Continental J. Biome ical Sciences 5 (1): 1 - 4, 2011 © Wilolud Journals, 2 11 ` Printed in Nigeria
ISSN: 2141 – 419X http://w w.wiloludjournal.com
CHANGES IN SERUM TRIACY GLYCEROL LEVEL AND BLOOD PRESSURE M ASURES INDUCED BY ARYING DOSES OF ALCOHOL IN MAN
Department of Medical
Opajobi A.O iochemistry, College of Health Sciences, Delta State University
ABSTRACT The alteration in serum Triacyl lycerol (TAG) and Blood pressure (BP), caused by .4g ethanol/kg and 0.8g ethanol/kg weight administered orally were studied during the post oxidati on period. Results obtained indicate that the admiinistered doses increased both serum TAG and BP. The changes were found to be dose and sex depe ndent. Positive correlations were demonstrated at the different doses in both genders. The percentage changes were higher among the female participants. xcept the changes in BP produced by the higher d se, none again was shown to be significantly differen t at 5% probability level using ANOVA. Notwithstanding, alcohol induced increase in serum TAG and the attendant increase in BP could be risk fac tors of hypertension and other allied diseases. KEYWORDS: Blood Pressure, Hypertension, Triacylglycerol, Alcohol. INTRODUCTION Alcohol (ethanol) is one of the sub tances most frequently abused among several drugs Terry, et al., 1994). In beverage, it is consumed in the for of beer, wine, gin, whisky or spirit (Ellenhorn, 1997) but locally in form of palmwine, ‘ogogoro’, burukutu or “akpeteshi” with variable concentrations. Alcohol is absorbed from all parts f the gastro intestinal tract but, principally from the uodenum and jejunum largely by simple diffusion into blo od (Ellenhorn, 1997) which distributes the absorbed mount to the liver, the main site of oxidation, and to other well vascularised tissues, including the brain, kidney nd lungs. Alcohol is neither accumulated to a ny extent by specific organ nor preferentially bound t o cellular components. It is eliminated almost entirely by o idative metabolism in the liver. The basic pathway of alcohol metabolism involves the progressive oxidation to ac tate via acetaldehyde, respectively catalyzed by alcohol d hydrogenase (ADH) and aldehyde dehydrogenase (A LDH) (Lieber, 1997). However, about 2-10% is eliminate unchanged through breath, sweat, faeces faeces breast milk and saliva (Feinman, et al 1987). Ethanol consumption has been shown to affect blood chemistry values and this ref lects its influences on essential metabolic pathways includ ing those of lipids. Ethanol has been demonstrated t cause a rise in plasma TAG (Hodge, et al, 1993). A posi tive correlation between chronic alcohol intake, BP and the prevalence of hypertension has been described i epidemiological surveys. In such studies utilizing free-living individuals selected at random, it was observe that the ingestion of 30g ethanol/day increased bot systolic and diastolic BP in Men and Women (Moreira, et al, 1998). Other studies on the pattern of alco ol intake showed that pressure response to alcohol consu mption is similar in magnitude in weekend and dail drinkers (Rakic et al, 1998). However, such influence ha s a rapid onset and offset in weekend drinkers, but it is more sustained in daily drinkers (Pickering, et al, 1 95). Increase in plasma TAG has been reported in hospitalized Nigerian alcoholics (Onyesom, et al, 2000). Since environment and ethnicity in luence the manner alcohol affects metabolic process, It becomes imperative to study the changes in TAG and B P induced by different doses in free-living Nigerian Men and Women with very weak drinking habits. This cou ld be a baseline study to establishing a pattern for Nig erians.
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Opajobi A.O: Continental J. Biomedical Sciences 5 (1): 1 - 4, 2011
MATERIALS AND METHODS STUDY CENTRE AND PERIOD: This study was carried out in the Research unit, Department of Medical Biochemistry, Delta State University, Abraka, Nigeria between September and November 2008. Subjects:Fifteen (eight male and seven female) free-living undergraduates in apparent good health were selected at random and tested. Conditions that could interfere with lipid metabolism and BP were eliminated in this study. ADMINISTRATION OF THE ALCOHOL DOSES: The subjects were tested on two different occasions on the first occasion, 0.40g ethanol/kg body weight was administered as a single dose, and during the second occasion separated by ten days, 0.80g ethanol/kg body weight was administered. These were administered orally after about 2 hours of taking snacks (biscuits and squash) as supper. This practice ensures gastric empting, since food in the stomach could affect alcohol bioavailability and its attendant effects. In all cases, the equivalent volume of the amount administered was calculated as previously described (Onyesom and Atakuo, 1998). The basal values were determined using water in lieu of alcohol. Blood samples were collected from the participants the next morning before breakfast. COLLECTION OF BLOOD SPECIMEN: Five milliliters (5ml) of venous (whole) blood was collected from each volunteer into plain sterile bottles then, allowed to clot and centrifuged at 1200 x g for 5 minutes at room temperature. The serum was separated from the debris using dropping pipette in bijou bottle for analysis. ANALYSIS OF SERUM SAMPLES: The serum TAG was determined using the end-point colorimetric method (Searcy, 1961). The commercial kit containing the reagents was supplied by TECO diagnostics, USA. The BP was measured in a well seated position using sphygmomanometer after some few minutes of rest prior to blood collection. RESULTS Statistical analysis of the data obtained using ANOVA demonstrate that the dose and sex-dependent increase in serum TAG were not significant (P >0.03) (Table 1.0). However, the increase in the systolic and diastolic BP induced by the higher dose were statistically found to be significant (P < 0.05) using ANOVA (Table 1). The Pearson’s movement product correlation analysis of results indicates positive relationship between serum TAG and BP at both doses except for the female group at the higher dose. It was also observed that percentage increases in TAG and BP (from the respective basal values) were higher among the female subjects. DISCUSSION In this study, alcohol has been demonstrated to increase plasma TAG and BP (table 1.0) and these observations + agree with earlier reports (Hodge, et al, 1993, Onyesom, et al, 2000). Ethanol oxidation generates NADH + H + and the excess H stimulates the synthesis of fatty acids which are diverted from their normal energy producing pathways into TAG synthesis due to impairment in the carnitine transferase transport mechanism. Alcohol consumption has also been reported to induced high BP (Itoh, et al, 1997) and cause hypertension (Lee, et al, 1998) due to a number of overlapping factors including increase blood acetaldehyde levels and release of epinephrine that accompanies alcohol intoxication stress. More recently, the alcohol-induced hypertriglyceridemia demonstrated in this study, could be implicated as yet another aetiologic factor. The long-term effect of alcohol misuse could lead to cardiovascular complications, although Lip and Beevers (1995) argued that moderate alcohol consumption may be protective against these complications, and that alcohol only results in a rapid reversible risk in BP which does not cause cardiovascular damage. However, Onyesom and Atakuo (1998) stated that if moderate drinking persists over a fairly long period of time, such damage could develop due to the cost and pressure of extracting TAG in l ieu of free fatty acids (FFA) by the myocardium. The association of the alcohol-induced increase in plasma TAG and increase BP put female drinkers especially, at greater risk of developing hypertension in this context. Therefore, long-term control trial involving large sample size is currently being investigated. Nonetheless in the interim, drinking by Nigerian women especially should be sparingly if at all necessary since it has been speculated that they cannot easily adjust to any particular dose due to the effects of hormones that control the menstrual cycle. 2
Opajobi A.O: Continental J. Biomedical Sciences 5 (1): 1 - 4, 2011
TABLE 1: CHANGES IN MEAN SERUM TAG AND BP INDUCED BY DIFFERENT DOSES OF ALCOHOL ADMINISTERED ORALLY TO MAN DOSE (ethanol/kg BW) 0.04
SEX
TAG (mmol/l)
% INCREASE FROM BASAL VALUES
M F M F M
1.150±0.043 18.07 1.230±0.035 33.26 0.8 1.224±0.034 25.67 1.210±0.012 31.09 Basal value 0.974±0.033 0.923±0.002 *Significantly different from their respective basal values (P<0.05)
SYSTOLIC BP 112+2.0 *103+2.0 *116±1.0 *106±2.0 106±3.0 94±4.0
% INCREASE FROM BASAL VALUES 5.66 9.58 9.43 12.77
DIASTOLIC BP 93±30 80±1.0 *96±1.0 82±1.5 88±3.0 75±2.5
% INCREASE FROM BASAL VALUES 5.66 6.67 9.09 9.33
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Opajobi A.O: Continental J. Biomedical Sciences 5 (1): 1 - 4, 2011
Further research and caution are important because this speculation could complicate the observed trend. ACKNOWLEDGEMENT Gratitude goes to the management of Vantex Research Laboratory Sapele. REFERENCES nd Ellanbom, M.J. (1997). Ellanbom’s Medical Toxicology: Diagnosis and Treatment of Human Poisoning, 2 (ed), Williams and Wilkins, London. Feinman, L., Baraona, E., Matsuzaki, S. karsten, M. and Lieber, C.S. (1978). Concentration dependence of ethanol metabolism in vivo in rats and Man. Alcohol, Clin. Exp. Ros. 2:38-385. Hodge, A.M., Dowse, G.K., Collins, V.R. and Zimmet, P.Z (1993). Abnormal glucose tolerance and consumption in the population in high risk of non- I nsulin dependent diabetes mellitus. Am. J. Epidemiol 137 (2): 178-189. Itoh, T., Matsumoto, M., Okada, A. Shirashi, N. and Hougaku, H. (1997). Effect of daily alcohol intake on blood pressure differ depending on an individual’s sensitivity to alcohol: Oriental flushing as a sign to stop drinking for health reasons. J. Hypertension 15 (11): 1211-1217. Lee,K.S., Park, C.Y., Meng, k., Bush,A., Lee, S.H., Lee,N.G., Koo, J.W and Chuma, C.K., (1998). T he ociation of Cigarette Smoking and Alcohol Consumption with other Cardiovascular Cardiovascular risk factors in men from Seoul, Korea. Ann. Epidemiol. 8 (1): 31-38. Lieber, C.S (1997): Ethanol Metabolism, Cirrhosis and alcoholism. Clinical Chemical Acta : 257(1): 59-84. Lip, G.Y. and Beevers, D.G. (1995). Alcohol hypertension, Coronary disease and stroke. Clin. Exp. Pharmacol.
Opajobi A.O: Continental J. Biomedical Sciences 5 (1): 1 - 4, 2011
Further research and caution are important because this speculation could complicate the observed trend. ACKNOWLEDGEMENT Gratitude goes to the management of Vantex Research Laboratory Sapele. REFERENCES nd Ellanbom, M.J. (1997). Ellanbom’s Medical Toxicology: Diagnosis and Treatment of Human Poisoning, 2 (ed), Williams and Wilkins, London. Feinman, L., Baraona, E., Matsuzaki, S. karsten, M. and Lieber, C.S. (1978). Concentration dependence of ethanol metabolism in vivo in rats and Man. Alcohol, Clin. Exp. Ros. 2:38-385. Hodge, A.M., Dowse, G.K., Collins, V.R. and Zimmet, P.Z (1993). Abnormal glucose tolerance and consumption in the population in high risk of non- I nsulin dependent diabetes mellitus. Am. J. Epidemiol 137 (2): 178-189. Itoh, T., Matsumoto, M., Okada, A. Shirashi, N. and Hougaku, H. (1997). Effect of daily alcohol intake on blood pressure differ depending on an individual’s sensitivity to alcohol: Oriental flushing as a sign to stop drinking for health reasons. J. Hypertension 15 (11): 1211-1217. Lee,K.S., Park, C.Y., Meng, k., Bush,A., Lee, S.H., Lee,N.G., Koo, J.W and Chuma, C.K., (1998). T he ociation of Cigarette Smoking and Alcohol Consumption with other Cardiovascular Cardiovascular risk factors in men from Seoul, Korea. Ann. Epidemiol. 8 (1): 31-38. Lieber, C.S (1997): Ethanol Metabolism, Cirrhosis and alcoholism. Clinical Chemical Acta : 257(1): 59-84. Lip, G.Y. and Beevers, D.G. (1995). Alcohol hypertension, Coronary disease and stroke. Clin. Exp. Pharmacol. Physiol. 22 (3):189-194. Moreira, L. B., Fuchus, F.D., Moracs, R.S., Bredemeier, M. and Duncan, B.B. (1998). Alcohol intake and blood pressure: the importance of time elapsed since last drink. J. Hypertens. 16 (2):175-180. Onyesom, I. and Atakuo, E.O., (1998). An investigation into the relationship between alcohol induced changes in serum triacylglycerol and blood pressure. Nig.J. Biochem. Mol. Biol. 13:79-83. Onyesom, I., Obodoruku, S. and Imafidon, E.E. (2000). The influence of duration of alcoholism on plasma plasma triacylglycerol, lipoprotein, cholesterol and blood pressure in Nigerian alcoholics. alcoholics. Med. Lab. 9:9398. Pickering, T.G., Schwartz. J.E. and James G.D. (1995). Ambulatory blood pressure monitoring for evaluating the relationship between life style, hypertension and cardiovascular risk. Clin. Exp Pharmacol.Physiol. 1(3) 226- 237. Rakic, V. Puddey, I.B., Barke, V., Dimmit, S.B. and Belin, I.J. ( 1998). Influence of pattern of alcohol intake on blood pressure in regular drinkers: a controlled trial. Hypertension, 16 (20): 165-174. Trey, S.Z., Bridget, F.G., Fredrick, S.S. And Daryl, B. (1994). Alcohol involvement in fatal traffic crashes in the United States. 1979-1990. Addiction 89:228-229. Received for Publication: 02/02/2011 Accepted for Publication: 12/03/2011
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