High fat programming of beta-cell failure

Adv Exp Med Biol. 2010;654:77-89. doi: 10.1007/978-90-481-3271-3_5.


High saturated fat intake contributes to insulin resistance, beta-cell failure, and type 2 diabetes. Developmental programming refers to a stimulus or insult during critical periods of life which includes fetal and subsequent early neonatal life. Programming alters offspring physiology and metabolism with both immediate and lasting consequences. Maternal nutrition in gestation and lactation shapes offspring development and health. A high saturated fat diet ingested by mothers during gestation and/or lactation is a form of nutritional insult that induces diabetogenic changes in offspring physiology and metabolism. High fat programming is induced by maternal high saturated fat intake during defined periods of gestation and/or lactation and programs the physiology and metabolism of the offspring in early life. This more recently adopted form of developmental programming reflects society in both affluent and developing countries. High fat programming induces adverse changes in beta-cell development and function in neonatal and weanling offspring. These changes are characterized by compromised beta-cell development and function, evident by altered expression of key factors that maintain the beta-cell phenotype. High fat programming is likely to result in beta-cell failure and eventual type 2 diabetes.

Publication types

  • Review

MeSH terms

  • Adipose Tissue / physiology*
  • Animals
  • Blood Glucose / metabolism
  • Developmental Biology / methods
  • Diabetes Mellitus, Type 2 / diagnosis*
  • Diabetes Mellitus, Type 2 / genetics
  • Diabetes Mellitus, Type 2 / pathology
  • Diabetes Mellitus, Type 2 / therapy
  • Female
  • Gene Expression Regulation
  • Humans
  • Insulin-Secreting Cells / cytology*
  • Insulin-Secreting Cells / metabolism
  • Insulin-Secreting Cells / physiology
  • Maternal Nutritional Physiological Phenomena
  • Models, Biological
  • Pancreas / metabolism
  • Phenotype
  • Pregnancy
  • Rats


  • Blood Glucose