and IFG subjects. Plasma insulin was significantly higher in IFG and IGT compared with control subjects (median [range], pmol/l; control, 38 [28-55]; IFG, 49 [40-56] and IGT, 60 [20-91]). HOMA %B was significantly lower in IFG and significantly higher in IGT subjects compared with the controls (median [range], %; control, 81 [53-156]; IFG, 52 [40-63] and IGT, 95 [33-195]). HOMA %S was significantly decreased in IGT and also in IFG compared to controls (median (range), %; control, 137 [95-187]; IFG, 104 [88-127] and IGT, 86 [57-255]). Plasma amylin was significantly raised in IFG and IGT compared to control subjects (mean ± standard deviation, pmol/l; control, 5.0 ± 0.63; IFG, 6.43 ± 0.67 and IGT, 8.0 ± 1.18). In binary logistic regression analysis, it has been found that plasma amylin concentration is positively associated with impaired glucose regulation and in bivariate correlation analysis it has been found that plasma amylin is positively associated with HOMA %B and negatively associated with fasting glucose. Conclusion: The present data suggested that increased amylin concentration may be contributed to the development of pre-diabetic condition or vice versa.

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