Chronic high-fat diet in fathers programs ß-cell dysfunction in female rat offspring
Research output: Contribution to journal › Journal article › Research › peer-review
The global prevalence of obesity is increasing across most ages in both sexes. This is contributing to the early emergence of type 2 diabetes and its related epidemic. Having either parent obese is an independent risk factor for childhood obesity. Although the detrimental impacts of diet-induced maternal obesity on adiposity and metabolism in offspring are well established, the extent of any contribution of obese fathers is unclear, particularly the role of non-genetic factors in the causal pathway. Here we show that paternal high-fat-diet (HFD) exposure programs ß-cell 'dysfunction' in rat F(1) female offspring. Chronic HFD consumption in Sprague-Dawley fathers induced increased body weight, adiposity, impaired glucose tolerance and insulin sensitivity. Relative to controls, their female offspring had an early onset of impaired insulin secretion and glucose tolerance that worsened with time, and normal adiposity. Paternal HFD altered the expression of 642 pancreatic islet genes in adult female offspring (P¿
Original language | English |
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Journal | Nature |
Volume | 467 |
Issue number | 7318 |
Pages (from-to) | 963-6 |
Number of pages | 4 |
DOIs | |
Publication status | Published - 21 Oct 2010 |
- Adenosine Triphosphate, Adiposity, Aging, Animals, Apoptosis, Body Weight, Cations, Cell Cycle, Cytoskeleton, DNA Methylation, Diabetes Mellitus, Type 2, Diet, Dietary Fats, Epigenesis, Genetic, Fathers, Female, Gene Expression Profiling, Gene Expression Regulation, Glucose, Glucose Intolerance, Glucose Tolerance Test, Homeostasis, Insulin, Insulin-Secreting Cells, Litter Size, Male, Obesity, Paternal Exposure, Rats, Rats, Sprague-Dawley, Signal Transduction
Research areas
ID: 45577275