scholarly journals In Utero Exposure to a High-Fat Diet Programs Hepatic Hypermethylation and Gene Dysregulation and Development of Metabolic Syndrome in Male Mice

Endocrinology ◽  
2017 ◽  
Vol 158 (9) ◽  
pp. 2860-2872 ◽  
Author(s):  
Yoshinori Seki ◽  
Masako Suzuki ◽  
Xingyi Guo ◽  
Alan Scott Glenn ◽  
Patricia M Vuguin ◽  
...  
2014 ◽  
Vol 210 (1) ◽  
pp. S42-S43
Author(s):  
Melissa Suter ◽  
Jun Ma ◽  
Patricia Vuguin ◽  
Kirsten Hartil ◽  
Ariana Fiallo ◽  
...  

2009 ◽  
Vol 201 (6) ◽  
pp. S31
Author(s):  
Melissa Suter ◽  
Kirsten Hartil ◽  
Patricia Vuguin ◽  
Ariana Fiallo ◽  
Maureen Charron ◽  
...  

Endocrinology ◽  
2015 ◽  
Vol 156 (7) ◽  
pp. 2482-2491 ◽  
Author(s):  
Hisashi Masuyama ◽  
Takashi Mitsui ◽  
Etsuko Nobumoto ◽  
Yuji Hiramatsu

Recent studies demonstrate that epigenetic changes under malnutrition in utero might play important roles in transgenerational links with metabolic diseases. We have previously shown that exposure to a high-fat diet (HFD) in utero may cause a metabolic syndrome-like phenomenon through epigenetic modifications of Adiponectin and Leptin genes. Because an association of obesity between mother and offspring endured in multiple generations, we examined whether HFD exposure in utero might affect the metabolic status of female offspring through multigenerational epigenetic changes of Adiponectin and Leptin genes and whether a normal diet in utero for multiple generations might abolish such epigenetic changes after exposure to a HFD in utero using ICR mice. We observed that the effect of maternal HFD on offspring over multiple generations in metabolic syndrome-like phenomenon such as weight and fat mass gain, glucose intolerance, hypertriglyceridemia, abnormal adiponectin and leptin levels, and hypertension, were accumulated with expression and epigenetic changes in Adiponectin and Leptin genes. A normal diet in utero in the subsequent generations after HFD exposure in utero diminished, and a normal diet in utero for 3 generations completely abolished, the effect of HFD in utero on weight and fat mass gain, insulin resistance, serum triglyceride, adiponectin, and leptin levels, with epigenetic changes of Adiponectin and Leptin genes. Exposure to a HFD in utero might affect glucose and lipid metabolism of female offspring through epigenetic modifications to Adiponectin and Leptin genes for multiple generations. Obesogenic and diabetogenic traits were abolished after a maternal normal diet for 3 generations.


Endocrinology ◽  
2012 ◽  
Vol 153 (6) ◽  
pp. 2823-2830 ◽  
Author(s):  
Hisashi Masuyama ◽  
Yuji Hiramatsu

The links between obesity in parents and their offspring and the role of genes and a shared environment are not completely understood. Adipocytokines such as leptin and adiponectin play important roles in glucose and lipid metabolism. Therefore, we examined whether the offspring from dams exposed to a high-fat diet during pregnancy (OH mice) exhibited hypertension, insulin resistance, and hyperlipidemia along with epigenetic changes in the expression of adipocytokine genes. OH mice were significantly heavier than the offspring of dams exposed to a control diet during pregnancy (OC mice) from 14 wk of age after an increased caloric intake from 8 wk. OH mice exhibited higher blood pressure and worse glucose tolerance than the OC mice at 24 wk. Total triglyceride and leptin levels were significantly higher and the adiponectin level was significantly lower in OH compared with OC mice at 12 wk of age. This was associated with changes in leptin and adiponectin expression in white adipose tissue. There were lower acetylation and higher methylation levels of histone H3 at lysine 9 of the promoter of adiponectin in adipose tissues of OH mice at 2 wk of age as well as at 12 and 24 wk of age compared with OC mice. In contrast, methylation of histone 4 at lysine 20 in the leptin promoter was significantly higher in OH compared with OC mice. Thus, exposure to a high-fat diet in utero might cause a metabolic syndrome-like phenomenon through epigenetic modifications of adipocytokine, adiponectin, and leptin gene expression.


2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
martin ronis ◽  
Huijing Xia ◽  
samya lima rodrigues ◽  
Eli El Haji ◽  
Alexandra Noel ◽  
...  

2009 ◽  
Vol 66 (4) ◽  
pp. 368-373 ◽  
Author(s):  
Kirsten Hartil ◽  
Patricia M Vuguin ◽  
Michael Kruse ◽  
Esther Schmuel ◽  
Ariana Fiallo ◽  
...  

2014 ◽  
Vol 210 (5) ◽  
pp. 463.e1-463.e11 ◽  
Author(s):  
Melissa A. Suter ◽  
Jun Ma ◽  
Patricia M. Vuguin ◽  
Kirsten Hartil ◽  
Ariana Fiallo ◽  
...  

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e84209 ◽  
Author(s):  
Sarah J. Borengasser ◽  
Ping Kang ◽  
Jennifer Faske ◽  
Horacio Gomez-Acevedo ◽  
Michael L. Blackburn ◽  
...  

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