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1.
Br J Med Med Res ; 2014 Mar; 4(9): 1938-1942
Article in English | IMSEAR | ID: sea-175097

ABSTRACT

Introduction: Serum leptin levels are increased in chronic kidney disease (CKD) patients primarily due to decreased clearance by kidneys. As leptin is a 16 Kda protein, it is also not cleared even by dialysis using conventional dialyzers or by continuous ambulatory peritoneal dialysis (CAPD). Studies have shown that elevated leptin levels are corrected after successful renal transplantation. With this intention, we determined if restoration of renal function with kidney transplantation can reduce serum leptin concentration in CKD patients. Materials and Methods: A total of 21 Patients undergoing living donor kidney transplantation were studied. There were 13 men and 8 women, from 16 to 45 years of age. All patients were receiving Hemodialysis prior to transplant. All patients received triple immunosuppressant therapy after the surgery. There were no graft rejections. Blood samples were collected under fasting conditions before and 6 days after transplantation. Results: The mean age of the patients was 28.38±9.38 years. Pre transplantation leptin concentration was 9.96 + 3.48 ng/ml and this decreased to 4.07±1.7 ng/ml within six days of transplantation (p<0.0001). However there was no concomitant change in Body Mass Index (BMI) as the follow-up was too short. Plasma Creatinine level declined from 7.5±1.6 mg/dl to 1.1±0.7 mg/dl within six days after transplantation. Conclusion: Successful renal transplantation immediately reduces serum leptin levels along with serum creatinine. The reduction in serum leptin levels after renal transplantation is likely due to reversal of renal function. Neither pre nor post transplant plasma Leptin levels correlated significantly with BMI in our study.

2.
Article in English | IMSEAR | ID: sea-153951

ABSTRACT

Background: Experimental evaluation of antidepressants (ADs) in diverse animal models is the need of time. There is a constant search for newer models with ease and rapid screening of AD activity. As earlier studies highlight AD effect of tramadol in animal models, the study was undertaken to compare antidepressant-like effect of tramadol in two models of behavioural despair in mice. Methods: Tramadol was administered intraperitoneally (i.p.) at two different doses of 20 and 40 mg/kg, once daily for 7 days to Swiss albino mice. The immobility period of control and drug-treated mice was recorded in tail suspension test (TST) and forced swim test (FST). The antidepressant (AD) effect of tramadol was compared with control (NS) and reference drug imipramine (10 mg/kg, p.o.), administered orally (p.o.) for seven successive days. Results: Tramadol in tail suspension test (TST) produced significant antidepressant effect at 20 and 40 mg/kg doses, as depicted by reduction in immobility period of drug-treated mice compared to control group. The efficacy of tramadol at dose of 40 mg/kg was comparable to that of imipramine treated group (p<0.001). Tramadol in forced swim test (FST) produced significant antidepressant effect only at the dose of 40 mg/kg as compared to control, while the results were insignificant as compared to imipramine treated group (p>0.05). Conclusion: The results of the present study depict antidepressant-like activity of tramadol in both the models of depression TST and FST. But TST in mice seems to be more efficacious in appraising the antidepressant like effect of tramadol.

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