ISSN 1470-3947 (print)
ISSN 1479-6848 (online)

Searchable abstracts of presentations at key conferences in endocrinology

Published by BioScientifica
Endocrine Abstracts (2010) 22 P351 
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Increased serum nesfatin-1 levels in patients with impaired glucose tolerance

Nese Ersoz Gulcelik1, Safak Cavus Akin1, Duygu Yazgan Aksoy1, Jale Karakaya2 & Aydan Usman1

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Objective: Nesfatin was found to be co-localized with insulin in pancreatic β cells and its levels were decreased in type 2 diabetic patients. In order to investigate the role of nesfatin in carbohydrate metabolism, we measured baseline nesfatin-1 levels and its response to glucose load in patients with impaired glucose tolerance (IGT) and in healthy subjects.

Subjects and methods: Fourteen patients with IGT and, 13 age and body mass index matched controls were included in the study. Oral glucose tolerance test was performed for each subject and blood samples were taken at 0, 60 and 120 min at which glucose, insulin and nesfatin-1 levels were measured.

Results: Baseline glucose, insulin and nesfatin-1 levels were significantly higher in patients with IGT than controls. Two-way repeated-measures of ANOVA revealed that change in time (CIT) for glucose and insulin was significant (P<0.001 and P<0.001, respectively). CIT for glucose and insulin was significantly different between IGT patients and controls (P<0.001 and P=0.003, respectively). CIT for nesfatin-1 was not significant (P=0.467) and it was not different between the two groups (P=0.331). Since variables have different units, two-way repeated measures of ANOVA on both factors were used to evaluate percentage change of variables within times. Interactions of groups, times and factors (glucose, nesfatin-1, insulin) were also examined. Percentage of CIT was different for glucose, insulin and nesfatin-1 (P<0.001). Percentage of CIT for each factor was similar in both groups (P=0.120).

Conclusion: Nesfatin-1 levels were not affected by acute changes in glycemic status. In contrast to the previous reports showing decreased levels of nesfatin-1 levels in diabetic patients, we found elevated levels in patients with IGT. This controversial finding may be explained by a defensive increase in nesfatin-1 to regulate impaired glucose metabolism in IGT patients, which is disturbed by the development of diabetes.

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