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Neuroprotection of estrogen on hypoglycemic attack is through AKT/GSK3b pathway
Author(s) -
Alecea Eilliut,
Yohanan Darien,
Cohen Joshua,
Addya Sankar,
Chakraborty Sanjoy,
Chakraborty Tandra R.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.969.9
Subject(s) - neuroprotection , estrogen , protein kinase b , endocrinology , medicine , hypoglycemia , chemistry , apoptosis , diabetes mellitus , biochemistry
Glucose is the main metabolic fuel of the brain. and its availability is directly linked to neuronal activity. In the absence of glucose i.e. hypoglycemia, there is loss of neurons, impaired IQ and can ultimately lead to morbidity. In the present study we have reported the neuroprotection of estrogen on hypoglycemic injury in hypothalamic cell line. There was a marked decrease in the cell count and mitochondrial function when exposed to hypoglycemia which increased in presence of estrogen (42.8 vs 98.5, 24 hours, p<0.0001). The attenuation of the death pathways was only seen within the first 24 hours and gradually decreased with time. DNA microarray studies showed AKT, a promoter of cell survival, was down‐regulation in the absence of glucose and in the presence of estrogen an increase in gene expression. RTPCR showed decrease in AKT expression with a slight increase in presence of estrogen. PRAS 40, proline rich substrate for AKT was measured. Results show low expression of PRAS40 in hypoglycemic conditions in 24 hours and 72 hours with a trend to increase in presence of estrogen. Therefore, it seems that one of the mechanism by which estrogen shows its neuroprotection is through the Akt‐GSK3b pathway activation.