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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kujoth, Gregory C. Wada, Youichiro Kim, Hyung-suk Smithies, Oliver Prolla, Tomas A. Tsutsumi, Shuichi Reddick, Robert L. Fox, Raymond Maeda, Nobuyo |
| Description | Author Affiliation: Fox R ( Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC 27599, USA.); |
| Abstract | Diabetes and the development of its complications have been associated with mitochondrial DNA (mtDNA) dysfunction, but causal relationships remain undetermined. With the objective of testing whether increased mtDNA mutations exacerbate the diabetic phenotype, we have compared mice heterozygous for the Akita diabetogenic mutation (Akita) with mice homozygous for the D257A mutation in mitochondrial DNA polymerase gamma (Polg) or with mice having both mutations (Polg-Akita). The Polg-D257A protein is defective in proofreading and increases mtDNA mutations. At 3 mo of age, the Polg-Akita and Akita male mice were equally hyperglycemic. Unexpectedly, as the Polg-Akita males aged to 9 mo, their diabetic symptoms decreased. Thus, their hyperglycemia, hyperphagia and urine output declined significantly. The decrease in their food intake was accompanied by increased plasma leptin and decreased plasma ghrelin, while hypothalamic expression of the orexic gene, neuropeptide Y, was lower and expression of the anorexic gene, proopiomelanocortin, was higher. Testis function progressively worsened with age in the double mutants, and plasma testosterone levels in 9-mo-old Polg-Akita males were significantly reduced compared with Akita males. The hyperglycemia and hyperphagia returned in aged Polg-Akita males after testosterone administration. Hyperglycemia-associated distal tubular damage in the kidney also returned, and Polg-D257A-associated proximal tubular damage was enhanced. The mild diabetes of female Akita mice was not affected by the Polg-D257A mutation. We conclude that reduced diabetic symptoms of aging Polg-Akita males results from appetite suppression triggered by decreased testosterone associated with damage to the Leydig cells of the testis. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 21 |
| Volume Number | 108 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2011-05-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Appetite Genetics DNA, Mitochondrial DNA-Directed DNA Polymerase Diabetes Mellitus Mice, Inbred Strains Mutation Aging Animals Pathology Physiopathology Hyperglycemia Leydig Cells Mice Phenotype RNA Editing Testis Testosterone Blood Research Support, N.I.H., Extramural Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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