Early determinants of type-2 diabetes

L M Berends, S E Ozanne

Research output: Contribution to journalArticle

79 Citations (Scopus)

Abstract

The global prevalence of type-2 diabetes (T2D) has more than doubled in the last 30 years and is predicted to continue to rise at an alarming rate. The associated health and financial burdens are considerable. The aetiology of common forms of T2D is multifactorial and involves a complex interplay between genetic, epigenetic and environmental factors. The influential role of the environment, in particular our diet and sedentary lifestyles, in diabetes risk is well established. Of major concern is the increasing prevalence of early onset T2D or pre-diabetic characteristics in children. In recent years, the role of the early life environment in programming diabetes risk has been the focus of numerous human and animal studies. Historical studies highlighted an association between low birthweight, a proxy for suboptimal in utero growth, and diabetes risk in adulthood. Over more recent years it has become apparent that a variety of expositions, including maternal obesity and/or maternal diabetes, can have a significant effect on offspring health outcomes. Further complicating matters, paternal and transgenerational transmission of T2D can occur thus mediating a perpetuating cycle of disease risk between generations. It is imperative for the underlying mechanisms to be elucidated so that interventions can be introduced. In doing so, it may be possible to prevent, delay or reverse a pre-programmed risk for T2D induced by pre- and/or postnatal environmental factors to improve health outcomes and curb premature metabolic decline. This review presents evidence for how the early life environment may programme T2D risk and suggests some mechanisms by which this may occur.
Original languageEnglish
Pages (from-to)569-580
Number of pages12
JournalBest Practice and Research: Clinical Endocrinology & Metabolism
Volume26
Issue number5
DOIs
Publication statusPublished - Oct 2012

Keywords

  • Models, Animal
  • Obesity
  • Animals
  • Pregnancy Complications
  • MicroRNAs
  • Infant, Low Birth Weight
  • Humans
  • Infant, Newborn
  • Child
  • Diabetes, Gestational
  • Epigenesis, Genetic
  • Pregnancy
  • Child, Preschool
  • Insulin-Secreting Cells
  • Risk Factors
  • Oxidative Stress
  • Adult
  • Diabetes Mellitus, Type 2
  • Diet
  • Adolescent
  • Infant, Small for Gestational Age
  • Female
  • Fetal Growth Retardation
  • Prenatal Exposure Delayed Effects

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