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Mitochondrial Diabetology

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Mitochondrial Medicine

Diabetes mellitus (DM) is a chronic disease caused by disorder of insulin secretion in pancreatic β-cells, and/or its effect in tissues. Insulin acts to lower blood glucose by stimulation of glucose transport to muscle and fat cells and inhibition of its generation in the liver. Insulin promotes storage of the polysaccharide glycogen in the liver and muscles and stimulates glycogen synthesis.

Classification of DM is based on etiopathogenic mechanisms. Type 1 (characterized by β-cell destruction), type 2 (resistance to insulin action), other specific forms (mitochondrial DM included) and pregnancy diabetes.

Chronic hyperglycemia destroys many organs: eyes, kidneys, nervous tissue, heart and blood vessels. These changes are manifested as chronic diabetic complications.

Insulin deficiency and resistance to insulin action lead not only to changes in the metabolism of saccharides but also of proteins and lipids. The main pathobiochemical mechanisms of these changes are: (a) glycation of proteins, lipids, lipoproteins and DNA, (b) oxidative stress induced by hyperglycemia, (c) elevated flux via polyolic metabolic pathway of glucose, (d) changes linked with insulin signal pathway.

Abnormalities in metabolism which are typical for DM influence also functions of mitochondria. Disbalance between oxidative and reductive forms of supporting redox system create conditions for dysfunction of terminal oxidation. Mitochondria are assumed to be the key location for free radical generation because of the higher potential of reduced forms in this system (NADH). There is also a correlation between lower respiratory function of mitochondria and glycation of proteins in Complex II in the respiratory chain.

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Čársky, J., Gvozdjáková, A., Mikulecký, M., Kucharská, J., Singh, R.B. (2008). Mitochondrial Diabetology. In: Gvozdjáková, A. (eds) Mitochondrial Medicine. Springer, Dordrecht. https://doi.org/10.1007/978-1-4020-6714-3_8

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