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Hepatosteatosis is a disease present worldwide, which presents a number of health problems. Recently, thiazolidinedione (TZD) has been used as a therapy for lipid disorders. The present study demonstrates the potential of TZD as a treatment for hepatosteatosis and its mechanism of action, particularly focusing on its role in lipid metabolism. A total of 60 (80-90 g) rats were divided into three groups: A normal group with a standard diet, a high-fat, high-carbohydrate diet (HFCD) group or a HFCD+TZD group (n=20/group). The HFCD induced hepatosteatosis over a period of 12 weeks and the HFCD+TZD group were administered TZD in weeks 13-16. Blood and tissue samples were collected to measure hepatic function, the lipid profile, metabolism and hormone biomarkers, including serum triglyceride (TG), lipoprotein lipase (LPL), stearoyl-CoA desaturase (SCD-1), leptin and resistin. The HFCD-fed rats exhibited a significant increase in serum TG, total cholesterol, low-density lipoproteins, alanine transaminase and bilirubin compared with the normal group as well as a significant decrease in high-density lipoprotein. In addition, serum leptin and resistin were significantly elevated in the HFCD group compared with the normal group. The administration of TZD significantly increased SCD-1 activity and significantly inhibited LPL activity. It also attenuated the changes in the lipid profiles and normalized serum leptin and resistin levels. The results of the present study indicated that HFCD induced lipid abnormalities associated with hypertriglyceridemia, hypercholesterolemia and hepatosteatosis. These changes resulted from disruption to leptin and resistin, which may be due to alterations in LPL and SCD-1 activity. TZD mitigated the effects of HFCD-induced hepatosteatosis, indicating a possible regulatory effect of TZD in the development of hepatosteatosis. The authors suggest that the manipulation of SCD-1 and lipase by TZD may be useful as a treatment for hepatosteatosis. [ABSTRACT FROM AUTHOR]

Background: A high fat diet has an essential role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). This condition is characterized by hepatic fat accumulation (steatosis) and is associated with obesity, diabetes, and fibrosis or cirrhosis of the liver. Probiotics may be useful in the treatment of steatosis. This study examined the effects of an ingested probiotic formulation on the lipid profiles, liver functions, leptin levels, and inflammatory marker levels of rats with NAFLD that had been induced via high fat and sucrose diet (HFSD). Methods: Young male albino rats were randomly divided into three groups: a control group that was fed a standard diet; a second group that was fed a HFSD; and a third group that was given both a HFSD and ingestible probiotic mixtures. The groups were fed these diets for 16 weeks, and were then examined. Results: HFSD-only rats showed hypertriglyceridemia, hypercholesterolemia, and elevated low density lipoprotein (LDL) levels, and their serum alanine transaminase (ALT) and bilirubin levels were significantly higher than those of the control group. Compared to rats on the standard diet, HFSD-only rats showed higher levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6), increased serum leptin levels, and increased resistin hormone levels in the adipose tissues. In the third group, the inclusion of the probiotic mixture seemed to ameliorate the effects of the HFSD diet. The NAFD + probiotics group showed improved lipid profiles, better leptin and resistin levels, and better TNF-α and IL-6 levels than the NAFD-only group. They also showed no signs of NAFLD. Conclusions: The probiotic mixture showed promise as a treatment for NAFLD pathogenesis, and may improve HFSD-induced steatosis through its effects on leptin, resistin, inflammatory biomarkers, and hepatic function markers. We also established that gut microbiota-mediated regulation of lipid profiles was dependent on dietary lipids and carbohydrates. [ABSTRACT FROM AUTHOR]

Background. We evaluated the effect of maintaining highly active antiretroviral therapy (HAART) on the development of new acquired immunodeficiency syndrome (AIDS)-related events in patients with late-stage human immunodeficiency virus (HIV) infection who had suboptimal CD4+ cell count and viral load responses to HIV therapy. Methods. In patients with pretreatment CD4+ cell counts of <200 cells/mm³, incidence rates of new AIDS-related events occurring during HIV treatment were calculated during period 1 (pre-HAART era, 1990-1995; 88 patients) and period 2 (HAART era, 1996-2004; 214 patients) according to CD4+ cell count responses while receiving treatment. Cox multivariate model was used to compare rates of AIDS-related events from period 2 with those from period 1 according to specific CD4+ cell count response categories and rates of AIDS-related events for various viral load ranges within CD4+ cell count categories during period 2. Results. For period 2 patients with CD4+ cell counts <50 cells/mm³ and viral loads >100,000 copies/mL, the rate of AIDS-related events (39.3 events per 100 person-years) was significantly lower than that for period 1 patients with CD4+ cell counts <50 cells/mm³ (76.4 events per 100 person-years; P = .02). This held true for patients with CD4+ cell counts <100 cells/mm³ there were also significantly fewer AIDS-related events in period 2 (18 events per 100 person-years) than in period 1 (65.2 events per 100 person-years; P = .001), including those events occurring among period 2 patients with viral loads >100,000 copies/mL (29.5 events per 100 person-years; P = .01). Similarly, for patients with CD4+ cell counts of 100-200 cells/mm³, there were fewer AIDS-related events in period 2 (7.8 events per 100 person-years) than in period 1 (34.5 events per 100 person-years; P = .001); even for patients in period 2 with viral loads >100,000 copies/mL (15.4 events per 100 person-years; P = .04). Conclusions. Our data suggest that, even among patients with late-stage HIV infection and inadequate CD4+ cell count and viral load responses to HIV therapy, maintaining HAART may reduce the incidence of AIDS-related events. [ABSTRACT FROM AUTHOR]