Abstract
Background: Metabolic syndrome is a group of different disorders mainly includes, insulin resistance, obesity, cerebrovascular disorders, dyslipidemia, which leads to increase mortality. Patients suffering from related psychotic disorders such as schizophrenia are at the higher risk of developing metabolic syndrome. The aim of this study was to evaluate the association between the first episode of schizophrenia, metabolic syndrome and insulin resistance-related proteins in blood and adipose tissue of mice.Materials and Methods: Twelve, female Balb/c mice were randomly divided into two groups; one group was injected intraperitoneal MK-801 (0.6mg/kg/d) to induce schizophrenia, and other group received the 0.9% normal saline for two weeks. Body weight, fasting blood glucose (FBG), oral glucose tolerance (OGT), and Homeostatic model assessment (HOMA), were observed. Blood and adipose tissue were collected and Western blotting was done to evaluate the insulin resistance related proteins (GGPPS, FAT, PTP-1B, GRK2, ATGL, FGF21, and PGC-1α) by using GAPDH as an internal standard. Results: There was a significant increase in mean body weight in schizophrenic group (21.76 vs 22.81, P=004). On day 14, the FBG, insulin concentrations and Homeostatic model assessment and insulin resistance (HOME-IR) were high in schizhphrenic group vs control group, e.g. 5.3±0.6 vs 3.47±0.2 (P=0.0001), 28.9±2.2 vs 23.3±0.6 (P<0.005) and 9.2±1.3 vs 3.9±0.2 (P=0.0001) . Impaired glucose tolerance deranged from 4.8mmol/L to 6.4mmol/L. Western blotting showed a marked increase in the expression of GGPPS, FAT, ATGL, and FGF21 proteins in monocytes and PTP-1B, GRK2, and PGC-1α ratios in adipose tissues.Conclusion: There was a positive relation between schizophrenia and metabolic syndrome e.g. insulin resistance and obesity. Certain proteins in adipocytes and blood were responsible for causing insulin resistance. [GMJ.2018;7:e692]
Highlights
The prevalence of metabolic syndrome among schizophrenic patients is poorly understood
Some discovered proteins such as geranylgeranyl diphosphate synthase (GGPPS), fatty acid translocase (FAT), protein tyrosine phosphatase-1B (PTP-1B), G-protein–coupled receptor kinase-2 (GRK2), adipose triglyceride lipase (ATGL), fibroblast growth factor 21 (FGF21) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) in mice adipocytes and muscle tissues that were found to be associated with the pathogenesis of insulin resistance
The GGPPS, FAT, PTP-1B, GRK2, ATGL, FGF21 and PGC-1α proteins have been studied for the pathogenesis of insulin resistance by evaluating these proteins either in muscle or fat tissues, but no study have been performed to evaluate these protein levels in blood monocytes.This study was designed to assess the relationship between the first episode of schizophrenia and metabolic syndrome, and whether after the development of metabolic syndrome, these proteins levels have any impact on insulin resistance in the schizophrenic animal model and to show the relationship between the expression of these proteins in adipocytes and monocytes
Summary
The prevalence of metabolic syndrome among schizophrenic patients is poorly understood. The GGPPS, FAT, PTP-1B, GRK2, ATGL, FGF21 and PGC-1α proteins have been studied for the pathogenesis of insulin resistance by evaluating these proteins either in muscle or fat tissues, but no study have been performed to evaluate these protein levels in blood monocytes.This study was designed to assess the relationship between the first episode of schizophrenia and metabolic syndrome, and whether after the development of metabolic syndrome, these proteins levels have any impact on insulin resistance in the schizophrenic animal model and to show the relationship between the expression of these proteins in adipocytes and monocytes. Blood and adipose tissue were collected and Western blotting was done to evaluate the insulin resistance related proteins (GGPPS, FAT, PTP-1B, GRK2, ATGL, FGF21, and PGC-1α) by using GAPDH as an internal standard. Certain proteins in adipocytes and blood were responsible for causing insulin resistance. [GMJ.2018;7:e692] DOI:10.22086/gmj.v0i0.692
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