The role of mitochondrial DNA in the development of type 2 diabetes caused by fetal malnutrition

Epidemiological studies have revealed strong and reproducible links between indices of poor fetal growth and susceptibility to the development of glucose intolerance and insulin resistance syndrome in adult life. To explain these associations, the thrifty phenotype hypothesis has been proposed. Mito...

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Veröffentlicht in:	The Journal of nutritional biochemistry 2005-04, Vol.16 (4), p.195-204
Hauptverfasser:	Lee, Yun Yong, Park, Kyong Soo, Pak, Youngmi Kim, Lee, Hong Kyu
Format:	Artikel
Sprache:	eng
Schlagworte:	Base Sequence Biological and medical sciences Diabetes Mellitus, Type 2 - genetics Diabetes. Impaired glucose tolerance DNA, Mitochondrial - genetics Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female fetal development Fetal malnutrition glucose tolerance Humans insulin resistance Insulin Resistance - genetics literature reviews Malnutrition - embryology maternal effect maternal nutrition Medical sciences Metabolic diseases metabolic syndrome Miscellaneous Mitochondrial DNA Molecular Sequence Data noninsulin-dependent diabetes mellitus Nucleic Acid Conformation Other metabolic disorders Pregnancy pregnancy outcome Prenatal Exposure Delayed Effects protein energy malnutrition risk factors RNA, Transfer, Lys - genetics Thrifty phenotype Type 2 diabetes
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Zusammenfassung:	Epidemiological studies have revealed strong and reproducible links between indices of poor fetal growth and susceptibility to the development of glucose intolerance and insulin resistance syndrome in adult life. To explain these associations, the thrifty phenotype hypothesis has been proposed. Mitochondrial DNA abnormalities have been known to cause insulin deficiency, insulin resistance and diabetes mellitus. In this review, we propose that mitochondrial dysfunction is a link between malnutrition during early life and disease in adult life. The potential mechanism for mitochondrial dysfunction will be focused on availability of the taurine and nucleotides, and imprinting on the genes.
ISSN:	0955-2863 1873-4847
DOI:	10.1016/j.jnutbio.2004.11.002