Possible candidates are the peroxisome proliferator activated receptors, as dietary fats are the endogenous ligands for PPARs. PPARa-agonists decrease Gimeracil 11b-HSD1 in the liver in mice, while PPARc-agonists decrease 11b-HSD1 in rodent adipose tissue. Interestingly, these effects are not acutely observed in humans, which could potentially account for the differences in dietary regulation observed between species. The liver X receptor is another potential mediator of these effects, as LXR decreases 11b-HSD1 in the liver and adipose tissue. Further work is required to fully understand these mechanisms. To conclude, we have shown that diet-induced obesity in rats increases hepatic glucocorticoid metabolism by reducing 11bHSD1 and increasing 5a- and 5b-reductase expression, recapitulating the abnormal metabolism observed in human obesity. However, unlike in humans, a low carbohydrate diet does not increase hepatic 11b-HSD1 in rats, indeed lower carbohydrate content may decrease hepatic 11b-HSD1 further. Confirming previous results in rodents, high dietary fat content reduces glucocorticoid signalling by decreasing 11b-HSD1, and also GRa, in adipose tissue. Conversely, hepatic 5a-reductase is increased in association with increases in weight. Manipulation of dietary composition may chronically regulate 11b-HSD1 resulting in altered local glucocorticoid concentrations, which may modify the metabolic efficacy of various dietary strategies. The HCV genome is a positive sense, single-stranded RNA molecule of around 9.6-kb. It encodes a single polyprotein that is proteolytically processed by a combination of cellular and viral proteases into structural and nonstructural proteins. Based mainly on phylogenetic analyses, six major lineages, namely genotypes 1 to 6, have been identified. These groups are further subdivided into DY131 several subtypes. HCV genotypes 1a, 1b and 3a are distributed worldwide as a result of HCV transmission through blood transfusion, use of inadequately sterilized medical equipment and intravenous drug use. However, a non-negligible proportion of HCV infections have an ����undefined���� route of transmission.