American Journal of Medicine Studies. 2014, 2(3), 46-49
DOI: 10.12691/ajms-2-3-2
Open AccessArticle
Sabitha Kandi1, Neelesh deshpande2, Pragna rao3 and K.V. Ramana4,
1Department of Biochemistry, Chalmeda Anandrao Institute of Medical Sciences, Karimnagar, India
2Department of Biochemistry, Government Medical College, Nagpur, India
3Department of Biochemistry, Manipal University, Manipal, India
4Department of Microbiology, Prathima Institute of Medical Sciences, Karimnagar, India
Pub. Date: September 12, 2014
Cite this paper:
Sabitha Kandi, Neelesh deshpande, Pragna rao and K.V. Ramana. Alcoholism and Its Relation to Hypoglycemia – An Overview. American Journal of Medicine Studies. 2014; 2(3):46-49. doi: 10.12691/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 CO2 and H2O utilizing NAD+ and Cytochrome P450 E1 (CYPE1). Thus alcohol metabolism decreases NAD+ / 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+ / NADH, and since the gluconeogenic pathway is dependent on the NAD+ / 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.Keywords:
alcoholism alcoholic hypoglycemia alcoholic ketosis redox state
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