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The perception of a salty flavor is facilitated by sodium ions within the oral salivary fluid. Upon consumption of a salty substance, salt crystals disassemble, leading to the liberation of its constituents—Na+ and Cl- ions. These ions subsequently dissolve into the salivary fluid present in the oral cavity. The external environment of the gustatory cells experiences an elevation in Na+ concentration, thereby establishing a potent concentration gradient. This gradient propels the...
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Related Experiment Video

Updated: Jun 11, 2025

Simultaneous Detection of c-Fos Activation from Mesolimbic and Mesocortical Dopamine Reward Sites Following Naive Sugar and Fat Ingestion in Rats
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Gastrodin attenuates high fructose-induced sweet taste preference decrease by inhibiting hippocampal neural stem cell

Chuan-Feng Tang1, Hong Ding1, Ya-Qian Wu1

  • 1State Key Laboratory of Pharmaceutical Biotechnology, Institute of Chinese Medicine, Nanjing Drum Tower Hospital, School of Life Sciences, Nanjing University, Nanjing, PR China.

Journal of Advanced Research
|October 1, 2024
PubMed
Summary
This summary is machine-generated.

High fructose intake causes neural stem cell ferroptosis, leading to behavioral changes. Gastrodin protects against this by downregulating ZIC2 and CISD1, improving sweet taste preference.

Keywords:
CISD1FerroptosisGastrodinHigh fructoseNSCsSweet taste preference

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • High fructose consumption is linked to behavioral disorders via central nervous system ferroptosis.
  • Neural stem cells (NSCs) are vital for hippocampal neurogenesis and resisting behavioral alterations.
  • Gastrodin, from Gastrodia elata, exhibits neuroprotective properties.

Purpose of the Study:

  • To investigate how high fructose induces sweet taste preference.
  • To determine the effect of gastrodin on hippocampal NSC ferroptosis.

Main Methods:

  • Mice and cultured NSCs were treated with high fructose and/or gastrodin.
  • Assessed NSC ferroptosis via lipid peroxidation and DNA double-strand breaks.
  • Utilized RNA-seq, Western blotting, and ChIP to explore mechanisms; manipulated gene expression using lentivirus.

Main Results:

  • Gastrodin reduced sweet taste preference decline and hippocampal NSC ferroptosis in fructose-fed mice.
  • Identified CDGSH iron-sulfur domain 1 (CISD1) as a ferroptosis mediator upregulated by fructose.
  • Zic family member 2 (ZIC2) overexpression increased CISD1 transcription; gastrodin downregulated ZIC2, inhibiting CISD1.

Conclusions:

  • High fructose induces hippocampal NSC ferroptosis by upregulating ZIC2 and CISD1, impairing sweet taste preference.
  • Gastrodin shows potential in mitigating NSC ferroptosis and enhancing sweet taste preference.