Mitochondrial Diabetes
Open accessAbstract
Mutations in mitochondrial DNA (mtDNA) associate with various disease states. A few mtDNA mutations strongly associate with diabetes, with the most common mutation being the A3243G mutation in the mitochondrial DNA-encoded tRNA(Leu,UUR) gene. This article describes clinical characteristics of mitochondrial diabetes and its molecular diagnosis. Furthermore, it outlines recent developments in the pathophysiological and molecular mechanisms leading to a diabetic state. A gradual development of pancreatic beta-cell dysfunction upon aging, rather than insulin resistance, is the main mechanism in developing glucose intolerance. Carriers of the A3243G mutation show during a hyperglycemic clamp at 10 mmol/l glucose a marked reduction in first- and second-phase insulin secretion compared with noncarriers. The molecular mechanism by which the A3243G mutation affects insulin secretion may involve an attenuation of cytosolic ADP/ATP levels leading to a resetting of the glucose sensor in the pancreatic beta-cell, such as in maturity-onset diabetes of the young (MODY)-2 patients with mutations in glucokinase. Unlike in MODY2, which is a nonprogressive form of diabetes, mitochondrial diabetes does show a pronounced age-dependent deterioration of pancreatic function indicating involvement of additional processes. Furthermore, one would expect that all mtDNA mutations that affect ATP synthesis lead to diabetes. This is in contrast to clinical observations. The origin of the age-dependent deterioration of pancreatic function in carriers of the A3243G mutation and the contribution of ATP and other mitochondrion-derived factors such as reactive oxygen species to the development of diabetes is discussed.
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The most common mutation leading to mitochondrial diabetes is the A3243G mutation in the mitochondrial encoded tRNA (Leu, UUR) gene.
“The most common mutation leading to mitochondrial diabetes is the A3243G mutation in the mitochondrial encoded tRNA (Leu, UUR) gene (205, 206).”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [205]
Mitochondrial diabetes is more likely to result from a gradual deterioration of β-cell function than from an acute functional impairment due to insufficient ATP production.
“These data suggest that mitochondrial diabetes is more likely to result from a gradual deterioration of -cell function, rather than from an acute functional impairment due to insufficient ATP production (246).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [246]
Mitochondrial diabetes only develops upon aging, with an average age of onset between 35 and 40 years for MIDD and 48 years for the 14577 T>C mutation.
“Interestingly, mitochondrial diabetes only develops upon aging, with an average age of onset between 35 and 40 yr for MIDD and 48 yr for 14577 TϾC.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [246]
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- Authors
- Maassen, J. A., ‘t Hart, L. M., van Essen, E., Heine, R. J., Nijpels, G., Jahangir Tafrechi, R. S., Raap, A. K., Janssen, G. M. C., & Lemkes, H. H. P. J.
- Affiliations
- Leiden University Medical Center (NL)
- Department of Molecular Cell Biology, Leiden University Medical Centre, Leiden, the Netherlands
- Department of Endocrinology and Metabolic Diseases, Leiden University Medical Centre, Leiden, the Netherlands
- Amsterdam UMC Location Vrije Universiteit Amsterdam (NL)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2004-02-01
- Volume
- 53
- Issue
- suppl_1
- Pages
- S103-S109
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2101260083
- Cited by
- 439
- References
- 47
- Citations by year
- 2026: 6 · 2025: 23 · 2024: 12 · 2023: 21 · 2022: 19 · 2021: 23 · 2020: 19 · 2019: 17 · 2018: 18 · 2017: 17 · 2016: 17 · 2015: 18 · 2014: 18 · 2013: 27 · 2012: 28
- FWCI
- 1.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- European Commission
- Diabetes Fonds
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- mitochondrial diabetes, mitochondrial DNA mutations, A3243G mutation, tRNA-Leu(UUR), beta-cell dysfunction, insulin secretion, impaired glucose tolerance, glucose sensor, maturity-onset diabetes of the young, glucokinase, reactive oxygen species, ATP production
- MeSH terms
- Insulin Secretion, Animals, Base Sequence, Diabetes Mellitus, Humans, Insulin, Mitochondria, Molecular Sequence Data, Nucleic Acid Conformation, RNA, Transfer, Leu, Incidence, Glucose Intolerance
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