Obesity increases monocyte chemoattractant protein-1 and inflammatory markers in rats

Objectives: To investigate the effect of high fat diet on inflammatory markers monocyte chemoattractant protein-1 [MCP-1] and C-reactive protein [CRP] in rats. And to investigate changes in these markers during weight reduction with diet control and orlistat treatment

Setting: Biochemistry Department, Faculty of Pharmacy and Faculty of Medicine, Suez Canal University

Design: Case control study

Materials and Methods: This study was conducted on sixty female albino rats, 15 rats received normal diet for three months and act as control. Remaining rats received high fat diet for three months and divided equally into three groups, one group continue on high fat diet, second group returned to normal diet and the third group returned to normal diet and treated with orlistat for two months. Body weight, scrum lipid profile, plasma free fatty acids [FFA] were assessed by High performance liquid chromatography [HPLC]. MCP-1 and C-reactive protein were evaluated using ELISA. Results: Feeding with high fat diet for 3 months induced significant increase in body weight [247.0 +/- 14.66] compared to control group [126. 37 +/- 23.26]. Serum total cholesterol [TC], triacylglyceroles [TAG], FFA , MCP-1 and CRP were significantly elevated in obese compared to control rats. Reduction of body weight by diet control and tetrahydrolipstatin [orlistat] treatment successfully reduced the level of MCP-1 and CRP

Conclusion: Our data showed that obesity increases chemokine levels and inflammation. Intervention to reduce these markers may help in avoidance of obesity related complications

Human telomerase enzyme activity in human hepatoma cell line [HEPG2] and its interaction with the heme oxygenase gene

Objective: to examine the contribution of telomerase and HO-1 in the adaptive cellular response to survive exposure to oxidative stresses in human hepatoma cell line [HepG2]

Materials and Methods: induction and activities of HO and telomerase enzymes were assessed in HepG2 cells in response to oxidative stress [represented by treatment with heme, SnC12 and H202] and in the presence of the HO inhibitor stannic mesoporphyrin [SnMP]. Induction of HO and telomerase mRNA were assessed using RT-PCR and western blotting techniques, while HO and telomerase enzyme activities were assessed spectrophotometrically Cytoprotection against oxidative stress was measured by assessing cell viability using a novel colorimetric method

Results: upregulation of HO-1 provided cytoprotection against oxidative stress while its downregulation increased oxidative stress mediated cell injury without altering telomerase activity. Telomerase was active in hepatocellular carcinoma cell line [HepG2] and human telomerase enzyme catalytic subunit [hTERT] was expressed in telomerase positive cancer cells. However, telomerase activity was not affected by oxidants, heme and H[2]O[2] or downregulation of HO gene activity by SnMP, similarly. hTERT, which is considered as the major regulator of telomerase activity, was not affected by oxidants, inducers or inhibitors of HO activity. On the other hand, HO-1 gene induction stimulated cell proliferation and accelerates cell cycle in HepC2 cells, while inhibition of HO activity augmented the damaging effects of oxidants

Conclusion: Induction of HO-1 gene mediates protection against oxidants and increases cell survival by a mechanism independent of telomerase enzyme activity