@article{ajms2014232,
author={{Kandi, Sabitha and deshpande, Neelesh and rao, Pragna and Ramana, K.V.},
title={Alcoholism and Its Relation to Hypoglycemia ¨C An Overview},
journal={American Journal of Medicine Studies},
volume={2},
number={3},
pages={46--49},
year={2014},
url={http://pubs.sciepub.com/ajms/2/3/2},
abstract={Alcohol (ethanol) is metabolized in the liver by enzymes alcohol dehydrogenase and aldehyde dehydrogenase to acetate, which is spontaneously broken down to CO<SUB>2</SUB> and H<SUB>2</SUB>O utilizing NAD<SUP>+</SUP> and Cytochrome P<SUB>450</SUB> E<SUB>1 </SUB>(CYPE1). Thus alcohol metabolism decreases NAD<SUP>+</SUP><SUP> </SUP>/ NADH ratio(redox state). Gluconeogenesis, the synthetic pathway of glucose from non-carbohydrate sources(propionate, lactate, aminoacids, glycerol, alanine) predominantly takes place in liver. The significance of gluconeogenic pathway is that it helps in maintaining blood glucose levels in fasting or starvation conditions. Alcoholism (>120ml /day) leads to an increase in the ratio of NAD<SUP>+</SUP><SUP> </SUP>/ NADH, and since the gluconeogenic pathway is dependent on the NAD<SUP>+</SUP><SUP> </SUP>/ NADH ratio, increased ratio slows down the pathway leading to hypoglycemia. There is enhanced ketone body metabolism due to hypoglycemia, leading to the accumulation of beta hydroxy butyrate resulting in alcoholic ketosis. Thus alcoholic hypoglycemia and alcoholic ketosis are associated with each other and gross change in liver can be seen after chronic alcoholism with malnutrition. Further studies are required to better understand how liver is able to maintain the redox states longer even during alcoholism.},
doi={10.12691/ajms-2-3-2}
publisher={Science and Education Publishing}
}