| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2026-03-10 |
| タイトル |
|
|
タイトル |
Maternal fructose intake predisposes rat offspring to metabolic disorders via abnormal hepatic programming |
|
言語 |
en |
| 言語 |
|
|
言語 |
eng |
| 資源タイプ |
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|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
| 著者 |
Munetsuna, Eiji
Yamada, Hiroya
Yamazaki, Mirai
Ando, Yoshitaka
Mizuno, Genki
Hattori, Yuji
Kageyama, Itsuki
Teshigawara, Atsushi
Nouchi, Yuki
Ishikawa, Hiroaki
Fujii, Ryosuke
Ohta, Yoshiji
Suzuki, Koji
Shimono, Yohei
Ohashi, Koji
Hashimoto, Shuji
|
| Abstract |
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内容記述タイプ |
Abstract |
|
内容記述 |
Given that fructose consumption has increased by more than 10-fold in recent decades, it is possible that excess maternal fructose consumption causes harmful effects in the next generation. This study attempted to elucidate the mechanism of the harmful effects of excessive maternal fructose intake from the perspective of offspring liver function. Female rats during gestation and lactation were fed water containing fructose, and their offspring were fed normal water. We attempted to elucidate the mechanism of fructose-induced transgenerational toxicity by conducting a longitudinal study focusing on hepatic programming prior to disease onset. Impaired Insulin resistance and decreased high-density lipoprotein-cholesterol levels were observed at 160 days of age. However, metabolic disorders were not observed in 60-day-old offspring. Microarray analysis of 60-day-old offspring livers showed the reduction of hepatic insulin-like growth factor-1 (Igf1) mRNA expression. This reduction continued until the rats were aged 160 days and attenuated Igf1 signaling. Hepatic microRNA-29 (miR-29a) and miR-130a, which target Igf1 mRNA, were also found to be upregulated. Interestingly, these miRNAs were upregulated in the absence of metabolic disorder. In this study, we found that maternal fructose intake resulted in dysregulated expression of Igf1 and its target miRNAs in the offspring liver, and that these offspring were more likely to develop metabolic disorders. Abnormal hepatic programming induced by an imbalanced maternal nutritional environment is maintained throughout life, implying that it may contribute to metabolic disorders. |
|
言語 |
en |
| 書誌情報 |
The FASEB Journal
巻 35,
号 12,
p. e22030-e22030,
発行日 2021-11-08
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| 出版者 |
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出版者 |
Wiley |
| DOI |
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|
識別子タイプ |
DOI |
|
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関連識別子 |
10.1096/fj.202101276R |
| 著者版フラグ |
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出版タイプ |
AM |
|
出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |
| 査読 |
|
|
内容記述タイプ |
Other |
|
内容記述 |
査読あり |
R1_FASEB_Munetsuna-2021-Ver-Submitted.pdf (351 KB)
