Anda di halaman 1dari 4

Continental J.

Biomedical Sciences 5 (1): 1 - 4, 2011 ISSN: 2141 – 419X


© Wilolud Journals, 2011 http://www.wiloludjournal.com
http://www.wilol
` Printed in Nigeria

CHANGES IN SERUM TRIACYLGLYCEROL


TRIACYLGLYCEROL LEVEL AND BLOOD PRESSURE MEASURES
MEASURE INDUCED
BY VARYING DOSES OF ALCOHOL IN MAN

Opajobi A.O
Department of Medical
edical Biochemistry, College of Health Sciences, Delta State University

ABSTRACT
The alteration in serum Triacylglycerol (TAG) and Blood pressure (BP), caused by 0.4g ethanol/kg and
0.8g ethanol/kg weight administered orally were studied during the post oxidation
oxidation period. Results
obtained indicate that the administered doses increased both serum TAG and BP. The changes were
found to be dose and sex dependent. Positive correlations were demonstrated at the different doses in
both genders. The percentage changes were higher among the female participants. Except the changes
in BP produced by the higher dose, none again was shown to be significantly different at 5% probability
level using ANOVA. Notwithstanding, alcohol induced increase in serum TAG and the attendant attendan
increase in BP could be risk factors of hypertension and other allied diseases.

KEYWORDS: Blood Pressure, Hypertension, Triacylglycerol, Alcohol.

INTRODUCTION
Alcohol (ethanol) is one of the substances most frequently abused among several drugs (Terry, et al., 1994). In
beverage, it is consumed in the form 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 of the gastro intestinal tract but, principally from the duodenum and jejunum
largely by simple diffusion into blood (Ellenhorn, 1997) which distributes the absorbed amount to the liver, the
main site of oxidation, and to other well vascularised tissues, including the brain, kidney and lungs.

Alcohol is neither accumulated to any extent by specific organ nor preferentially bound to cellular components.
It is eliminated almost entirely by oxidative metabolism in the liver.

The basic pathway of alcohol metabolism involves


involves the progressive oxidation to acetate via acetaldehyde,
respectively catalyzed by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) (Lieber, 1997).

However, about 2-10%


10% is eliminated unchanged through breath, sweat, faeces breast milk and saliva
sal (Feinman,
et al 1987).

Ethanol consumption has been shown to affect blood chemistry values and this reflects its influences on
essential metabolic pathways including those of lipids. Ethanol has been demonstrated to cause a rise in plasma
TAG (Hodge, et al,, 1993). A positive correlation between chronic alcohol intake, BP and the prevalence of
hypertension has been described in epidemiological surveys. In such studies utilizing free-living
free individuals
selected at random, it was observed that the ingestion
ingestion of 30g ethanol/day increased both systolic and diastolic
BP in Men and Women (Moreira, et al,, 1998). Other studies on the pattern of alcohol intake showed that
pressure response to alcohol consumption is similar in magnitude in weekend and daily drinkers (Rakic et al,
1998). However, such influence has a rapid onset and offset in weekend drinkers, but it is more sustained in
daily drinkers (Pickering, et al,, 1995). Increase in plasma TAG has been reported in hospitalized Nigerian
alcoholics (Onyesom, et al, 2000).

Since environment and ethnicity influence the manner alcohol affects metabolic process, It becomes imperative
to study the changes in TAG and BP induced by different doses in free-living
free living Nigerian Men and Women with
very weak drinking habits. Thiss could be a baseline study to establishing a pattern for Nigerians.

1
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 lieu 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 SEX TAG (mmol/l) % INCREASE FROM SYSTOLIC % INCREASE FROM DIASTOLIC % INCREASE
(ethanol/kg BW) BASAL VALUES BP BASAL VALUES BP FROM BASAL
VALUES
0.04 M 1.150±0.043 18.07 112+2.0 5.66 93±30 5.66
F 1.230±0.035 33.26 *103+2.0 9.58 80±1.0 6.67
0.8 M 1.224±0.034 25.67 *116±1.0 9.43 *96±1.0 9.09
F 1.210±0.012 31.09 *106±2.0 12.77 82±1.5 9.33
Basal value M 0.974±0.033 106±3.0 88±3.0
0.923±0.002 94±4.0 75±2.5
*Significantly different from their respective basal values (P<0.05)

3
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
Ellanbom, M.J. (1997). Ellanbom’s Medical Toxicology: Diagnosis and Treatment of Human Poisoning, 2nd
(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- Insulin 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). The ociation
of Cigarette Smoking and Alcohol Consumption with other 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
triacylglycerol, lipoprotein, cholesterol and blood pressure in Nigerian alcoholics. Med. Lab. 9:93-
98.

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

Anda mungkin juga menyukai