ArticleAIMS neuroscience2021
Neuroestradiol regulation of ventromedial hypothalamic nucleus 5'-AMP-activated protein kinase activity and counterregulatory hormone secretion in hypoglycemic male versus female rats.
Article in AIMS neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 1 citations in OpenAlex.
- Brain-derived estrogen and neural function.Neuroscience and biobehavioral reviews · 2022Review
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2 authors at 1 institution in 1 country.
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Abstract
Hypoglycemia activates the ultra-sensitive energy gauge 5'-AMP-activated protein kinase (AMPK) in ventromedial hypothalamic nucleus (VMN) gluco-regulatory neurons. The VMN is exemplified by high levels of expression of the enzyme aromatase, which converts testosterone to estradiol. This study examined the hypothesis that neuroestradiol imposes sex-dimorphic control of VMN AMPK activity during eu- and/or hypoglycemia. VMN tissue corresponding to distinct rostro-caudal segments was obtained by micropunch dissection from testes-intact male and estradiol-replaced ovariectomized female rats that were infused intracerebroventricularly with the aromatase inhibitor letrozole (Lz) before subcutaneous insulin (INS) injection. In euglycemic rats, Lz treatment elevated (male) or decreased (female) middle VMN phosphoAMPK content, with concurrent effects on total AMPK expression. Lz prevented hypoglycemic up-regulation of the mean pAMPK/AMPK ratio in rostral and middle segments of the male VMN, and significantly inhibited this proportion throughout the VMN of hypoglycemic female rats. Lz prevented glucagon secretion in hypoglycemic rats of each sex, and abolished hypoglycemic hypercorticosteronemia in males. Results show that neuroestradiol regulation of VMN AMPK activity during euglycemia is region-specific and gender-divergent, e.g. inhibitory in males versus stimulatory in females. Intra-VMN distribution of hypoglycemia-activated AMPK varies between sexes, but in each sex, locally-generated estradiol is critical for sensor reactivity to this stimulus. Coincident Lz attenuation of VMN AMPK and counter-regulatory hormone responses to hypoglycemia infers a possible cause-and-effect association. Further effort is needed to elucidate the cellular and molecular mechanisms that underlie sex-dimorphic neuroestradiol control of VMN total AMPK and phosphoAMPK expression during distinct metabolic states.
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