Sex-specific basal and hypoglycemic patterns of in vivo caudal dorsal vagal complex astrocyte glycogen metabolic enzyme protein expression

Tamrakar, Pratistha; Shrestha, Pooja; Briski, Karen P.

doi:10.1016/j.brainres.2014.08.042

Cited by 4 publications

(2 citation statements)

References 32 publications

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“…For each animal, thin (10 µm-thick) sections were mounted on PEN membrane-coated slides (Carl Zeiss Microscopy, LLC, Thornwood, NY) for immunocytochemical labeling of the astrocyte marker protein glial fibrillary acid protein (GFAP) [Tamrakar et al, 2014, 2015; Tamarkar and Briski, 2015]. Briefly, tissues were fixed with acetone, blocked with 1.5% normal horse serum (prod.…”

Section: Methodsmentioning

confidence: 99%

Sex differences in forebrain estrogen receptor regulation of hypoglycemic patterns of counter-regulatory hormone secretion and ventromedial hypothalamic nucleus glucoregulatory neurotransmitter and astrocyte glycogen metabolic enzyme expression

et al. 2018

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The female ventromedial hypothalamic nucleus (VMN) is a focal substrate for estradiol (E) regulation of energy balance, feeding, and body weight, but how E shapes VMN gluco-regulatory signaling in each sex is unclear. This study investigated the hypothesis that estrogen receptor-alpha (ERα) and/or -beta (ERβ) control VMN signals that inhibit [γ-aminobutyric acid] or stimulate [nitric oxide, steroidogenic factor-1 (SF-1)] counter-regulation in a sex-dependent manner. VMN nitrergic neurons monitor astrocyte fuel provision; here, we examined how these ER regulate astrocyte glycogen metabolic enzyme, monocarboxylate transporter, and adrenoreceptor protein responses to insulin-induced hypoglycemia (IIH) in each sex. Testes-intact male and E-replaced ovariectomized female rats were pretreated by intracerebroventricular ERα antagonist (MPP) or ERβ antagonist (PHTPP) administration before IIH. Data implicate both ER in hypoglycemic inhibition of neuronal nitric oxide synthase protein in each sex and up-regulation of glutamate decarboxylase65/67 and SF-1 expression in females. ERα and -β enhance astrocyte AMPK and glycogen synthase expression and inhibit glycogen phosphorylase in hypoglycemic females, while ERβ suppresses the same proteins in males. Differential VMN astrocyte protein responses to IIH may partially reflect ERα and -β augmentation of ERβ and down-regulation of alpha1, alpha2, and beta1 adrenoreceptor proteins in females, versus ERβ repression of GPER and alpha2 adrenoreceptor profiles in males. MPP or PHTPP pretreatment blunted counter-regulatory hormone secretion in hypoglycemic males only, suggesting that in males one or more VMN neurotransmitters exhibiting sensitivity to forebrain ER may passively regulate this endocrine outflow, whereas female forebrain ERα and -β are apparently uninvolved in these contra-regulatory responses.

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Section: Methodsmentioning

confidence: 99%

Sex differences in forebrain estrogen receptor regulation of hypoglycemic patterns of counter-regulatory hormone secretion and ventromedial hypothalamic nucleus glucoregulatory neurotransmitter and astrocyte glycogen metabolic enzyme expression

et al. 2018

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“…In line with the literature, our results also reveal that lower GS activity enhances lifespan ( elav>GSRNAi ), whereas higher enzyme activity results in a shorter lifespan ( elav>hMGS-wt ). Brain glycogen metabolism is also suggested to be sexually dimorphic ( Tamrakar et al, 2014 ), as gonadal steroids are known to affect brain and body bioenergetics (viz., glucose uptake, mitochondrial oxidative phosphorylation, oxidative stress, etc.) ( Rettberg et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Alterations in brain glycogen levels influence life-history traits and reduce the lifespan in female Drosophila melanogaster

2021

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Sexual dimorphism in lifespan, wherein females outlive males, is evident across all animal taxa. The longevity difference between sexes is controlled by multiple physiological processes with complex relationships to one another. In recent years, glycogen, the storage form of glucose, has been shown to cause rapid aging upon forced synthesis in healthy neurons. Glycogen in the form of corpora amylacea in the aging brain is also widely reported. While these studies did suggest a novel role for glycogen in aging, most of them have focused on pooled samples, and have not looked at sex-specific effects, if any. Given the widespread occurrence of sex-biased expression of genes and the underlying physiology, it is important to look at the sex-specific effect of metabolic processes. In the present study, using transgenic fly lines for the human glycogen synthase, we investigated the sex-specific effect of glycogen on stress resistance, fitness, and survival. We demonstrate that Drosophila females with altered levels of glycogen in the brain display a shortened lifespan, increased resistance to starvation, and higher oxidative stress than male flies. The present study thus provides a novel insight into the sex-specific effect of glycogen in survival and aging and how differences in metabolic processes could contribute to sex-specific traits.

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State-Dependent Changes in Brain Glycogen Metabolism

DiNuzzo

Walls

Öz

et al. 2019

Advances in Neurobiology

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Sex-specific basal and hypoglycemic patterns of in vivo caudal dorsal vagal complex astrocyte glycogen metabolic enzyme protein expression

Cited by 4 publications

References 32 publications

Sex differences in forebrain estrogen receptor regulation of hypoglycemic patterns of counter-regulatory hormone secretion and ventromedial hypothalamic nucleus glucoregulatory neurotransmitter and astrocyte glycogen metabolic enzyme expression

Sex differences in forebrain estrogen receptor regulation of hypoglycemic patterns of counter-regulatory hormone secretion and ventromedial hypothalamic nucleus glucoregulatory neurotransmitter and astrocyte glycogen metabolic enzyme expression

Alterations in brain glycogen levels influence life-history traits and reduce the lifespan in female Drosophila melanogaster

State-Dependent Changes in Brain Glycogen Metabolism

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