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2017 ; 6
(9
): 1040-1051
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Transcribing ?-cell mitochondria in health and disease
#MMPMID28951827
Mulder H
Mol Metab
2017[Sep]; 6
(9
): 1040-1051
PMID28951827
show ga
BACKGROUND: The recent genome-wide association studies (GWAS) of Type 2 Diabetes
(T2D) have identified the pancreatic ?-cell as the culprit in the pathogenesis of
the disease. Mitochondrial metabolism plays a crucial role in the processes
controlling release of insulin and ?-cell mass. This notion implies that
mechanisms controlling mitochondrial function have the potential to play a
decisive pathogenetic role in T2D. SCOPE OF THE REVIEW: This article reviews
studies demonstrating that there is indeed mitochondrial dysfunction in islets in
T2D, and that GWAS have identified a variant in the gene encoding transcription
factor B1 mitochondrial (TFB1M), predisposing to T2D due to mitochondrial
dysfunction and impaired insulin secretion. Mechanistic studies of the nature of
this pathogenetic link, as well as of other mitochondrial transcription factors,
are described. MAJOR CONCLUSIONS: Based on this, it is argued that transcription
and translation in mitochondria are critical processes determining mitochondrial
function in ?-cells in health and disease.
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