Literature DB >> 23291363

Development of hyperglycemia and diabetes in captive Polish bank voles.

Aleksandra Bartelik1, Maciej Ciesla, Jerzy Kotlinowski, Stanislaw Bartelik, Dominik Czaplicki, Anna Grochot-Przeczek, Krzysztof Kurowski, Paweł Koteja, Jozef Dulak, Alicja Józkowicz.   

Abstract

Diabetes has been detected in Danish and Swedish bank voles (Myodes glareolus). There are no data, however, concerning the prevalence of diabetes in populations from other geographic regions. We investigated the frequency and physiological effects of glucose metabolism disorders in captive bank voles from Poland. Single measurement of fasting blood glucose concentration performed in the 3-4month old captive-born bank Polish voles without any disease symptoms showed that 8% of individuals (22/284) displayed an impaired fasting glucose (IFG, blood glucose (BG) ≥100mg/dL) and 1% (4/284) showed hyperglycemia (BG ≥126mg/dL) which could suggest diabetes. Next, we analyzed blood glucose in samples taken once a month from an additional cohort of bank voles with (FHD), or without (H), a family history of diabetes. The prevalence of IFG at age six months was 26% (16/62) among bank voles from the H group. In the FHD group the prevalence increased to 49% (43/88), and additional 12% (11/88) became diabetic (DB, BG ≥126mg/dL at two time points). Postnatal stress (three maternal deprivations before weaning) did not affect the risk of developing IFG or DB in H voles, but significantly reduced the frequency of glucose metabolism disorders (IFG and DB combined) in FHD voles. IFG was associated with hyperinsulinemia, but not with other biochemical disturbances. Diabetic animals displayed a progressive malformation and vacuolization of β-cells in the pancreas, without visible leukocytic infiltrations. In summary, our results indicate that Polish captive bank voles can develop diabetes, which shows features of both type 1 and type 2 diabetes in humans. Risk of diabetes is higher in animal with FHD.
Copyright © 2012 Elsevier Inc. All rights reserved.

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Year:  2013        PMID: 23291363     DOI: 10.1016/j.ygcen.2012.12.006

Source DB:  PubMed          Journal:  Gen Comp Endocrinol        ISSN: 0016-6480            Impact factor:   2.822


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