Neuropsychological state of the population living in the Aral Sea region (zone of ecological crisis)

Background: The Aral Sea crisis has led to harmful effects on human habitat. In recent years, mild cognitive impairment is a growing problem.

Objectives: This article provides the results of studying the neuropsychological state of residents living in the crisis zone of the Aral Sea region in the case of Shalkar city. We have provided an assessment of the neuropsychological state of examined population and determined the leading pathology in this region.

Methods: The survey sample included 344 persons of reproductive age from 21 to 45 years. We have obtained results in biochemical studies, indicating perturbations of proteometabolism and lipid metabolism.

Results: A correlation analysis showed dependence between a decrease of albumin and high-density lipoproteins, an increase of low-density lipoproteins and parameters of cognitive function.

Conclusions: The research suggests a high prevalence of cerebrovascular pathology among the population, changes in cognitive function parameters, long-term and short-term memory problems and high levels of depression.     

GnRH increases glucose transporter-1 expression and stimulates glucose uptake in the gonadotroph

GnRH is the main regulator of the hypothalamic-pituitary-gonadal (H-P-G) axis. GnRH stimulates the pituitary gonadotroph to synthesize and secrete gonadotrophins (LH and FSH), and this effect of GnRH is dependent on the availability of glucose and other nutrients. Little is known about whether GnRH regulates glucose metabolism in the gonadotroph. This study examined the regulation of glucose transporters (Gluts) by GnRH in the LβT2 gonadotroph cell line. Using real-time PCR analysis, the expression of Glut1, -2, -4, and -8 was detected, but Glut1 mRNA expression level was more abundant than the mRNA expression levels of Glut2, -4, and -8. After the treatment of LβT2 cells with GnRH, Glut1 mRNA expression was markedly induced, but there was no GnRH-induction of Glut2, -4, or -8 mRNA expression in LβT2 cells. The effect of GnRH on Glut1 mRNA expression is partly mediated by ERK activation. GnRH increased GLUT1 protein and stimulated GLUT1 translocation to the cell surface of LβT2 cells. Glucose uptake assays were performed in LβT2 cells and showed that GnRH stimulates glucose uptake in the gonadotroph. Finally, exogenous treatment of mice with GnRH increased the expression of Glut1 but not the expression of Glut2, -4, or -8 in the pituitary. Therefore, regulation of glucose metabolism by GnRH via changes in Gluts expression and subcellular location in the pituitary gonadotroph reveals a novel response of the gonadotroph to GnRH.