Individual epidemiologic studies as well as the pooled analysis of observational studies have indicated the association between type 2 diabetes (T2D) and hepatitis C virus infection (HCV). Whether HCV infection is the cause of diabetes or diabetic patients are more prone to get HCV infection is still in question. The objective of the present review was to provide answers to this issue, based on available evidence from epidemiologic, molecular, experimental and therapeutic studies. Our current understanding of how chronic HCV infection could induce T2D is incomplete, but it seems twofold based on both direct and indirect roles of the virus. HCV may directly induce insulin resistance (IR) through its proteins. HCV core protein was shown to stimulate suppressor of cytokine signaling, resulting in ubiquitination and degradation of tyrosine kinase phosphorylated insulin receptor substrates (IRS1/2) in proteasomes. HCV-nonstructural protein could increase protein phosphatase 2A which has been shown to inactivate the key enzyme Akt by dephosphorylating it. Insulin signaling defects in hepatic IRS-1 tyrosine phosphorylation and PI3-kinase association/activation may contribute to IR, which leads to the development of T2D in patients with HCV infection. The peroxisome proliferator-activated receptors (PPARs) are also implicated. PPARα/γ, together with their obligate partner RXR, are the main nuclear receptors expressed in the liver. PPARα upregulates glycerol-3-phosphate dehydrogenase, glycerol kinase, and glycerol transport proteins, which allows for glucose synthesis during fasting states. Decreased activity of PPARs could attribute to HCV-induced IR. Immune-mediated mechanisms may be involved in the indirect role of HCV in inducing IR. It is speculated that TNF-alpha plays a major role in the pathogenesis of IR through lowering IRS1/2. Furthermore, HCV infection- triggered ER stress could lead to the activation of PP2A, which inhibits both Akt and the AMP-activated kinase, the regulators of gluconeogenesis. In summary, we illustrate that HCV infection is accompanied by multiple defects in the upstream insulin signaling pathway in the liver that may contribute to the observed prevalence of IR and diabetes. Future studies are needed to resolve this issue.

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There has been no literature on analysing short answer questions (SAQs) to assess how well the students captured the essence of core concepts in basic sciences disciplines. The objective of this study was to assess the performance of students and marking process in core concept-intensive SAQs on physiology and pathology in a professional examination of the undergraduate medical curriculum. Two faculties, each from physiology and pathology disciplines identified the core concept-intensive SAQs. Consensus was taken on how core are the concepts and a marking scheme was developed by ranking of the elements of the concept. Based on their overall performance, top 20 students, middle 20 students and bottom 20 were identified, and their answers were graded (parameters: not attempted, wrong concept, incomplete or irrelevant, and how well the essence of critical key concepts was captured). This communication focused on the discrepancies in the marks awarded by the marker (examiner) and by the investigators. The discrepancy was higher in the middle 20 group while most of the bottom 20 had no marks awarded as they had not attempted or had a wrong or irrelevant concept. The construction of model answers in the examinations should be improved to unlock how much students could capture the underlying key critical concepts. Alternatively, the marker should be a content expert capable of going beyond the given model answer.