RESUMEN
BACKGROUND: Obesity is a multifactorial metabolic disease resulting from behavioral and genetic factors. Obesity is linked to diabetes mellitus and hypertension, which are considered as major risk factors for chronic kidney disease (CKD); moreover, it has a direct effect on developing CKD and end stage renal disease (ESRD). Here was aimed to examine the association between uncoupling protein 2 (UCP2) gene expression and obesity in CKD patients. METHODS: UCP2 gene expression was analyzed by real time polymerase chain reaction (RT-PCR) in 93 participants divided into three groups. The groups included 31 non-obese CKD patients, 31 obese CKD patients, and 31 healthy, age-matched, unrelated volunteers as a control group. RESULTS: UCP2 gene expression was significantly relevant when comparing the non-obese CKD and obese CKD groups to the control group (p< 0.001). No significant association was found when the groups were compared by gender; Chi-square (X2) was 2.38 and p= 0.304. A significant negative correlation was found between UCP2 gene expression and BMI in CKD (p< 0.05). CONCLUSION: These results indicate that UCP2 gene expression plays a significant role as a risk factor for obesity in CKD patients.
RESUMEN
It is well known that females are more vulnerable than males to stress-related psychiatric disorders, particularly during perimenopausal and postmenopausal periods. Hormone replacement therapy (HRT) has been widely used for the management of postmenopausal depression. However, HRT could be associated with severe adverse effects, including increased risk for coronary heart disease, breast cancer and endometrial cancer. Thus, there is a pressing demand for novel therapeutic options for postmenopausal depression without sacrificing uterine health. Simvastatin (SIM) was proven to have neuroprotective activities besides its hypocholesterolemic effect, the former can be attributed to its, antioxidant, anti-apoptotic and anti-inflammatory activities. Moreover, many reports highlighted that SIM has estrogenic activity and was able to induce the expression of estrogen receptors in rats. The present study showed that SIM (20 mg/kg, p.o.) markedly attenuated depressive-like behavior in ovariectomized (OVX) rats. Moreover, SIM prohibited hippocampal microglial activation, abrogated P2X7 receptor, TLR2 and TLR4 expression, inhibited NLRP3 inflammasome activation, with subsequent reduction in the levels of pro-inflammatory mediators; IL-1ß and IL-18. Furthermore, a marked elevation in hippocampal expression of ERα and ERß was noted in SIM-treated animals, without any significant effect on uterine relative weight or ERα expression. Taken together, SIM could provide a safer alternative for HRT for the management of postmenopausal depression, without any hyperplastic effect on the uterus.