Life Sciences 79 (2006) 1578 – 1584

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Effects of soy protein and genistein on blood glucose, antioxidant enzyme

activities, and lipid profile in streptozotocin-induced diabetic rats
Jeong-Sook Lee ⁎
Department of Food and Nutrition, Kosin University, Busan, 606-701, South Korea
Received 18 May 2006; accepted 19 June 2006

Abstract

In the current study, the effect of soy protein and genistein, one of the main isoflavones in soybeans, on blood glucose, lipid profile, and
antioxidant enzyme activities in streptozotocin (STZ)-induced diabetic rats was investigated. Male Sprague–Dawley rats were divided into
nondiabetic control, STZ, STZ-genistein supplemented group (STZ-G; 600 mg/kg diet), and STZ-isolated soy protein supplemented group (STZ-
ISP; 200 g/kg diet). Diabetes was induced by a single injection of STZ (50 mg/kg BW) freshly dissolved in 0.1 mol/L citrate buffer (pH 4.5) into
the intraperitonium. Diabetes was confirmed by measuring the fasting blood glucose concentration 48-h post-injection. The rats with blood
glucose level above 350 mg/dL were considered to be diabetic. Genistein and ISP were supplemented in the diet for 3 weeks.
The supplementation of genistein and ISP increased the plasma insulin level but decreased the HbAIC level of the STZ-induced diabetic rats.
The supplementation of genistein and ISP increased the glucokinase level of the STZ-induced diabetic rats. A significant reduction in glucose-6-
phosphatase was observed in the groups treated with genistein and ISP in comparison with the diabetic control group. Hepatic superoxide
dismutase, catalase, and glutathione peroxidase activities of the STZ-induced diabetic rats were significantly decreased in comparison with the
control rats. Administering genistein and ISP to the STZ-induced diabetic rats significantly increased those enzyme activities. The concentration of
thiobarbituric acid reactive substances in the STZ-induced diabetic rats was significantly elevated, while the genistein and ISP supplement
decreased it to the control concentration. Genistein and ISP supplements seem to be beneficial for correcting the hyperglycemia and preventing
diabetic complications.
© 2006 Elsevier Inc. All rights reserved.

Keywords: Soy protein; Genistein; Streptozotocin-induced diabetic rats; Antioxidant enzymes

Introduction
Diabetes mellitus is a major endocrine disorder and growing
health problem in most countries (Gavard et al., 1993; Anderson
et al., 2001). Recently, it was suggested that formation of free
radicals is involved in the pathogenesis of diabetes and the
development of diabetic complications because prolonged
exposure to hyperglycemia increases the generation of free
radicals and reduces capacities of the antioxidant defense system
(Sanders et al., 2001). In spite of the presentation of many
hypoglycemic agents, diabetes and its related complications are
still a major medical problem.
⁎ Tel.: +82 51 990 2328; fax: +82 51 403 3760.
E-mail address: jslee@Kosin.ac.kr.
0024-3205/$ - see front matter © 2006 Elsevier Inc. All rights reserved.
doi:10.1016/j.lfs.2006.06.030
The interest in the potential health effects of soy and soy
isoflavones is growing as epidemiological studies have associated
with a diet rich in isoflavones with a lower risk of certain diseases
(Anderson et al., 1995; Potter, 1998; Hermansen et al., 2001). Soy
intake has been linked to the improved blood lipid levels in
humans and animals and decreased arterial fatty streaks in ani-
mals, therefore reducing the risk of developing atherosclerosis
(Adams et al., 2002; Lichtenstein, 2001; Iqbal et al., 2002).
Recently, isoflavones as an important bio-active component of
soy also have been investigated (Adams et al., 2002; Clarkson,
2002; Nestel, 2002).
Considerable research efforts have focused on isoflavones as
the main hypolipidemic agent in soy because of their anti-
oxidative and mild estrogenic activity (Anthony, 2000; Polk-
owski and Mazurek, 2000; Wilson et al., 2002). Some studies
have shown that removal of the isoflavone-containing fraction of
 J.-S. Lee / Life Sciences 79 (2006) 1578–1584 1579

soy protein results in the loss of soy's beneficial effect on blood
lipids (Anthony et al., 1998; Crouse et al., 1999). It remains a
possibility that soy has a positive and direct effect on the man-
agement of diabetes by some yet-unrecognized mechanism.
However, the interaction between soy protein and isoflavone and
diabetic complications is little known. In this study, the possible
anti-diabetic effects of soy protein and genistein, one of the main
isoflavones in soybeans, in streptozotocin-induced diabetic rats
have been evaluated.
The food consumption and weight gain were measured
daily and weekly, respectively. At the end of the experimental
period (3 weeks), the rats were anesthetized with ether fol-
lowing a 16-h fast. Blood samples were taken from the ab-
dominal aorta using heparin-coated syringes for plasma and
regular syringes for serum. Plasma and serum were obtained
by centrifuging the blood at 3000 rpm for 15 min at 4 °C. The
livers were removed and rinsed with physiological saline. All
samples were stored at − 70 °C until analyzed.

Material and methods Glucose tolerance test

Animals and diets After 18 days of treatment, a fasting blood sample was taken
from all the groups of rats. Four more blood samples were
At the beginning of the experiment, Male Sprague–Dawley collected at 30-, 60-, 90-, and 120-min intervals after adminis-
rats weighing between 80 and 90 g were purchased from Daehan tration of glucose at a concentration of 2 g/kg of body weight
Laboratory Animal Research Center (Daegu, Korea). The ani- (Joy and Kuttan, 1999). All the blood samples were collected
mals were all individually housed in stainless steel cages in an with potassium oxalate and sodium fluoride solution for the
air-conditioned room with controlled temperature (20–22 °C) estimation of glucose.
and automatic lighting (alternation 12-h periods of light and
dark) and fed an AIN-93 (Reeves et al., 1993) standard Tissue preparations
laboratory diet for 21 days after arrival. The animals were di-
vided into two groups: a nondiabetic control and a diabetic The livers were homogenized in 20 parts (w/v) of a 0.25 mol/L
group. Diabetes was induced by a single injection of STZ sucrose solution using a tissue homogenizer with a Teflon pestle
(50 mg/kg BW; Sigma, USA) freshly dissolved in a 0.1 mol/L at 4 °C. The homogenate was centrifuged at 600 ×g for 10 min to
citrate buffer (pH 4.5) into the intraperitonium. The control rats discard any cell debris, then the supernatant was further centri-
were only injected with the citrate buffer. Diabetes was con- fuged at 10,000 ×g for 20 min to remove the mitochondria pellet.
firmed in the STZ-treated rats by measuring the fasting blood Finally, the supernatant was further ultracentrifuged at 105,000 ×g
glucose concentration 48-h post-injection. The rats with blood for 60 min to obtain the cytosol supernatant. The amounts of
glucose level above 350 mg/dL were considered to be diabetic protein in the mitochondrial and cytosolic fractions were
and were used in the experiment. The diabetic rats were measured using the method of Lowry et al. (1951) with bovine
randomly divided into three sub-groups, diabetic controls (STZ), serum albumin as the standard.
diabetic rats given genistein (STZ-G; 600 mg/kg diet), and
diabetic rats given isolated soy protein (STZ-ISP; 200 g/kg diet). Plasma insulin and glycosylated hemoglobin levels
In this study, 32 rats were used (eight control and 24 diabetic).
The composition of the experimental diet, as shown in Table 1, Plasma insulin was determined by using a rat insulin
was based on the AIN-93 standard laboratory diet. The rats were radioimmunoassay kit (Linco Research Inc., St. Charles, USA)
given free access to food and distilled water, and all animals were in a gamma counter (Peckard, USA) based on the method of
observed daily for any clinical signs of disease. Andersen et al. (1993). The glycosylated hemoglobin (HbAIC)
was determined using a commercial kit (Roche Co., Basel,
Switzland) based on the method of Goldstein et al. (1986).
Table 1
Composition of control and experimental diet (g/100 g diet)
Glucokinase and glucose-6-phosphatase activities
Component Control STZ-G STZ-ISP
Caseina 20.0 20.0 – The glucokinase activity was determined using the method of
Isolated soy proteinb – – 20.0 Davidson and Arion (1987). The activity of glucose-6-phospha-
Cornstarch 55.0 54.94 55.0
tase was measured using the method of Alegre et al. (1988).
Sucrose 10.0 10.0 10.0
Corn oil 5.0 5.0 5.0
Cellulose 5.0 5.0 5.0 Serum and hepatic lipids
Mineral mixturec 3.5 3.5 3.5
Vitamin mixtured 1.0 1.0 1.0 The serum total cholesterol level was determined using a
Choline bitartrate 0.2 0.2 0.2
commercial kit (Sigma, USA) based on a modification of the
DL-methione 0.3 0.3 0.3
Genistein – 0.06 – cholesterol oxidase method of Allain et al. (1974). The HDL-
a fractions were separated using a Sigma kit based on the heparin-
Casein (ICN Biomedicals, Costa Mesa, USA).
b
Soy protein isolates (Protein Technologies International, St. Louis, USA). manganese precipitation procedure (Warnick and Albers, 1978),
c
AIN-93 mineral mixture. and the HDL-cholesterol concentration was determined using the
d
AIN-93 vitamin mixture. same enzymatic method. The serum triglyceride concentration
1580 J.-S. Lee / Life Sciences 79 (2006) 1578–1584

was measured enzymatically using a kit from Sigma Chemical

Co., a modification of the lipase-glycerol phosphate oxidase
method (McGrowan et al., 1983). The hepatic lipids were
extracted using the procedure of Folch et al. (1957). The dried
lipid residues were dissolved in 1 mL ethanol for cholesterol and
triglycerides assays. Triton X-100 and sodium cholate solutions
(in distilled H2O) were added to 200 μL of the dissolved lipid
solution to produce final concentrations of 5 g/L and 3 mmol/L,
respectively. The hepatic cholesterol and the triglyceride were
analyzed with the same enzymatic kit used in the plasma analysis.

Antioxidant enzyme activities and TBARS concentration

The hepatic superoxide dismutase (SOD) activity was de-

termined using Marklund and Marklund's method (Marklund
and Marklund, 1974). The hepatic catalase (CAT) activity was
measured using Abei's method (Abei, 1984). The activity of
hepatic glutathione peroxidase (GSH-Px) was measured using
Paglia and Valentine's method (Paglia and Valentine, 1967). The
hepatic thiobarbituric acid reactive substances (TBARS) were
monitored according to the method of Tarladgis et al. (1964).
Serum aminotransferase activity and plasma urea level
The serum aspartate aminotransferase (AST) and alanine ami-
notransferase (ALT) activities were determined using a commer-
cial kit (Eiken Co., Tokyo, Japan) based on the method of Reitman
and Frankel (1957). Plasma concentration of urea was determined
by the methods of Patton and Crouch (1977).
Statistical analyses
All data are presented as the mean ± SE. The data were eval-
uated by a one-way ANOVA using the SPSS program, and the
differences between the means assessed using Duncan's
Fig. 2. Plasma insulin level in experimental groups (n = 8). The insulin values
(mean ± SD) are expressed as ng/mL. The means sharing a common letter are not
significantly different ( p < 0.05).
multiple range test. Statistical significance was considered at
p < 0.05.
Results
Blood glucose, plasma insulin and glycosylated hemoglobin
levels
Fig. 1 shows the blood glucose levels of control and
experimental groups of rats after oral administration of glucose.
The blood glucose level in the control rats rose to a peak value
30 min after glucose load and decreased to near normal levels at
120 min. In diabetic control rats, the peak increase in blood
glucose concentration was observed after 30 min and remained
high over the 90 min. Genistein and ISP treated diabetic rats
showed significant decreases in blood glucose level at 30 and
120 min compared with diabetic rats.

Fig. 1. Oral glucose tolerance test in experimental groups (n = 8). The blood Fig. 3. Glacosylated hemoglobin level in experimental groups (n = 8). The gly-
glucose levels (mean ± SD) are expressed as mg/dL. The means sharing a cosylated hemoglobin values (mean ± SD) are expressed as mg/g of hemoglobin.
common letter are not significantly different ( p < 0.05). The means sharing a common letter are not significantly different ( p < 0.05).
 J.-S. Lee / Life Sciences 79 (2006) 1578–1584 1581

Table 2 Table 4
Effect of genistein and isolated soy protein on hepatic glucokinase and glucose- Effect of genistein and isolated soy protein on hepatic SOD, CAT, GSH-Px
6-phosphatase activities in diabetic rats activities and TBARS concentration in diabetic rats
Control STZ STZ-G STZ-ISP Control STZ STZ-G STZ-ISP
1 a d c b 1 a c b
Glucokinase 0.261 ± 0.023 0.079 ± 0.009 0.103 ± 0.012 0.133 ± 0.012 SOD 12.79 ± 0.75 6.50 ± 0.54 10.52 ± 1.06 11.00 ± 1.12b
Glucose-6- 0.165 ± 0.011d 0.457 ± 0.014a 0.396 ± 0.022b 0.302 ± 0.013c CAT2 18.60 ± 1.13a 11.06 ± 0.91d 12.41 ± 1.13c 14.30 ± 1.19b
2
phosphatase GSH-Px3 3.01 ± 0.46a 1.23 ± 0.46c 2.16 ± 0.46b 2.27 ± 0.77b
TBARS4 15.12 ± 0.14b 29.53 ± 2.12a 19.24 ± 1.06b 17.91 ± 1.23b
Values are mean ± SD of 8 rats from each group.
a,b,c
Means in the same row not sharing a common superscript are significantly Values are mean ± SD of 8 rats from each group.
a,b,c
different ( p < 0.05) between groups. Means in the same row not sharing a common superscript are significantly
1
Glucokinase: units/h/mg of protein. different ( p < 0.05) between groups.
2 1
Glucose-6-phosphatase: units/min/mg of protein. Superoxide dismutase: units/mg protein.
2
Catalase: deceased H2O2 nmol/min/mg protein.
3
Plasma insulin levels were lower in the STZ-induced diabetic Glutathione peroxidase: oxidized NADPH nmol/min/mg protein.
4
Thiobarbituric acid reactive substances: nmol/g.
rats compared with the control rats (Fig. 2). The supplementation
of genistein and ISP increased the plasma insulin level of the STZ-
induced diabetic rats. The effect was more pronounced in the ISP diabetic rats than in the control rats (Table 3). The supplemen-
supplemented rats than in the genistein-supplemented rats. tation of genistein and ISP suppressed the increase in the total
HbAIC levels were higher in the STZ-induced diabetic rats cholesterol and triglyceride levels in the serum and liver of the
compared to the control rats (Fig. 3). The supplementation of diabetic rats. The genistein and ISP supplementation decreased in
genistein and ISP decreased the HbAIC level of the STZ- the serum and hepatic triglyceride levels significantly to almost
induced diabetic rats. The effects were more potent in the STZ- the control concentration. The HDL-cholesterol concentration
ISP group than in the STZ-G group. was also significantly lowered by the induction of diabetes;
however it was higher in the genistein and ISP supplemented
Glucokinase and glucose-6-phosphatase activities groups compared to the other diabetic group.

Table 2 shows the effect of genistein and ISP on glucokinase
and glucose-6-phosphatase activities of normal and STZ diabetic
rats. The glucokinase activity was lower in the STZ-induced
diabetic rats compared with the control rats. The supplementation
of genistein and ISP increased the glucokinase level of the STZ-
induced diabetic rats. The glucose-6-phosphatase level was in-
creased in diabetic rats. A significant reduction in glucose-6-
phosphatase was observed in the groups treated with genistein and
ISP compared with the diabetic control group. The effects were
more potent in the STZ-ISP group than in the STZ-G group.
Serum and hepatic lipids
The total cholesterol and triglyceride concentrations in the
serum and liver were significantly higher in the STZ-induced
Antioxidant enzyme activities and TBARS concentration
The activities of SOD, CAT, GSH-Px and hepatic TBARS
concentration are given in Table 4. SOD and GSH-Px activities
in the liver of the STZ-induced diabetic rats were significantly
decreased compared to the control rats. Administering genistein
and ISP to the STZ-induced diabetic rats significantly increased
those enzyme activities. CAT activity of the rats treated with STZ
was significantly decreased, while genistein and ISP supplement
to the STZ-induced diabetic rats appeared to increase its activity.
The effect was more pronounced in the ISP supplemented group
than in the genistein-supplemented group.
The concentration of TBARS in the STZ-induced diabetic
rats was significantly elevated, the genistein and ISP supplement
decreased it significantly to almost the control concentration.

Serum aminotransferase activity and plasma urea level

Table 3
Effect of genistein and isolated soy protein on serum and hepatic lipids in
diabetic rats The activities of serum AST and ALT and plasma urea level
of control and experimental animals are given in Table 5.
Control STZ STZ-G STZ-ISP
Supplement with the genistein and ISP along with STZ showed
Serum
Total cholesterol 2.40 ± 0.16b 3.62 ± 0.20a 2.61 ± 0.09b 2.55 ± 0.08b
(mmol/L) Table 5
HDL-cholesterol 1.22 ± 0.05a 0.42 ± 0.05c 0.65 ± 0.06b 0.63 ± 0.06b Effect of genistein and isolated soy protein on serum ALT and AST activities and
(mmol/L) plasma urea level in diabetic rats
Triglyceride (mmol/L) 1.11 ± 0.09b 2.03 ± 0.16a 1.16 ± 0.09b 1.15 ± 0.13b
Control STZ STZ-G STZ-ISP
c a b
Liver ALT (unit/mL) 35.55 ± 1.62 63.88 ± 1.90 42.09 ± 1.06 43.19 ± 1.06b
Cholesterol (mmol/g) 0.13 ± 0.02b 0.23 ± 0.04a 0.16 ± 0.03b 0.15 ± 0.03b AST (unit/mL) 70.60 ± 2.13c 101.66 ± 3.06a 82.19 ± 1.56b 80.34 ± 1.69b
Triglyceride (mmol/g) 0.24 ± 0.02b 0.45 ± 0.05a 0.28 ± 0.03b 0.26 ± 0.03b Urea (mg/dL) 32.62 ± 1.52c 61.60 ± 2.52a 43.14 ± 1.36b 41.06 ± 2.02b
Values are mean ± SD of 8 rats from each group. Values are mean ± SD of 8 rats from each group.
a,b,c a,b,c
Means in the same row not sharing a common superscript are significantly Means in the same row not sharing a common superscript are significantly
different ( p < 0.05) between groups. different ( p < 0.05) between groups.
1582 J.-S. Lee / Life Sciences 79 (2006) 1578–1584
significantly reduced levels of AST and ALT as compared with
those of the unsupplemented STZ-treated rats. The STZ-induced
diabetic group resulted in a significant increase in plasma urea
concentration compared to the control group; Supplementation
of genistein and ISP decreased the level of urea as compared
with that of the STZ-treated group.
Discussion
Diabetes arises from destruction of the β-islet cells of the
pancreas, due to degranulation or reduction of insulin secretion
(Ramkumar et al., 2004). The elevation in plasma insulin in the
genistein and ISP-treated STZ-diabetic rats could be due to the
insulinotropic substances present in the fractions, which induce
the intact functional β-cells of the Langerhans islet to produce
insulin, or the protection of the functional β-cells from further
deterioration so that they remain active and produce insulin.
Diabetic rats induced by STZ show an increased sensitivity to
oxygen free radicals and hydrogen peroxide, the breakdown
products of the liver, which impose oxidative stress in diabetes
and would damage inner endothelial tissue; this would even-
tually be directly responsible for high blood glucose (Reddi and
Bollineni, 2001). The experimentally induced diabetes signif-
icantly (p < 0.05) increased the fasting blood glucose level by
148% of the control level. However, the treatment of STZ-
induced diabetic rats with the genistein and ISP reduced their
blood glucose levels by 19.6% and 24.9%, respectively, in
comparison to the diabetic group. The genistein and ISP sup-
plementations improved glucose tolerance in diabetic rats. It
seems that the hypoglycemic effects of genistein and ISP are
due to the increased level of serum insulin and the enhancement
of peripheral metabolism of glucose (Skim et al., 1999).
Supplement with ISP was found to increase the plasma insulin
level more effectively than genistein. It seems that ISP contains
one or more constituents that could increase the bioavailability
of genistein. Further study will be necessary to elucidate the
mechanism of blood glucose regulation by genistein and ISP.
HbAIC was found to increase in diabetic rats up to 176%.
And this increase is directly proportional to the fasting blood
glucose levels (Saravanan and Pugalendi, 2005). Since the
diabetic animals had prior higher blood glucose levels, elevated
levels of HbAIC were observed. Genistein and ISP fed diabetic
rats showed the decrease in HbAIC level, which seems to be the
reduction of blood glucose level.
Insulin increases hepatic glycolysis by increasing the activity
and amount of several key enzymes including glucokinase, phos-
phofructokinase and pyruvate kinase. In the liver, glucokinase is
an important regulator of glucose storage and disposal (Saravanan
and Pugalendi, 2005). In this study, glucokinase activity was
decreased in the liver of diabetic fats which may be due to a
deficiency of insulin. Genistein and ISP fed diabetic rat showed an
elevated activity of glucokinase, which may be associated with
reduced blood glucose. Therefore, the ISP appears to be more
potent than the genistein.
Insulin decreases gluconeogenesis by decreasing the activities
of key enzymes such as glucose-6-phosphatase, fructose 1,6-
bisphosphatase, phosphoenolpyruvate carboxykinase and pyru-
vate carboxykinase (Murray et al., 2000). Glucose-6-phosphatase
plays an important role in glucose homeostasis in liver and kidney
(Berg et al., 2002). In this study, the increased activity of glucose-
6-phosphatase in liver of diabetic rats seems to be insulin de-
ficiency. In genistein and ISP fed diabetic rats, the activity of that
enzyme was significantly reduced, which may be responsible for
the improved glycemic control. The ISP seems to be more potent
than the genistein, and contains other active constituents that
could potentiate the effect.
Hyperglycemia also generates reactive oxygen species which
in turn cause lipid peroxidation and membrane damage in this
study (Hunt et al., 1988). In the current study, the concentration
of hepatic TBARS was significantly increased after treatment of
STZ in the rats. The increased concentration of TBARS suggests
that an increase in oxygen free radicals could be due to either
their increased production or decreased destruction (Kakkar
et al., 1995). The level of hepatic TBARS in genistein and ISP
supplemented rats showed a significant reduction, which indi-
cates a decreased rate of lipid peroxidation. Several studies have
shown increased lipid peroxidation in clinical and experimental
diabetes (Sundaram et al., 1996; Kakkar et al., 1998). The
present results show increased lipid peroxidation in tissues of the
diabetic group. The increase of oxygen free radicals in diabetes
could be due to an increase of blood glucose level, since an
autoxidation generates free radicals (Ivorra et al., 1989). STZ has
been shown to produce oxygen free radicals. Lipid peroxide-
mediated tissue damages have been observed in the development
of type I and type II mellitus. Previous studies have reported that
lipid peroxidation in liver, kidney, and brain of diabetic rats was
increased (Latha and Pari, 2003; Venkateswaran and Pari, 2002).
Concerning to the changes in lipid peroxidation, the diabetic
tissue showed decreased activity of the key antioxidants SOD,
CAT, glutathione, GPx, and glutathione S-transferase, which play
an important role in scavenging the toxic intermediate of in-
complete oxidation. The decrease in the activity of these anti-
oxidants can lead to an excess availability of the superoxide anion
(O2−) and hydrogen peroxide in biological systems, which in turn
generate hydroxyl radicals resulting in initiation and propagation
of lipid peroxidation. Administration of genistein and ISP
increased the activity of enzymes and may help to control free
radicals (Kumuhekar and Katyane, 1992).
The induction of SOD activity by genistein and ISP may be
attributed to inhibition of the generation of active oxygen spe-
cies from autoxidation of glucose generation from the action of
STZ. The increased activity of SOD accelerates dismutation of
superoxide radicals to H2O2, which is removed by CAT. This
indicates that the genistein and ISP supplements have altered the
SOD, CAT, and GSH-Px activities and reduced oxidative stress
in the diabetic rats, resulting in a lower TBARS concentration.
The diabetic hyperglycemia induces the elevation of plasma
levels of urea and creatinine which are considered as sig-
nificant markers of renal dysfunction (Almdal and Vilstrup,
1988). In this study plasma urea in the diabetic groups in-
creased by 88.8% of the control level. While after the supple-
ment of genistein and ISP to the diabetic rats, the level of urea
was significantly ( p < 0.05) decreased in plasma by 30.0% and
32.5%, respectively, compared with the diabetic group. This
 J.-S. Lee / Life Sciences 79 (2006) 1578–1584
result indicates that genistein and ISP are capable of amelio-
rating the impaired diabetic kidney function in addition to its
hypoglycemic control.
Increased activities of AST and ALT are used as indices of
liver damage. When the liver is damaged, these enzymes leak out
of liver cells in large quantities, so their concentrations in the
blood are increased (Tawta et al., 2000). Possible explanation for
the differential effects of genistein and ISP on the activities of
AST and ALT in plasma is that genistein and ISP may inhibit the
liver damage induced by STZ.
Genistein and ISP would appear to contribute to alleviating
the adverse effect of diabetes mellitus by enhancing the lipid
metabolism as well as the hepatic antioxidant defense system.
Genistein and ISP supplements may be beneficial for correcting
the hyperglycemia and preventing diabetic complications. The
ISP appears to be more potent than the genistein. Hence further
biochemical and pharmacological studies are being carried out
to elucidate their mechanism of action.
Acknowledgements
The author is grateful for the financial support provided by
the foundation of Kosin University.
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