Background/Aim: Hepatitis C virus infection is a known risk factor of impaired glucose metabolism and diabetes mellitus. Whether hepatitis B virus (HBV) infection is also associated with impaired glucose tolerance remains uncertain. The aim of the study was to conduct a systematic review on the association between HBV infection and impaired glucose metabolism Methods: Studies reporting the association between HBV infection and markers of impaired glucose metabolism were identified through keyword search in PubMed and Google Scholar. 10 studies (out of 320) were included in this systematic review. Results were included. Majority (n=7) of the included studies were conducted among the Asian populations. Of the 10 included studies, eight studies reported a significant association between HBV infection and impaired glucose metabolism, proxied by impaired glucose tolerance, impaired fasting glucose, diabetes mellitus, insulin resistance, and metabolic syndromes. The remaining two studies using diabetes mellitus and insulin resistance as outcome measures did not find a positive association with HBV infection. Conclusions: The association between HBV and impaired glucose metabolism is suggestive from the evidence compiled from included articles. However, whether the development of glucose intolerance or diabetes mellitus is linked to an infectious cause of HBV is still inconclusive. Further studies that could improve on the current understanding of the associations between HBV infection and impaired glucose metabolism are necessary. / published_or_final_version / Public Health / Master / Master of Public Health

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Treatments aimed at modifying cardiac substrate utilisation are designed to improve metabolic efficiency. In the fasting state, the heart mainly relies on fatty acid oxidation for its energy production. The heart can adapt to metabolise glucose, lactate and amino acids depending on the predominate milieu and demands placed upon it. A shift from fatty acid oxidation to carbohydrate oxidation leads to a lower oxygen consumption per unit of adenosine triphosphate produced. It is this concept of improving cardiac efficiency by a reduction in oxygen demand that underpins the use of metabolic manipulating agents as a therapeutic strategy in heart failure. Cardiac energy starvation is increasingly recognised as playing a central role in the pathophysiology of heart failure. Alterations in substrate utilisation thus underlie the hope that metabolic manipulating agents will be of benefit in heart failure of both ischaemic and non-ischaemic origin. This metabolic shift is achieved by promoting glucose utilisation and reducing the utilisation of fatty acids. This leads to a greater production of adenosine triphosphate per unit of oxygen consumed. With an ongoing demand for treatment options in ischaemic heart disease and the growing burden of chronic heart failure, new treatment modalities beyond contemporary therapy warrant consideration. This thesis aims to investigate the short term effects of metabolic manipulation on changes in cardiac energetic status, cardiac function, efficiency and substrate utilisation.

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