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American Journal of Medicine Studies

ISSN (Print): 2333-8881

ISSN (Online): 2333-889X

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Alcoholism and Its Relation to Hypoglycemia – An Overview

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

American Journal of Medicine Studies. 2014, 2(3), 46-49
doi: 10.12691/ajms-2-3-2
Copyright © 2014 Science and Education Publishing

Cite this paper:
Sabitha Kandi, Neelesh deshpande, Pragna rao, 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.

Correspondence to: K.V.  Ramana, Department of Microbiology, Prathima Institute of Medical Sciences, Karimnagar, India. Email:


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.



[1]  Sabitha kandi, Neelesh Deshpande, Venkata Bharath Kumar Pinnelli, Ramakrishna Devaki, Pragna Rao, K.V. Ramana. Alcoholism and its role in the development of oxidative stress and DNA damage: An Insight. American Journal of Medical Sciences and Medicine, 2014:2(3):64-66.
[2]  U. Sitarama acharya. Biochemistry Questions and Answers. Chapter 8: Carbohydrate Metabolism. Honna – Padma printers. 1998; 99.
[3]  Dittmar EA, Hetenyi G Jr. The effect of ethanol on glucose homeostasis. Can J Physiol Pharmacol. 1978; 56(1): 54-61.
[4]  Krebs HA, Freeland RA, Hems R, Stubbs M. Inhibition of hepatic gluconeogenesis by ethanol. Biochem J. 1969; 112:117.
[5]  Stubbs M, Veech RL, Krebs HA. Control of the redox state of the nicotinamide – adenine dinucleotide couple in rat liver cytoplasm. Biochem J. 1972;126: 59-65.
Show More References
[6]  Heather Hammerstedt, Stacey L Chamberlain, Sara W Nelson and Mark C Bisanzo. Alcohol – related hypoglycemia in rural Uganda: Socioeconomic and physiologic contrasts. Int J Emerg Med. 2011: 4:5.
[7]  Huang Z, Sjoholm A. Ethanol acutely stimulates islet blood flow, amplifies insulin secretion, and induces hypoglycemia via nitric oxide and vagally mediated mechanisms. Endocrinology. 2008:149: 232-236.
[8]  American diabetes association. Standards of medical care in diabetes. 2013 36: suppl: S11-S66.
[9]  Williams HE. Alcoholic hypoglycemia and ketoacidosis. Med Clin North Am. 1984; 68(1): 33-8.
[10]  Jain H, Beriwal S, Singh S. Alcohol induced ketoacidosis, severe hypoglycemia and irreversible encephalopathy. Med Sci Monit. 2002; 8(11): CS77-9.
[11]  Field JB, Williams HE, Mortimorge GE. Studies on the mechanism of ethanol- induced hypoglycemia. J Clin Invest. 1963; 42:497-506.
[12]  Arky RA, Freinkel N: Alcohol hypoglycemia Vs Alcohol infusion to test gluconeogenesis in starvation, with special reference to obesity. N Engl J Med. 1996: 274: 426-433.
[13]  Rubin E, Lieber CS: Experimental alcoholic hepatic injury in man: Ultra structural changes. Fed Proc. 1967:26:1458-67.
[14]  Lefevre A, Adlex H, Lieber CS: Effect of ethanol on ketone metabolism. J Clin Invest. 1970:49: 1775-82.
[15]  Forsander OA, Maenpaa PH, Salaspuro MP: Influence of ethanol on the lactate/pyruvate and betahydroxy butyrate/acetoacetate ratios in rat liver experiments. Acta Chem Scand. 1965: 19: 1770 -71.
[16]  Milford Fulop MD: Alcoholic Hypoglycemia and ketosis. The Western journal of medicine. 1979: 4; 321-322.
[17]  Devenyi P : Alcoholic hypoglycemia and alcoholic ketoacidosis: sequential events of the same process?. CMA Journal. 1982; 127: 513.
Show Less References


Cystic Lymphangioma of the Adrenal Gland: A Case Report and a Review of the Literature

1Department of endocrinology, Hedi Chaker Hospital, Sfax, Tunisia

2Department of radiology, Habib Bourguiba Hospital, Sfax, Tunisia

American Journal of Medicine Studies. 2015, 3(1), 1-3
doi: 10.12691/ajms-3-1-1
Copyright © 2015 Science and Education Publishing

Cite this paper:
Faten hadjkacem, Mouna Ammar, Ayman Maalej, Mouna Elleuch, Nessrine Cheikrouhou, Mouna Mnif, Nabila Rekike, Fatma Mnif, Nadia Charfi, Mohamed Abid. Cystic Lymphangioma of the Adrenal Gland: A Case Report and a Review of the Literature. American Journal of Medicine Studies. 2015; 3(1):1-3. doi: 10.12691/ajms-3-1-1.

Correspondence to: Mouna  Elleuch, Department of endocrinology, Hedi Chaker Hospital, Sfax, Tunisia. Email:


Adrenal lymphangiomas, also known as cystic adrenal lymphangiomas are benign vascular lesions, most often found incidentally during abdominal imaging studies, abdominal surgery or at autopsy. We present a case of a 45-year-old female who was evaluated for recurrent abdominal pain. Imaging studies revealed a large cystic lesion in the right adrenal region considered as a hydatid cyst. Right adrenalectomy was performed. Histopathologic examination demonstrates that the definite diagnosis is cystic lymphangioma of the right adrenal gland.



[1]  C. L. Ellis, P. Banerjee, E. Carney, R. Sharma, and G. J. Netto. Adrenal lymphangioma: clinicopathologic and immunohistochemical characteristics of a rare lesion. Human Pathology( 2011);( 42): 1013-1018.
[2]  Khoda J, Hertzanu Y, Sebbag G, Lantsberg L, Barky Y. Adrenal cysts: diagnosis and therapeutic approach. Int Surg. (1993); (78): 239-242.
[3]  J.M. Longo, S.Z. Jafri, andK. B. Bis, “Adrenal lymphangioma: a case report,”. Clinical Imaging.(2000); (24): 104 106.
[4]  Kalof AN, Cooper K. D2-40 immunohistochemistry-so far. Adv Anat Pathol. (2009); (16): 62-4.
[5]  L. A. Erickson, R. V. Lloyd, R. Hartman, and G. Thompson. Cystic adrenal neoplasms. Cancer. (2004);(101): 1537-1544.
Show More References
[6]  Y. Tanuma, M. Kimura, and S. Sakai. Adrenal cyst: a review of the japanese literature and report of a case. International Journal of Urology. (2001); (8): 500-503.
[7]  J.M. Longo, S.Z. Jafri, andK. B. Bis. Adrenal lymphangioma: acase report. Clinical Imaging. (2000);(24): 104-106.
[8]  Y.-K. Guo, Z.-G. Yang, Y. Li et al.Uncommon adrenal masses: CT and MRI features with histopathologic correlation. European Journal of Radiology.(2007); (62): 359-370.
[9]  Satou T, Uesugi T, Nakai Y, Hayashi Y, Imano M, Hashimoto S. Case of adrenal lymphangioma with atypical lymphocytes in aspirate cytology. Diagn Cytopathol. (2003); ( 29): 87-90.
[10]  Goel MC, Agarwal MR, Misra A. Percutaneous drainage of renal hydatid cyst: early results and follow-up. Br J Urol. (1995); (75):724-8.
[11]  A. A. Kasperlik-Załuska, M. Otto, A. Cichocki et al.1,161 patients with adrenal incidentalomas: indications for surgery. Langenbeck’s Archives of Surgery. (2008); (393): 121-126.
Show Less References


Researches on the Pharmacological Effects of Eicosapentaenoic Acid

1School of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan 250355, People’s Republic of China

American Journal of Medicine Studies. 2015, 3(1), 4-7
doi: 10.12691/ajms-3-1-2
Copyright © 2015 Science and Education Publishing

Cite this paper:
Zunting Pang, Qiang Zhang, Zhixiang Tian, Chunchao Han. Researches on the Pharmacological Effects of Eicosapentaenoic Acid. American Journal of Medicine Studies. 2015; 3(1):4-7. doi: 10.12691/ajms-3-1-2.

Correspondence to: Chunchao  Han, School of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan 250355, People’s Republic of China. Email:


Fish oils are the most common source of omega-3 polyunsaturated fatty acids (n-3 PUFAs), mainly eicosapentaenoic acid(EPA). It has been pointed out protective effects and beneficial effects of EPA on body weight reduction, heart health, blood lipid profile, cardiovascular diseases and other diseases. Based on its biological activities, EPA may be developed to a complementary and alternative medicine through further research. In this paper, the pharmacological effects of EPA were summarized by reviewing the recent related literatures.



[1]  Dyerberg J, Bang HO. (1970).Lipid metabolism, atherogenesis, and haemostasis in Eskimos: The role of the prostaglandin-3 family. Haemostasis 8(3-5):227-233.
[2]  Eunice Molinar-Toribio1, Jara Pe ´rez-Jime ´nez1, Sara Ramos-Romero, et al. (2015) Effect of n-3 PUFA supplementation at different EPA:DHA ratios on the spontaneously hypertensive obese rat model of the metabolic syndrome. British Journal of Nutrition 113: 878-887
[3]  WHIMS-MRI. (2014) Higher RBC EPA+DHA corresponds with larger total brain and hippocampal volumes. American Academy of Neurology 82(5):435-42.
[4]  Hajime Ishii, Yasuo Horie, Shigetoshi Ohshima, et al. (2009). Eicosapentaenoic acid ameliorates steatohepatitis and hepatocellular carcinoma in hepatocytespecific Pten-deficient mice. J Hepatol 50(3):562-71.
[5]  Y.A. Carpentier, L. Portois, W.J. Malaisse. (2006). N-3 fatty acids and the metabolic syndrome. Am. J. Clin. Nutr 83:1499S-1504S.
Show More References
[6]  G. Schmitz, J. Ecker. (2008). The opposing effects of n-3 and n-6 fatty acids. Prog Lipid Res 47(2):147-55.
[7]  Kunesova M. (2006). The influence of n-3 polyunsaturated fatty acids and very low calorie diet during a short-term weight reducing regimen on weight loss and serum fatty acid composition in severely obese women. Physiol Res Acad Sci Bohemoslov 55:63-72.
[8]  Thorsdottir I, Tomasson H, Gunnarsdottir I, Gisladottir E, Kiely M, Parra MD, et al. (2007). Randomized trial of weight-loss-diets for young adults varying in fish and fish oil content. Int J Obes 31:1560-1566.
[9]  LeMieux MJ, Kalupahana NS, Scoggin S, Moustaid-Moussa N. (2015) Eicosapentaenoic acid reduces adipocyte hypertrophy and inflammation in diet-induced obese mice in an adiposity-independent manner. J Nutr 145(3):411-7.
[10]  Huerta AE, Navas-Carretero S, et al. (2015) Effects of α-lipoic acid and eicosapentaenoic acid in overweight and obese women during weight loss.Obesity (Silver Spring) 23(2):313-21.
[11]  Balk EM, Lichtenstein AH, Chung M, Kupelnick B, Chew P, Lau J. (2006) Effects of omega-3 fatty acids on serum markers of cardiovascular disease risk: a systematic review. Atherosclerosis 189(1):19-30.
[12]  Jacobson TA. (2008)Role of n-3 fatty acids in the treatment of hypertriglyceridemia and cardiovascular disease. Am J Clin Nutr 87 (Suppl):S1981-S1990.
[13]  Fletcher B, Berra K, Ades P, et al. (2005)Managing abnormal blood lipids: a collaborative approach. Circulation 112:3184-3209.
[14]  Musa-VelosoK, Binns MA, Kocenas AC, et al. (2010) Long-chain omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid dose-dependentlyreduce fasting serum triglycerides. Nutr Rev 68(3):155-67.
[15]  Durante W. (2010). Targeting heme oxygenase-1 in vascular disease. Curr Drug Targets 11(12):1504-1516.
[16]  Idriss NK, Blann AD, Lip GY. (2008)Hemoxygenase-1 in cardiovascular disease. J Am Coll Cardiol 52(12):971-978.
[17]  Lee SE, Kim GD, Yang H, Son GW, Park HR, Cho JJ, Ahn HJ, Park CS, Park YS. (2015)Effects of eicosapentaenoic acid (EPA) on the cytoprotection via Nrf2-mediated heme oxygenase-1 inhuman endothelial cells. J Cardiovasc Pharmacol 26.
[18]  H. Chamras, A. Ardashian, D. Heber, J.A. Glaspy. (2002)Fatty acid modulation of MCF-7 human breast cancer cell proliferation, apoptosis and differentiation. J Nutr Biochem 13:711-717.
[19]  Eser PO, Vanden Heuvel JP, Araujo J, Thompson JT. (2013) Marineand plant-derived omega-3 fatty acids differentially regulate prostate cancer cell proliferation. Mol Clin Oncol 1(3):444-452.
[20]  Fukui M, Kang KS, Okada K , Zhu BT. (2013)EPA, an omega-3fatty acid, induces apoptosis in human pancreatic cancer cells:role of ROS accumulation, caspase-8 activation, and autophagyinduction. J Cell Biochem 114(1):192-203.
[21]  Hossain Z, Hosokawa M, Takahashi K. (2009)Growth inhibition and induction of apoptosis of colon cancer cell lines by applying marine phospholipid. Nutr Cancer 61:123-130.
[22]  B.E.S. Hashem, K.L. Rudolph. (2007)Hepatocellular carcinoma: epidemiology and molecular carcinogenesis. J Gastroenterol 132:2557-2576.
[23]  J. Whang Peng, A.L. Cheng, C. Hsu, C.M. Chen. (2010)Clinical development and future direction for the treatment of hepatocellular carcinoma. J Exp Clin Med 2:93-103.
[24]  Zhang Y, Han L, Qi W, Cheng D, Ma X, Hou L, Cao X, Wang C. (2015) Eicosapentaenoic acid (EPA) induced apoptosis in HepG2 cells through ROS-Ca(2+)-JNK mitochondrial pathways. Biochem Biophys Res Commun 456(4):926-32.
[25]  Fietkau R, Lewitzki V, Kuhnt T, Holscher T, Hess CF, Berger B, Wiegel T, Rodel C, Niewald M, Hermann RM , Lubgan D. (2013)A disease-specific enteral nutrition formula improves nutritional status and functional performance in patients with head and neck and esophageal cancer undergoing chemoradiotherapy: results of a randomized, controlled, multicenter trial. Cancer 119: 3343-3353.
[26]  Mizoguchi K, Ishiguro H, Takahashi H, Sakamoto N, et al. (2014)Induction of apoptosis by eicosapentaenoic acid in esophageal squamous cell carcinoma. Anticancer Res 34(12):7145-9.
[27]  Jump DB. (2002)The biochemistry of n-3 polyunsaturated fatty acids. J Biol Chem 277: 8755-8758.
[28]  Konuma K, Itoh M, Suganami T, Kanai S, et al. (2015)Eicosapentaenoic Acid ameliorates non-alcoholic steatohepatitis in a novel mouse model using melanocortin 4 receptor-deficient mice. PLoS One 27, 10(3):e0121528.
[29]  Wirth S, Ribes-Koninckx C, Calzado MA, et al. (2010)High sustained virologic response rates in children with chronic hepatitis C receiving peginterferon alfa-2b plus ribavirin. J Hepatol 52:501-7.
[30]  Sokal EM, Bourgois A, Stephenne X, et al. (2010)Peginterferon alfa-2a plus ribavirin for chronic hepatitis C virus infection in children andadolescents. J Hepatol 52: 827-31.
[31]  Tajiri H, Inui A, Kiyohara Y, et al. (2009)Peginterferon alpha-2b and ribavirin for the treatment of chronic hepatitis C in Japanese pediatric and young adult patients: a survey of the Japan Society of Pediatric Hepatology. Eur J Gastroenterol Hepatol 21:1256-60.
[32]  Baker RD, Dee D, Baker SS. (2007) Response to pegylated interferon alpha-2b and ribavirin in children with chronic hepatitis C. J Clin Gastroenterol 41: 111-4.
[33]  McHutchison JG, Manns MP, Longo DL. (2006)Definition and management of anemia in patients infected with hepatitis C virus. Liver Int 26: 389-98.
[34]  Suzuki M, Inage E, et al. (2012)Prophylaxis for ribavirin-related anemia using eicosapentaenoic acid in chronic hepatitis C patients. Pediatr Int 54(4):528-31.
[35]  Rowan AD. (2001)Cartilage catabolism in arthritis: factors that influence homeostasis. Expert Rev Mol Med 1-20.
[36]  Hashimoto S, Nishiyama T, Hayashi S, et al. (2009)Role of p53 in human chondrocyte apoptosis in response to shear strain. Arthritis Rheum 60:2340-2349.
[37]  Takebe K, Nishiyama T, Hayashi S, et al. (2011)Regulation of p38 MAPK phosphorylation inhibits chondrocyte apoptosis in response to heat stress or mechanical stress. Int J Mol Med 27:329-335.
[38]  Sakata S, Hayashi S, Fujishiro T, et al. (2015)Oxidative Stress-induced Apoptosis and Matrix Loss of Chondrocytes Is Inhibited by Eicosapentaenoic Acid. J Orthop Res 33(3):359-65.
[39]  Jump DB, Depner CM, Tripathy S. (2012)Omega-3 fatty acid supplementation and cardiovascular disease. J Lipid Res 53:2525–2545.
[40]  Eslick GD, Howe PR, Smith C, Priest R, Bensoussan A. (2009) Benefits of fish oil supplementation in hyperlipidemia: a systematic review and metaanalysis. Int J Cardiol 136(1):4-16.
[41]  Verduci E, Agostoni C, et al. (2014)Blood lipids profile in hyperlipidemic children undergoing different dietary long chain polyunsaturated supplementations: a preliminary clinical trial. Int J Food Sci Nutr 65(3):375-9.
[42]  Angela Pirillo. (2013)Omega-3 polyunsaturated fatty acids in the treatment of hypertriglyceridaemia. Int J Cardiol.
Show Less References