Maternal fructose intake predisposes rat offspring to metabolic disorders via abnormal hepatic programming-Reference-Cited by-同舟云学术

Maternal fructose intake predisposes rat offspring to metabolic disorders via abnormal hepatic programming

Published:2021-11-08 Issue:12 Volume:35 Page:
ISSN:0892-6638
Container-title:The FASEB Journal
language:en
Short-container-title:The FASEB Journal

Author:

Munetsuna Eiji¹,Yamada Hiroya²,Yamazaki Mirai³,Ando Yoshitaka⁴,Mizuno Genki⁵⁶,Hattori Yuji⁶,Kageyama Itsuki⁴,Teshigawara Atsushi⁴⁵,Nouchi Yuki⁴,Ishikawa Hiroaki⁴,Fujii Ryosuke⁶,Ohta Yoshiji⁷,Suzuki Koji⁶,Shimono Yohei¹,Ohashi Koji⁴,Hashimoto Shuji²

Affiliation:

1. Department of Biochemistry Fujita Health University School of Medicine Toyoake Japan

2. Department of Hygiene Fujita Health University School of Medicine Toyoake Japan

3. Department of Medical Technology Kagawa Prefectural University of Health Sciences Takamatsu Japan

4. Department of Clinical Biochemistry Fujita Health University School of Medical Sciences Toyoake Japan

5. Deparment of Joint Research Laboratory of Clinical Medicine Fujita Health University Hospital Toyoake Japan

6. Department of Preventive Medical Sciences Fujita Health University School of Medical Sciences Toyoake Japan

7. Department of Chemistry Fujita Health University School of Medicine Toyoake Japan

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1096/fj.202101276R

Reference49 articles.

1. Obesity at the age of 50 y in men and women exposed to famine prenatally

2. Early onset of coronary artery disease after prenatal exposure to the Dutch famine

3. Maternal high-fat feeding through pregnancy and lactation predisposes mouse offspring to molecular insulin resistance and fatty liver

4. Maternal high-fat feeding primes steatohepatitis in adult mice offspring, involving mitochondrial dysfunction and altered lipogenesis gene expression

5. Maternal obesity programs offspring non-alcoholic fatty liver disease through disruption of 24-h rhythms in mice

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