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

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)259-264
Number of pages6
JournalNutrition Research
Volume35
Issue number3
DOIs
Publication statusPublished - 01-03-2015

Fingerprint

Fructose
Mothers
Messenger RNA
Lactation
Hippocampus
Sweetening Agents
Pregnancy
Body Weight Changes
Monosaccharides
Blood-Brain Barrier
Reverse Transcriptase Polymerase Chain Reaction
Synapses
Neurotransmitter Agents
Real-Time Polymerase Chain Reaction
Milk
Fetus
Steroids
Hormones
Water
Brain

All Science Journal Classification (ASJC) codes

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

Cite this

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title = "Maternal fructose consumption alters messenger RNA expression of hippocampal StAR, PBR, P450(11β), 11β-HSD, and 17β-HSD in rat offspring",
abstract = "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.",
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Maternal fructose consumption alters messenger RNA expression of hippocampal StAR, PBR, P450(11β), 11β-HSD, and 17β-HSD in rat offspring. / Ohashi, Koji; Ando, Yoshitaka; Munetsuna, Eiji; Yamada, Hiroya; Yamazaki, Mirai; Nagura, Ayuri; Taromaru, Nao; Ishikawa, Hiroaki; Suzuki, Koji; Teradaira, Ryouji.

In: Nutrition Research, Vol. 35, No. 3, 01.03.2015, p. 259-264.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Maternal fructose consumption alters messenger RNA expression of hippocampal StAR, PBR, P450(11β), 11β-HSD, and 17β-HSD in rat offspring

AU - Ohashi, Koji

AU - Ando, Yoshitaka

AU - Munetsuna, Eiji

AU - Yamada, Hiroya

AU - Yamazaki, Mirai

AU - Nagura, Ayuri

AU - Taromaru, Nao

AU - Ishikawa, Hiroaki

AU - Suzuki, Koji

AU - Teradaira, Ryouji

PY - 2015/3/1

Y1 - 2015/3/1

N2 - 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.

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