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Mitochondrial 16189 variant, thinness at birth, and type-2 diabetes

1999; Elsevier BV; Volume: 353; Issue: 9163 Linguagem: Inglês

10.1016/s0140-6736(98)05817-6

1474-547X

David B. Dunger, Kristina Casteels, Ken K. Ong, David Phillips, Holly Bendall, Marcus Pembrey, Jo Poulton,

Epigenetics and DNA Methylation

There has been great interest in the mechanisms whereby maternal restraint of fetal growth, resulting in small size and especially thinness at birth, may be associated with insulin resistance and type-2 diabetes in adulthood. 1 Hales CN Barker DJ Clark PM et al. Fetal and infant growth and impaired glucose tolerance at age 64. BMJ. 1991; 303: 1019-1022 Crossref PubMed Scopus (2174) Google Scholar Degree of maternal restraint varies greatly and is influenced not only by mother's size and nutrition, but also varies with parity and may be inherited as a trait through the maternal line. 2 Ounsted M Scott A Ounsted C Transmission through the female line of a mechanism constraining human fetal growth. Ann Hum Biol. 1986; 13: 143-151 Crossref PubMed Scopus (81) Google Scholar This could imply a role for genes that are exclusively maternally expressed (ie, paternally imprinted genes) or exclusively maternally transmitted, such as mitochondrial DNA.