Chronic high-fat diet in fathers programs ß-cell dysfunction in female rat offspring
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Chronic high-fat diet in fathers programs ß-cell dysfunction in female rat offspring. / Ng, Sheau-Fang; Lin, Ruby C Y; Laybutt, D Ross; Barres, Romain; Owens, Julie A; Morris, Margaret J.
In: Nature, Vol. 467, No. 7318, 21.10.2010, p. 963-6.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Chronic high-fat diet in fathers programs ß-cell dysfunction in female rat offspring
AU - Ng, Sheau-Fang
AU - Lin, Ruby C Y
AU - Laybutt, D Ross
AU - Barres, Romain
AU - Owens, Julie A
AU - Morris, Margaret J
PY - 2010/10/21
Y1 - 2010/10/21
N2 - 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¿
AB - 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¿
KW - Adenosine Triphosphate
KW - Adiposity
KW - Aging
KW - Animals
KW - Apoptosis
KW - Body Weight
KW - Cations
KW - Cell Cycle
KW - Cytoskeleton
KW - DNA Methylation
KW - Diabetes Mellitus, Type 2
KW - Diet
KW - Dietary Fats
KW - Epigenesis, Genetic
KW - Fathers
KW - Female
KW - Gene Expression Profiling
KW - Gene Expression Regulation
KW - Glucose
KW - Glucose Intolerance
KW - Glucose Tolerance Test
KW - Homeostasis
KW - Insulin
KW - Insulin-Secreting Cells
KW - Litter Size
KW - Male
KW - Obesity
KW - Paternal Exposure
KW - Rats
KW - Rats, Sprague-Dawley
KW - Signal Transduction
U2 - 10.1038/nature09491
DO - 10.1038/nature09491
M3 - Journal article
C2 - 20962845
VL - 467
SP - 963
EP - 966
JO - Nature
JF - Nature
SN - 0028-0836
IS - 7318
ER -
ID: 45577275