Background: Obestatin and ghrelin both have effects on the hypothalamus which controls food intake. We hypothesize that the circulating levels of obestatin and ghrelin may change after a meal and might be different between obesity and anorexia, which might be relevant to anorexia or obesity. Method: Fifteen children with obesity, 25 children with anorexia and 17 normal-weight healthy controls were enrolled in the study. The preprandial and postprandial glucose, insulin, total ghrelin and obestatin tests were completed in the three groups. The values of these indices were compared. Results: The obesity group had the highest values for BMI and fasting glucose (p < 0.001), while the anorexia group had the highest values for obestatin and ghrelin, followed by the control and obesity groups. No differences in ratios of ghrelin to obestatin were found between the anorexia and obesity groups (p > 0.05), but both were higher than that of the control group (p < 0.05). BMI was negatively correlated with preprandial obestatin (r = -0.8413, p < 0.001) and ghrelin (r = -0.7400, p < 0.001), but showed no significant correlations with the ghrelin-to-obestatin ratio. Conclusion: Although there is still controversy between the present and previous studies, the present study show that levels of obestatin and ghrelin are inversely correlated with BMI.

Epidemiological data have demonstrated that the prevalence of either obesity or hepatocellular carcinoma (HCC) is increasing worldwide during past decades, and obesity has been unequivocally shown to be a risk factor for HCC. It has been reported that a significant proportion of HCC in obesity develops in cryptogenic cirrhosis, which is largely associated with the progression of nonalcoholic fatty liver disease, especially nonalcoholic steatohepatitis. Since the HCC is a highly malignant tumor with a poor prognosis, a better understanding of the molecular mechanisms may help researchers to explore new approaches for preventing and treating the obesity-related HCC, and thereby facilitating a substantial reduction of morbidity and mortality. In this article, we reviewed the mechanisms underlying the relationship between obesity and HCC, with an emphasis on the roles of insulin/insulin-like growth factor axis, adipose tissue derived hormones, oxidative stress, and liver stem cells. In addition, we will discuss the impact of life-style modification on obesity-related HCC.

Cisplatin-induced short-term ORR was decreased in nasopharyngeal carcinoma patients with high ERCC1 expression, which increased the risk of metastasis.

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