ArticleMolecular and cellular biochemistry2020
Sex-dimorphic moderate hypoglycemia preconditioning effects on Hippocampal CA1 neuron bio-energetic and anti-oxidant function.
Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- Maternal Immune Activation Leads to Lasting Sex-Specific Changes in Behavior and Hippocampal Morphological and Molecular Features in 12-Month-Old Rat Offspring.International journal of molecular sciences · 2026Article
- Mechanistic insights into ferroptosis in thyroid cancer and its therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- The critical role of ferroptosis in thyroid cancer development and potential therapeutic implications.Frontiers in oncology · 2026Review
- Ferroptosis in thyroid cancer: mechanisms, current status, and treatment.Frontiers in oncology · 2025Review
- Deciphering the Heterogeneity of the Internal Environment of Hippocampal Neurons during Maturation by Raman Spectroscopy.ACS omega · 2022Article
- Effect of β-Hydroxybutyrate on Autophagy Dynamics During Severe Hypoglycemia and the Hypoglycemic Coma.Frontiers in cellular neuroscience · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hypoglycemia is a detrimental complication of rigorous management of type 1 diabetes mellitus. Moderate hypoglycemia (MH) preconditioning of male rats partially affords protection from loss of vulnerable brain neurons to severe hypoglycemia (SH). Current research investigated whether MH preconditioning exerts sex-dimorphic effects on hippocampal CA1 neuron bio-energetic and anti-oxidant responses to SH. SH up-regulated CA1 glucose or monocarboxylate transporter proteins in corresponding hypoglycemia-naïve male versus female rats; precedent MH amplified glucose transporter expression in SH irrespective of sex. Sex-differentiating SH effects on glycolytic and tricarboxylic pathway markers correlated with elevated tissue ATP content and diminished CA1 5'-AMP-activated protein kinase (AMPK) activation in females. MH-preconditioned suppression of mitochondrial energy pathway enzyme profiles and tissue ATP in SH rats coincided with amplified CA1 AMPK activity in both sexes. Anti-oxidative stress enzyme protein responses to SH were primarily sex-contingent; preconditioning amplified most of these profiles, yet exacerbated expression of lipid and protein oxidation markers in SH male and female rats, respectively. Results show that MH preconditioning abolishes female CA1 neuron neuroprotection of positive energy balance through SH, resulting in augmented CA1 AMPK activity and oxidative injury and diminished tissue ATP in hypoglycemia-conditioned versus naïve rats in each sex. It is unclear if SH elicits differential rates of CA1 neuronal destruction in the two sexes, or how MH may impact sex-specific cell loss. Further research is needed to determine if molecular mechanism(s) that maintain female CA1 neuron metabolic stability in the absence of MH preconditioning can be leveraged for therapeutic prevention of hypoglycemic nerve cell damage.
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