Maternal fructose consumption alters messenger RNA expression of hippocampal StAR, PBR, P450(11β), 11β-HSD, and 17β-HSD in rat offspring

Koji Ohashi, Yoshitaka Ando, Eiji Munetsuna, Hiroya Yamada, Mirai Yamazaki, Ayuri Nagura, Nao Taromaru, Hiroaki Ishikawa, Koji Suzuki, Ryouji Teradaira

研究成果: Article

14 引用 (Scopus)

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Hippocampal functions such as neuronal protection and synapse formation are positively modulated by neurosteroids, which are synthesized de novo within the brain. However, the mechanisms regulating neurosteroidogenesis remain unclear. Fructose, which is used as a sweetener, affects steroid hormone synthesis in peripheral endocrine organs. This monosaccharide can penetrate the blood-brain barrier and impair hippocampal function. Also, fructose is secreted into milk and is thus delivered to the fetus. Based on these observations, we hypothesized that the hippocampal neurosteroidogenesis in the offspring may be affected by maternal fructose consumption. Female rats were fed with normal water or 20% fructose solution during gestation and lactation. Maternal calorie intake did not change significantly, and no significant change in body weight was observed. The levels of messenger RNAs (mRNAs) for steroidogenic enzymes and proteins in the hippocampus of the offspring were analyzed by real-time reverse transcriptase polymerase chain reaction. Maternal fructose consumption during gestation and lactation increased mRNA levels of P450(11β)-2, 11β-HSD-2, and 17β-HSD-1 in the offspring hippocampus, and reduced levels of mRNAs for StAR, PBR, and 17β-HSD-3. Maternal fructose consumption might influence hippocampal neurosteroidogenesis in offspring.

元の言語English
ページ(範囲)259-264
ページ数6
ジャーナルNutrition Research
35
発行部数3
DOI
出版物ステータスPublished - 01-03-2015

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Nutrition and Dietetics

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