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
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container_title The Journal of nutritional biochemistry
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creator Lee, Yun Yong
Park, Kyong Soo
Pak, Youngmi Kim
Lee, Hong Kyu
description 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.
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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.</description><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>DNA, Mitochondrial - genetics</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. 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source MEDLINE; ScienceDirect Journals (5 years ago - present)
subjects 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
title The role of mitochondrial DNA in the development of type 2 diabetes caused by fetal malnutrition
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