Document Type
Original Study
Abstract
Endocannabinoid system (ECS) implicated in lipid and glucose metabolism, energy homeostasis expenditure and energy intake. In current study we focused on specific member of ECS which is CB2R . It is expressed in splenic tissue and immune cells. CB2R is one of the newest target of drug to treat chronic inflammatory diseases. This project aimed to assess the transcript level of CB2R in diabetic mellitus patients compare with its level in control group and evaluating some biochemical parameters including (glucose, cholesterol and triglyceride). As well as to characters the correlation type between above biochemical parameters and CB2R expression in patients group. mRNA of CN2R gene was extracted and cDNA was created to measure CB2R gene expression by using qRT-PCR assay. CB2R gene expression was significantly down regulated in blood samples of DM patients compared with its level in healthy group with fold change (0.563) fold. Biochemical parameters levels including (FBG, HbA1c, TC, TG, LDL, VLDL) were significantly increased in blood samples of DM patients compared with their levels in control group. However, HDL level was significantly reduced in DM patients (20.25±0.93) compared with its level in control group (35.66±9.34). there is no correlation coefficient was identified between CB2R gene expression and studied parameters while a non-significant negative correlation was demonstrated between cholesterol and CB2R gene expression (r=- 0.205. p-value = 0.625).these finding refers to possible association role of CB2R with DM disease as well as its association with lipid regulation this assay may provide useful target for new research to imply DM treatment.
Keywords
Endocannabinoid; CB2 receptor; CNR2 gene; Diabetes mellitus Introduction
Recommended Citation
Al Jebur, Shurooq Hussein
(2024)
"Association between CNR2 gene expression and the risk of diabetes mellitus disease,"
Al-Qadisiyah Journal of Pure Science: Vol. 29
:
No.
1
, Article 28.
Available at:
https://doi.org/10.29350/2411-3514.1273
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