Chronic high-fat diet in fathers programs ß-cell dysfunction in female rat offspring

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

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

Harvard

Ng, S-F, Lin, RCY, Laybutt, DR, Barres, R, Owens, JA & Morris, MJ 2010, 'Chronic high-fat diet in fathers programs ß-cell dysfunction in female rat offspring', Nature, vol. 467, no. 7318, pp. 963-6. https://doi.org/10.1038/nature09491

APA

Ng, S-F., Lin, R. C. Y., Laybutt, D. R., Barres, R., Owens, J. A., & Morris, M. J. (2010). Chronic high-fat diet in fathers programs ß-cell dysfunction in female rat offspring. Nature, 467(7318), 963-6. https://doi.org/10.1038/nature09491

Vancouver

Ng S-F, Lin RCY, Laybutt DR, Barres R, Owens JA, Morris MJ. Chronic high-fat diet in fathers programs ß-cell dysfunction in female rat offspring. Nature. 2010 Oct 21;467(7318):963-6. https://doi.org/10.1038/nature09491

Author

Ng, Sheau-Fang ; Lin, Ruby C Y ; Laybutt, D Ross ; Barres, Romain ; Owens, Julie A ; Morris, Margaret J. / Chronic high-fat diet in fathers programs ß-cell dysfunction in female rat offspring. In: Nature. 2010 ; Vol. 467, No. 7318. pp. 963-6.

Bibtex

@article{9cb973840d054ce79ba462b841868e26,
title = "Chronic high-fat diet in fathers programs {\ss}-cell dysfunction in female rat offspring",
abstract = "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¿",
keywords = "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",
author = "Sheau-Fang Ng and Lin, {Ruby C Y} and Laybutt, {D Ross} and Romain Barres and Owens, {Julie A} and Morris, {Margaret J}",
year = "2010",
month = oct,
day = "21",
doi = "10.1038/nature09491",
language = "English",
volume = "467",
pages = "963--6",
journal = "Nature",
issn = "0028-0836",
publisher = "nature publishing group",
number = "7318",

}

RIS

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