Eight-week old, IL-2 −/− and wild-type control (IL-2 +/+) male mice were compared for food intake, body weight, and serum TNF-α concentrations. The purpose of this study was to evaluate the role of tumor necrosis factor-α (TNF-α) in these altered leptin responses. Serum leptin concentrations in the IL-2 −/− mice in the fed state were lower than controls, but paradoxically increased in the starved state compared to controls. We showed altered leptin responses in interleukin-2 deficient (IL-2 −/−) mice, a model of IBD, with elevated pro-inflammatory cytokines. We postulated that pro-inflammatory cytokines in IBD elevate serum leptin concentration contributing to the anorexia. A small amount of weight loss may be associated with a reduction in steatosis and abnormal liver enzymes and an improvement in fibrosis, despite the persistence of the virus.Īnorexia is a major complication of inflammatory bowel disease (IBD). Those that have maintained weight have sustained improvements in their liver function. In these subjects the median fibrosis score decreased from 3 to 1 (p=0.01) To date, 12 patients have completed 6-12 months of the maintenance program with a 55% success rate. The degree of reduction in steatosis was significantly associated with the percentage of weight loss (p=0.005). Nine of the 10 patients with paired liver biopsies had a reduction in steatosis. Mean fasting insulin fell from 16 to 11 mmol/L (p<0.002). In 16 of the 19 patients, serum ALT levels fell progressively with weight loss. After 12 weeks there was a mean weight loss of 5.9 ± 3.2 kg and a mean reduction in waist circumference of 9.0 ± 5.0 cm. Patients then entered a 12 month weight maintenance program with monthly dietetic review. Biochemistry was monitored monthly and a liver biopsy was performed prior to and 3-6 months after the intervention period. We examined the effect of a 12 week diet and exercise program where all subjects were seen weekly by the Dietician, with the goal of achieving a 0.5 kg weight loss per week. This study investigated the effect of weight reduction on liver biochemistry and histology in patients with HCV and the success of weight maintenance after an intensive intervention. We propose that in patients with chronic HCV and steatosis, obesity contributes to fat in the liver, which results in increased fibrosis and progression to cirrhosis. Improvements in biochemical parameters may be seen with weight reduction, however the effects on liver histology have not been investigated. Steatosis is found in 60% of patients with HCV and is strongly associated with more severe fibrosis. For these reasons, additional therapies to limit the progression of liver disease are urgently required. Antiviral treatment is successful in less than 50% of patients, is costly and causes debilitating side effects.
Hepatitis C virus (HCV) is a major cause of chronic liver disease that may progress to cirrhosis.
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