INTAKE OF SARDIN ELLA LONGICEPS OIL AS ANTI DISLIPIDEMIA THROUGH DECREASE OF LDL-C ON RAT WISTAR.
INTAKE OF SARDIN ELLA LONGICEPS OIL AS ANTI DISLIPIDEMIA THROUGH
DECREASE OF LDL-C ON RAT WISTAR
Sri Wahjuni
Biochemistry Laboratory Chemistry Departement Faculty of Math and Science Udayana
University
ABSTRACT
Nowadays fish consumption behaviour needs to be improved since the chandes of consumption
paten to instant food. Fish, especially from deep see, is good for health, due to its rich content of
polyunsaturated fatty acid (omega-3) which level is investigated in this research using true
experimental study with randomized pre and posttest control group design. This research employed
50 Wistar rats which were divided into Sgroups, i.e.control group ()%SLO), treatment group l (10%
SLO), treatment group 2 (15% SLO),treatment group 3 (20%SLO), and treatment group 4
(25%SLO). To obtain dislipidemia, the rats were fed with food rich in factor for 8 weeks, followed
by determination of HDL level (pretest). After that, all rats were fed with sardinella longiceps oil
for 6 weeks for dislipidemia and followed by determination of HDL.
Intake of 20% SLO resulted in an increase of blood LDL levels of dislipidemia Wistar rat about
22,78% from 55,97 + 5.l,25 to 68,73 +1,25 MG/dL. Further research regarding of whether the
intake of SLO inhuman results in a similar effect to anti dislipidemia need to be carried out.
Keywords: Fish consumption, antidislipidemia, sardinella longiceps
INTRODUCTION
Nowdays, fish consumption behaviour needs to be improve since the changes of
consumption patern to instan food. Fish, especially from deep sea is good for health, due to the fish
rich of polyunsaturated fatty acid (omega-3). Such fish including Thunnus Scombridae, Euthymrus
sp, Scamberamorus, Decopterus, Rastrellinger, Sardinella Longiceps, Carangidae, Clupeidae, and
Psettodeserumei. Sardinella Longiceps are a highly abundance fish found in Indonesian sea.
Outbreak during peak season occures and as a consequence no economic value. Therefore, to
increase their economic value, the fish can be managed to produce oil (Abdullah, 200; Ihsan, 2009).
Research on fish oil advantages to decrease dislipidemia have already widely carried out.
This was intiated by the evidence that Japanese life longer compare to Mongolianese. This is as a
results of Japanese have much more fish on their diet compare to meat consumption by
Mongolianese. Fish consumption leads to lower of total cholesterol, LDL-cholesterol, and
trigliceride and higher HDL cholesterol compare to meat consumption. This is because of fish
contain much more polyunsaturated fatty acids omega-3 (Komatsu, et al., 2006; Fadilah, 2007).
Many researchs reported that there is a correlation between high lipid serum levels to
incidence of atheroschlerosis, a triger of coronary heart disease. Coronary heart disease occures as a
consequence of one of general mechanism, i.e. blood circulation disturbance and abnormality of
chardiac charge or any other form of aritmias. These will lead to the present of unorganize
myocardiac contraction, blood circulation obstruction, and blood circulation regugirtation. All of
these conditions result in shunting, abnormal circulation, and end up with congestive heart failure
(Vinay, et al. 2004). Ateroschlerosis is a slow progressive disease present in large to small muscular
and elastic arteris. Main sites of atheroschlerosis are abdominal aorta, coronaria arteri, poplitea
arteri, desendens toracali aorta, intern carotic arteri, and willisi circulation. Other risk factors, such
as hypertension, chronic hypercholesterolemia, immune system disturbance, toxin and virus have
also affect destruction of arteri endothelial wall cells. This destruction induces endotel cell
permeability changes and lead to plasma constituent, i.e. lipoprotein easily flow to the inner of
arterial wall. Endotel cell destruction will also change thrombocystein lumen arteri which is lead
to adhesion of thrombocyte to damaged and inflamated blood. Finally, results in contact of lower
connected tissue to other elements in blood circulation. If; this damage goes chronically and ages,
atherosclerosis process continually occurs and leads to thick tunica intima and disturbance of blood
circulation on that site (Szmitko, et al., 2003).
Dyslipidemia is an abnormal lipoprotein metabolism, generally correlated to decrease or
overproduction of lipoprotein. Dyslipidemia is frequently also known as hyperlipidemia associated
with increase of lipid serum as a risk factor of cardiovascular disease. This is because of there is a
cholesterol behavior which is play an important role on atherosclerosis in dyslipidemia. Therefore,
differentiation between hypercholesterolemia with dyslipidemia is hypercholesterolemia is define as
an increase of serum cholesterol more than 200 mg/Dl after 9-12 h starving. On the other hand,
dyslipidemia define as the present of increase LDL-cholesterol serum more than 160 mg/D1,
increase of triglyceride serum more than l50 mg/Dl or HDL-cholesterol below 40mg/Dl for man
and below 50 mg/Dl for women, besides hypercholesterolemia criteria. High cholesterol symptom
in dyslipidemia cannot be felt by dyslipidemia patients, however, this can only be known through
routine check of blood cholesterol. High cholesterol diet and genetic induce dyslipidemia (Anonym,
2009).
Based on background explained above, the author want to investigate the effect of anti
dislipidemia, through an decrease of LDL.
RESEARCH METHOD
Research Design
This is a true experimental study with randomized pre and posttest control group design.
This research employing 100 Wistar rats divided into two research, i.e. dislipidemia and
atheroschlerosis. Each researchs applying 50 Wistar rat classified into 5 groups, i.e. control group
(0% SLO), treatment group l (10% SLO), treatment group 2 (15% SLG), treatment group 3 (20%
SLO), and treatment group 4 (25% SLO).
Initial step is to prepaired all rats in similar condition, therefore, all rat were feeded with ITB
diet for 4 weeks. Then to obtain dislipidemiarat (Research I), rats were fed with food rich of fat
(UNAIR diet) for 8 weeks, followed by determination LDL-C levels (pretest data).
Location And Time Schedule
Rats preparation were carried out at Center Study of Animal Diseases(CSAD)Veterinary
Faculty Udayana University.LDL-C determination was carried out at UPT. Laboratorium Analitik
Universitas Udayana. Research was carried out for 12 months including data analysis and writing
the results.
Data Analysis
All data were analyzed descriptively. Mean difference decrease of decrease of LDL-C were
analyzed using anova one way at 5% significant levels.
RESULTS
Decrease of LDL-C levels of dislipidemia Wistar rat
Mean decrease data of LDL-C of dislipidemia Wistar rats for pre and posttest were listed on
Table 1. The data on Table l were normally distributed and their variance were also homogeneous
insicates by p > 0.05. Mean different profile of LDL-C levels after treatment of various SLO intake
was presented on
Figure l
Decrease of LDL-C levels of dislipidemia Wistar rat
Mean LDL-C levels of Wistar rat pretest and postest data were listed on Table l.
Table l Decrease of LDL-C Levels
Data on Table 1 are normaly distributed and their variance also homogeneous with p> 0 05
Mean profile different of LDL-C difference of various SLO intake was presented in Figure 1
Figure 1
Mean Different Profile of LDL-C Difference for Posttest
Anova test indicates that there is a significant different of SLO various intake with p< 0 05 Resume
of the test was presented on Table 2.
Tab1e2 Resume of Post 1-loc LDL-C Levels
DISCUSSION
Dyslipidemia
A number of 50 Wistar rat for dislipidemia have already investigated. Dislipidemia research
was applied by feeding of high fat diet (UNAIR diet) for 8 weeks, compare to 13 weeks for
atheroschlerotic research. Mean weight of initial Wistar rat is 49.78 dc 0.77) g. After the present of
dislipidemia, the mean weight is about 201.75 ± 0.51 g (pretest data). Mean weight of Wistar rat
alter intake of various SLO for 6 weeks is 203.78 ± 1.03 g (posttest data).
Decrease of LDL-C blood levels of dyslipidemia Wistar rat
In this research, it was obtained that intake of various SLO concentration decrease blood
LDL-C levels of dyslipidemia Wistar rat. Mean LDL-C blood levels of dyslipidemia Wistar rat
were presented on Table 1. Mean HDL-C blood levels of dyslipidemia Wistar rat for pretest with
intake of 0%, 10%, 15%, 20%, and 25% SLO were kolest-LDL pre danposttest (144,05;t0,02) and
(l41,06 :l:l,54) mg/dL, respectively. The mixture of MIL 10% results in the levels of kolest-LDL
pre and posttest (144,09 ± 0,08) and (140,99±1,38) mg/dL. The table also showd the level of kolestLDL for MIL 15%, 20% dan 25% pre and posttest (144,05±0,08) and (134,52i1,89) mg/dL;
(l44,08±0,02) and (126,12±1,61) mg/dL; (144,08±0,03) and (134,52±3,51) mg/dL respectively.
This research shows that lowering of the levels of kolest-LDL took place at all treatments (Figure
5.3). From the same table, it can also be seen that mean HDL-C blood levels of dyslipidemia Wistar
rat for posttest with intake of 0%, 10%, 15%, 20%, and 25% SLO were (56.84 ± 1.25); (58.14 ±
1.38); (59.26 ± 0.84); and (68.72 ± 0.86) mg/dL, respectively. The increase different of HDL-C
blood levels of dislipidemia Wistar rat caused by intake of 0%, 10%, 15%, 20%, and 25% SLO can
be seen on Table 4.10. This table reveals that the highest increase of 11.88 mg/dL HDL-C blood
levels of dislipidemia Wistar rat was observed for intake of 20% SLO, compare to 1.30 mg/dL for
intake of 10% SLO, and 2.72 mg/dL for intake of 15% SLO. These were compared towards HDL-C
blood levels of dislipidemia Wistar rat with intake of 0% SLO. An interesting trend observed in this
research was increase of 2.54 mg/dL HDL-C blood levels of dilipidemia rat due to intake of 25%
SLO, as indicated by Figure 4.5. However, that increase is not as big as for intake of 20% SLO
about 11.88 mg/dL. These trends occure in all treatments of SLO intake, including decrease of
LDL-C and MDA blood leves.
In dyslipidemia case, cell membrane was saturated of cholesterol due to exessive of LDL
acceptance and endogenebiosintesys. To overcome this situation, naturaly cholesterol balancing
occures trough pick cholesterol up and distributed to extracelular Hood and return it to liver. This
event known as reverse cholesterol transport and was carried out by HDL as an antithrombin
(Devlin, 1986; Murray, 2004). Possible mechanism is due to anti oxidant inactivation, that function
to break down unsaturated fatty acids. Long and continue exposure induce leucocyte adhesion to
vascular endotel which leads to endotel cells promote cholesterol effux that have as role to control
vascular (Tatong, 2003). This is conform to hypothesis 5, i.e intake of SLO increase HDL-C blood
levels of dislipidemia Wistar rat.
CONCLUSION
It can be concluded that:
1. Intake of 20% SLO results in increase of LDL-C blood levels of dislipidemia Wistar rat about
22.78%, from 55.97i1.25 to 68.73 il.25 mg/dL; and
2. Further research regarding of whether intake of SLO to human results in a similar effect for anti
dislipidemia.
REFERENCES
Abbas, K. A., Lichtman, A. H., and Pober, J _ S. 2000. Cytokin in Cellular and Moleculer
Immunology 4th ed. Philadelphia, WB Saunders; 233-267.
Abdullah-Rasyid. 2001. Prosiding Seminar IPT EK Kelautan Nasional, Pusat Penelitian
Oseanografi LIPI Jakarta.
Ahmed, E. 2001. Immune Mechanism in Atherosclerosis. Dissertation. ISSBN: 91-628-4612-4.
Konferensrummet, Centrum for Molekular Medicin, Karolinska Sjukhuset.
Ahmed, M. S., and Olfat, M. Y. 2010. Physiological Studies on the Risk Factors Responsible for
Atherosclerosis in Rats. Nature and Science. 8(5); 144-155.
Anonim. 2009. Health: Hypercholesterolemia. College of Medicine. Milton State Hershey Medical
Center Penn State. America.
Anonim. 2007. Minyak Ikan Berkhasiat Turunkan Serangam Jantung. Depot ikan Jakarta: Serpong.
Fadilah, S. 2007. Pengaruh diit minyak ikan lemuru terhadap kaclar lnoid plasma dan agregasi
platelet pada orang sehat. Journal colletion departemen kardiologi dan kedokteran vaskuler
Universitas Indonesia.
Gatot, S. L. 2005. Sindrom Metabolik Merupakan Manisfestasi dari Keadaan Inflamasi. Jurnal
Medicin. 26 (1). Universitas Hasanudin Makasar.
Murray, K. 2004. Harper Biochemestry twenty sixth edition. Mc Graw Hill Companie; New York.
Pramesti, G. 2007. Aplikasi SPSS 15.0 dalam Model Linier Statistika. Jakarta: Penerbit PT Elex
Media Komputindo.
Szmitko, P. E., Wang, C. H., Weisel, R. D., De-Almmeida, J. R., Anderson, T. J., and Verma, S.
2003. New Markers of Inflamamtion and Endothelial Cell Activation. Circulation 108: 19171923.
Tatong, H. 2003. Fungsi Endotel dan pengaruhnya pada berbagai gangguan fungsi kardiovaskuler.
Malang Press. Fakultas Kedokteran Universitas Brawijaya.
Vinay, K., Abbas, A. K., and Nelson, F. 2004. Pathologic basic of disease 7th ed. Elsevier Saunders.
New York
DECREASE OF LDL-C ON RAT WISTAR
Sri Wahjuni
Biochemistry Laboratory Chemistry Departement Faculty of Math and Science Udayana
University
ABSTRACT
Nowadays fish consumption behaviour needs to be improved since the chandes of consumption
paten to instant food. Fish, especially from deep see, is good for health, due to its rich content of
polyunsaturated fatty acid (omega-3) which level is investigated in this research using true
experimental study with randomized pre and posttest control group design. This research employed
50 Wistar rats which were divided into Sgroups, i.e.control group ()%SLO), treatment group l (10%
SLO), treatment group 2 (15% SLO),treatment group 3 (20%SLO), and treatment group 4
(25%SLO). To obtain dislipidemia, the rats were fed with food rich in factor for 8 weeks, followed
by determination of HDL level (pretest). After that, all rats were fed with sardinella longiceps oil
for 6 weeks for dislipidemia and followed by determination of HDL.
Intake of 20% SLO resulted in an increase of blood LDL levels of dislipidemia Wistar rat about
22,78% from 55,97 + 5.l,25 to 68,73 +1,25 MG/dL. Further research regarding of whether the
intake of SLO inhuman results in a similar effect to anti dislipidemia need to be carried out.
Keywords: Fish consumption, antidislipidemia, sardinella longiceps
INTRODUCTION
Nowdays, fish consumption behaviour needs to be improve since the changes of
consumption patern to instan food. Fish, especially from deep sea is good for health, due to the fish
rich of polyunsaturated fatty acid (omega-3). Such fish including Thunnus Scombridae, Euthymrus
sp, Scamberamorus, Decopterus, Rastrellinger, Sardinella Longiceps, Carangidae, Clupeidae, and
Psettodeserumei. Sardinella Longiceps are a highly abundance fish found in Indonesian sea.
Outbreak during peak season occures and as a consequence no economic value. Therefore, to
increase their economic value, the fish can be managed to produce oil (Abdullah, 200; Ihsan, 2009).
Research on fish oil advantages to decrease dislipidemia have already widely carried out.
This was intiated by the evidence that Japanese life longer compare to Mongolianese. This is as a
results of Japanese have much more fish on their diet compare to meat consumption by
Mongolianese. Fish consumption leads to lower of total cholesterol, LDL-cholesterol, and
trigliceride and higher HDL cholesterol compare to meat consumption. This is because of fish
contain much more polyunsaturated fatty acids omega-3 (Komatsu, et al., 2006; Fadilah, 2007).
Many researchs reported that there is a correlation between high lipid serum levels to
incidence of atheroschlerosis, a triger of coronary heart disease. Coronary heart disease occures as a
consequence of one of general mechanism, i.e. blood circulation disturbance and abnormality of
chardiac charge or any other form of aritmias. These will lead to the present of unorganize
myocardiac contraction, blood circulation obstruction, and blood circulation regugirtation. All of
these conditions result in shunting, abnormal circulation, and end up with congestive heart failure
(Vinay, et al. 2004). Ateroschlerosis is a slow progressive disease present in large to small muscular
and elastic arteris. Main sites of atheroschlerosis are abdominal aorta, coronaria arteri, poplitea
arteri, desendens toracali aorta, intern carotic arteri, and willisi circulation. Other risk factors, such
as hypertension, chronic hypercholesterolemia, immune system disturbance, toxin and virus have
also affect destruction of arteri endothelial wall cells. This destruction induces endotel cell
permeability changes and lead to plasma constituent, i.e. lipoprotein easily flow to the inner of
arterial wall. Endotel cell destruction will also change thrombocystein lumen arteri which is lead
to adhesion of thrombocyte to damaged and inflamated blood. Finally, results in contact of lower
connected tissue to other elements in blood circulation. If; this damage goes chronically and ages,
atherosclerosis process continually occurs and leads to thick tunica intima and disturbance of blood
circulation on that site (Szmitko, et al., 2003).
Dyslipidemia is an abnormal lipoprotein metabolism, generally correlated to decrease or
overproduction of lipoprotein. Dyslipidemia is frequently also known as hyperlipidemia associated
with increase of lipid serum as a risk factor of cardiovascular disease. This is because of there is a
cholesterol behavior which is play an important role on atherosclerosis in dyslipidemia. Therefore,
differentiation between hypercholesterolemia with dyslipidemia is hypercholesterolemia is define as
an increase of serum cholesterol more than 200 mg/Dl after 9-12 h starving. On the other hand,
dyslipidemia define as the present of increase LDL-cholesterol serum more than 160 mg/D1,
increase of triglyceride serum more than l50 mg/Dl or HDL-cholesterol below 40mg/Dl for man
and below 50 mg/Dl for women, besides hypercholesterolemia criteria. High cholesterol symptom
in dyslipidemia cannot be felt by dyslipidemia patients, however, this can only be known through
routine check of blood cholesterol. High cholesterol diet and genetic induce dyslipidemia (Anonym,
2009).
Based on background explained above, the author want to investigate the effect of anti
dislipidemia, through an decrease of LDL.
RESEARCH METHOD
Research Design
This is a true experimental study with randomized pre and posttest control group design.
This research employing 100 Wistar rats divided into two research, i.e. dislipidemia and
atheroschlerosis. Each researchs applying 50 Wistar rat classified into 5 groups, i.e. control group
(0% SLO), treatment group l (10% SLO), treatment group 2 (15% SLG), treatment group 3 (20%
SLO), and treatment group 4 (25% SLO).
Initial step is to prepaired all rats in similar condition, therefore, all rat were feeded with ITB
diet for 4 weeks. Then to obtain dislipidemiarat (Research I), rats were fed with food rich of fat
(UNAIR diet) for 8 weeks, followed by determination LDL-C levels (pretest data).
Location And Time Schedule
Rats preparation were carried out at Center Study of Animal Diseases(CSAD)Veterinary
Faculty Udayana University.LDL-C determination was carried out at UPT. Laboratorium Analitik
Universitas Udayana. Research was carried out for 12 months including data analysis and writing
the results.
Data Analysis
All data were analyzed descriptively. Mean difference decrease of decrease of LDL-C were
analyzed using anova one way at 5% significant levels.
RESULTS
Decrease of LDL-C levels of dislipidemia Wistar rat
Mean decrease data of LDL-C of dislipidemia Wistar rats for pre and posttest were listed on
Table 1. The data on Table l were normally distributed and their variance were also homogeneous
insicates by p > 0.05. Mean different profile of LDL-C levels after treatment of various SLO intake
was presented on
Figure l
Decrease of LDL-C levels of dislipidemia Wistar rat
Mean LDL-C levels of Wistar rat pretest and postest data were listed on Table l.
Table l Decrease of LDL-C Levels
Data on Table 1 are normaly distributed and their variance also homogeneous with p> 0 05
Mean profile different of LDL-C difference of various SLO intake was presented in Figure 1
Figure 1
Mean Different Profile of LDL-C Difference for Posttest
Anova test indicates that there is a significant different of SLO various intake with p< 0 05 Resume
of the test was presented on Table 2.
Tab1e2 Resume of Post 1-loc LDL-C Levels
DISCUSSION
Dyslipidemia
A number of 50 Wistar rat for dislipidemia have already investigated. Dislipidemia research
was applied by feeding of high fat diet (UNAIR diet) for 8 weeks, compare to 13 weeks for
atheroschlerotic research. Mean weight of initial Wistar rat is 49.78 dc 0.77) g. After the present of
dislipidemia, the mean weight is about 201.75 ± 0.51 g (pretest data). Mean weight of Wistar rat
alter intake of various SLO for 6 weeks is 203.78 ± 1.03 g (posttest data).
Decrease of LDL-C blood levels of dyslipidemia Wistar rat
In this research, it was obtained that intake of various SLO concentration decrease blood
LDL-C levels of dyslipidemia Wistar rat. Mean LDL-C blood levels of dyslipidemia Wistar rat
were presented on Table 1. Mean HDL-C blood levels of dyslipidemia Wistar rat for pretest with
intake of 0%, 10%, 15%, 20%, and 25% SLO were kolest-LDL pre danposttest (144,05;t0,02) and
(l41,06 :l:l,54) mg/dL, respectively. The mixture of MIL 10% results in the levels of kolest-LDL
pre and posttest (144,09 ± 0,08) and (140,99±1,38) mg/dL. The table also showd the level of kolestLDL for MIL 15%, 20% dan 25% pre and posttest (144,05±0,08) and (134,52i1,89) mg/dL;
(l44,08±0,02) and (126,12±1,61) mg/dL; (144,08±0,03) and (134,52±3,51) mg/dL respectively.
This research shows that lowering of the levels of kolest-LDL took place at all treatments (Figure
5.3). From the same table, it can also be seen that mean HDL-C blood levels of dyslipidemia Wistar
rat for posttest with intake of 0%, 10%, 15%, 20%, and 25% SLO were (56.84 ± 1.25); (58.14 ±
1.38); (59.26 ± 0.84); and (68.72 ± 0.86) mg/dL, respectively. The increase different of HDL-C
blood levels of dislipidemia Wistar rat caused by intake of 0%, 10%, 15%, 20%, and 25% SLO can
be seen on Table 4.10. This table reveals that the highest increase of 11.88 mg/dL HDL-C blood
levels of dislipidemia Wistar rat was observed for intake of 20% SLO, compare to 1.30 mg/dL for
intake of 10% SLO, and 2.72 mg/dL for intake of 15% SLO. These were compared towards HDL-C
blood levels of dislipidemia Wistar rat with intake of 0% SLO. An interesting trend observed in this
research was increase of 2.54 mg/dL HDL-C blood levels of dilipidemia rat due to intake of 25%
SLO, as indicated by Figure 4.5. However, that increase is not as big as for intake of 20% SLO
about 11.88 mg/dL. These trends occure in all treatments of SLO intake, including decrease of
LDL-C and MDA blood leves.
In dyslipidemia case, cell membrane was saturated of cholesterol due to exessive of LDL
acceptance and endogenebiosintesys. To overcome this situation, naturaly cholesterol balancing
occures trough pick cholesterol up and distributed to extracelular Hood and return it to liver. This
event known as reverse cholesterol transport and was carried out by HDL as an antithrombin
(Devlin, 1986; Murray, 2004). Possible mechanism is due to anti oxidant inactivation, that function
to break down unsaturated fatty acids. Long and continue exposure induce leucocyte adhesion to
vascular endotel which leads to endotel cells promote cholesterol effux that have as role to control
vascular (Tatong, 2003). This is conform to hypothesis 5, i.e intake of SLO increase HDL-C blood
levels of dislipidemia Wistar rat.
CONCLUSION
It can be concluded that:
1. Intake of 20% SLO results in increase of LDL-C blood levels of dislipidemia Wistar rat about
22.78%, from 55.97i1.25 to 68.73 il.25 mg/dL; and
2. Further research regarding of whether intake of SLO to human results in a similar effect for anti
dislipidemia.
REFERENCES
Abbas, K. A., Lichtman, A. H., and Pober, J _ S. 2000. Cytokin in Cellular and Moleculer
Immunology 4th ed. Philadelphia, WB Saunders; 233-267.
Abdullah-Rasyid. 2001. Prosiding Seminar IPT EK Kelautan Nasional, Pusat Penelitian
Oseanografi LIPI Jakarta.
Ahmed, E. 2001. Immune Mechanism in Atherosclerosis. Dissertation. ISSBN: 91-628-4612-4.
Konferensrummet, Centrum for Molekular Medicin, Karolinska Sjukhuset.
Ahmed, M. S., and Olfat, M. Y. 2010. Physiological Studies on the Risk Factors Responsible for
Atherosclerosis in Rats. Nature and Science. 8(5); 144-155.
Anonim. 2009. Health: Hypercholesterolemia. College of Medicine. Milton State Hershey Medical
Center Penn State. America.
Anonim. 2007. Minyak Ikan Berkhasiat Turunkan Serangam Jantung. Depot ikan Jakarta: Serpong.
Fadilah, S. 2007. Pengaruh diit minyak ikan lemuru terhadap kaclar lnoid plasma dan agregasi
platelet pada orang sehat. Journal colletion departemen kardiologi dan kedokteran vaskuler
Universitas Indonesia.
Gatot, S. L. 2005. Sindrom Metabolik Merupakan Manisfestasi dari Keadaan Inflamasi. Jurnal
Medicin. 26 (1). Universitas Hasanudin Makasar.
Murray, K. 2004. Harper Biochemestry twenty sixth edition. Mc Graw Hill Companie; New York.
Pramesti, G. 2007. Aplikasi SPSS 15.0 dalam Model Linier Statistika. Jakarta: Penerbit PT Elex
Media Komputindo.
Szmitko, P. E., Wang, C. H., Weisel, R. D., De-Almmeida, J. R., Anderson, T. J., and Verma, S.
2003. New Markers of Inflamamtion and Endothelial Cell Activation. Circulation 108: 19171923.
Tatong, H. 2003. Fungsi Endotel dan pengaruhnya pada berbagai gangguan fungsi kardiovaskuler.
Malang Press. Fakultas Kedokteran Universitas Brawijaya.
Vinay, K., Abbas, A. K., and Nelson, F. 2004. Pathologic basic of disease 7th ed. Elsevier Saunders.
New York