Sucrose Diet Elevates Cardiovascular Risk Factors in Male Albino Rats
Effects of various concentrations of sucrose diet were assessed on thirty weaning male albino
rats divided randomly into five equal groups as follows: G1 (baseline group); G2 (control group
given rat chow only); G3, G4 and G5 (groups with energy supply from sucrose at 10, 20 and 30%,
respectively). The four groups were fed for twelve weeks and then fasted overnight. They were then
anaesthetized with diethyl ether and venous blood was collected using cardio puncture method.
Plasma was collected by centrifugation and total plasma cholesterol, HDL cholesterol and serum
Triglycerides were assayed using Randox enzymatic kit while VLDL cholesterol, LDL cholesterol,
Atherogenic index and coronary risk indices were calculated. Sucrose diet increased energy density.
It also increased significantly (p<0.05). Plasma total cholesterol, LDL cholesterol, VLDL cholesterol,
Triglycerides, Atherogenic and Coronary risk indices while it decreased HDL cholesterol. Present
results indicated that sucrose diet at present level of consumption (about 25% energy supply)
elevated cardiovascular risk factors in male albino rats and may predispose one to cardiovascular
to cite this article:
B.A. Salau, W.E. Olooto, O.L. Adebayo, E.O. Ajani, K.T. Odufuwa and J.O. Olowookere, 2012. Sucrose Diet Elevates Cardiovascular Risk Factors in Male Albino Rats. International Journal of Biological Chemistry, 6: 61-68.
Received: January 27, 2012;
Accepted: March 17, 2012;
Published: May 29, 2012
Cardiovascular disease remains one of the leading causes of morbidity, mortality
and major public health problem in the developed and developing countries (Ignarro
et al., 2007; Burta et al., 2008;
Badaruddoza et al., 2011; Noroozi
et al., 2011).
An expanding body of evidence indicates that certain dietary patterns can influence
the aetiology, progression and treatment of cardiovascular disease (Osadolor
et al., 2005; Amadou et al., 2009).
This may occur by modifying risk factors such as obesity, dyslipidaemia, as
well as factors involved in systemic inflammation, oxidative stress and thrombosis
(Parikh et al., 2005; Napoli
et al., 2006, 2007; Laleye
et al., 2007).
Sucrose, a form of carbohydrate common in diet is widely consumed by humans
(Ahmed et al., 2001) and its consumption has
been linked to various disorders such as diabetes (Thomas
et al., 1982), metabolic syndrome (Sivabalan
and Menon, 2008), aging (Lee and Cerami, 1992) and
cancers (Dragsted et al., 2002). In spite of
the involvement of sucrose consumption in `the aetiology of many diseases of
which cardiovascular disease is inclusive, the last joint report of WHO/FAO
(WHO/FAO, 2003) apparently exonerated sucrose in the aetiology
of cardiovascular disease. This however is contrary to indictment by some other
investigators (Szanto and Yudkin, 1969; Albrink
and Ullrich, 1986; Johnson et al., 2009).
The WHO/FAO (2003) recommended that sucrose should not
supply more than ten 10% of energy requirement. The clause which sugar company
Death from cardiovascular disease may be sudden and sometime without warning;
however, there are some risk factors such as plasma total cholesterol (Richard
et al., 1989; Mazier-Patrioia and Jones-Peter,
1991), plasma triglycerides (Austin et al.,
2000; Van Lennep et al., 2002), HDL cholesterol
(Asia Pacific Cohort Studies Collaboration, 2004; Barter,
2005), LDL Cholesterol (Staprans et al., 1996),
VLDL cholesterol (Rosenfeld et al., 1987), Atherogenic
index (Abbott et al., 1988) and coronary risk
index (Alladi and Khada, 1989) which may serve as warning
signals. Thus, the assessment of these biochemical parameters may go a long
way in predicting cardiovascular diseases, thereby giving the opportunity to
abate or control the disease at earlier stage. Also, it may help to establish
cause-effect relationship with respect to a particular dietary factor such as
sucrose. In view of the above, we set to investigate the implications of excess
sucrose consumption on these cardiovascular risk factors.
MATERIALS AND METHODS
Experimental animals: Thirty weanling male Wistar rats purchased from the animal house, Physiology Department, Olabisi Onabanjo University, Ago-Iwoye were used for this experiment. The whole experiment was carried out in 2010 for a period of 15 weeks. The rats weight ranged between 57 to 63 g. The rats were acclimatized for 2 weeks in individual metal cages where water and rat chow were given ad libitum.
Feed preparation: The pellets (rat chow) obtained from Ladokun feed Ibadan, Nigeria were grounded with pestle and mortar and the powdery form was mixed with granulated sugar at different ratios. The combined mixture was moistened with distilled water and then palletized with the palletizing machine. It was then oven dried at 60°C for 2 days to maintain 5% initial water content of the pellets. These pellets were then kept in an air tight polythene bags and given to the animal according to their grouping.
Grouping and management of experimental animals: The experimental animals were randomly divided into 5 groups, labeled and managed as indicated below:
||Group 1 (G1, baseline): Rats in this group were sacrificed
at onset of investigation to serve as the baseline data
||Group 2 (G2, normal control): Rats in this group were
placed on commercial diet (rat chow)
||Group 3 (G3, test group 1): Rats in this group were
placed on experimental diet consisting 10% energy supplied from sucrose
||Group 4 (G4, test group 2): Rats in this group were
placed on experimental diet consisting of 20% energy supply from sucrose
||Group 5 (G5, test group 3): Rats in this group were
placed on experimental diet consisting of 30% energy supply from sucrose
The rats were maintained on each respective diet ad libitum for a period
of twelve weeks. After the 12 week period, the rats were fasted overnight, anaesthetized
with diethyl ether and sacrificed. Blood was then withdrawn from the rats by
cardiac puncture into EDTA bottle, properly mixed and processed for further
analysis. The blood was centrifuged at 3,000 rpm for twenty minutes and the
plasma was collected.
Biochemical analysis: Plasma cholesterol, HDL cholesterol and plasma
triglycerides were determined by enzymatic method using Randox kits. LDL cholesterol
was obtained by deduction using Friedewald equation (Friedewald
et al., 1972). Atherogenic index was calculated using the formula
of Abbott et al. (1988). Coronary risk index
was determined by the method of Alladi and Khada (1989).
VLDL cholesterol was estimated by dividing plasma triglyceride by 5.
Statistical analysis: All data were analyzed using one-way ANOVA, Level of significance was assessed using Duncan Multiple Range Test at p<0.05. SPSS 14.0 software was used for data analyses.
Table 1 showed the inclusion of sucrose in the diet of the
rats which linearly increased the energy contents of the feed, thereby increasing
the energy density. Table 2 is the lipid profile of albino
rats placed on diets supplying various percentage of energy from sucrose. Significant
differences (p<0.05) were observed in total plasma cholesterol. An increasing
trend in plasma total cholesterol from (G1 to G5) with increase in percentage
energy from sucrose was observed.
|| Energy content and energy density of the diet
|Sucrose 1 g supplies 3.98 kcal
|| Plasma cholesterol profile of rats fed with different concentrations
of sucrose diet
|Values are expressed as Mean±SEM for 6 rats per group,
Mean values were compared using one way-ANOVA, Level of significance 0 was
assessed using Duncans multiple range test (DMRT) of p<0.05, Values
with different superscript (in the same row) are significantly different
A reduction was observed in the LDL cholesterol concentration of normal control
group (G2) when compared with the baseline value group (G1). When the plasma
LDL concentration of the normal control rat was compared with those of the test
groups, significant increases (p<0.05) were observed in LDL cholesterol with
increasing percentage energy source from sucrose. Results of the VLDL cholesterol
indicated that there was no significant difference (p>0.05) in VLDL cholesterol
between the baseline and the normal control group. The VLDL cholesterol however
continued to increase with increase in sucrose diet.
Though the HDL cholesterol concentration did not vary between the baseline and the control group, increases in sucrose diet significantly decreased the plasma HDL concentration. This decrease was also observed to be concentration dependent. Triglyceride concentration was also observed to increase with increase in percentage energy source from sucrose, however, no significant difference (p>0.05) was observed in the triglyceride concentration of the rats placed on diet that supplied 10% energy source from sucrose and that which supplied 20% energy from sucrose. In addition, no significant difference (p>0.05) was observed in the triglyceride concentration of the rats placed on diet that supplied 20% energy from sucrose and that which supplied 30% energy from sucrose but a significant increases (p<0.05) was observed between rats placed on diet that supplied 10% energy from sucrose and that of 30% energy from sucrose. Table 3 showed average percentage risk. The table indicated that average percentage risk increases with increase in percentage energy source from sucrose. Results of atherogenic and coronary risk indices of albino rats consuming different concentration of sucrose in the diet is shown in Fig. 1. A significant increase (p<0.05) in atherogenic index was observed when G2 was compared with the test groups G3 to G5. A similar trend was observed in coronary risk index.
|| Plasma lipid profile percentage risk of rats fed with different
concentrations of sucrose diet
||Atherogenic and coronary risk indices of rats with fed different
concentrations of sucrose diet
In previous reports, contradictory claims abound as to what level of sucrose
consumption is optimal for good health. While WHO/FAO recommend intake of sucrose
not more than ten percent of energy supply (WHO/FAO, 2003).
The institute of medicine of Food and Nutrition Board reported 25% in energy
intake from sucrose may not cause any adverse effect (Food
and Nutrition Board, 2005). However, the present study showed the adverse
effect of high sucrose diet on lipid profiles that are associated with cardiovascular
Excess intake of sugar has been shown to increase energy density by adding
empty calories (Krebs-Smith et al., 1997) and
this may lead to imbalance diet. The prepared diet mimics sucrose diet consumed
by many individuals, thus such diet increases energy density of the food as
the sucrose concentration increases and decrease in other nutrient density (Salau
et al., 2011) which may lead to energy saving pathway such as lipogenesis
or sparing effect on other energy yielding nutrients such as protein and lipids
and may consequently increase body fat.
Association between sucrose intake and cholesterol level has been established
(Albrink and Ullrich, 1986; Richard
et al., 1989). Increase in sucrose consumption follows closely a
linear relationship with plasma cholesterol. Ten percent energy supply from
sucrose led to 15.18 percentage risk in plasma cholesterol when compared with
the control, while 20 and 30% energy supply from sucrose led to 25.62 and 34.54%
plasma cholesterol risk, respectively. One of the possible mechanisms could
be as a result of increase in fructose consumption (a component of sucrose)
which increases oxidative stress (Faure et al., 1977).
This in effect may depress the antioxidant status and it is in this process
that other molecules such as cholesterol picked up the oxidant, thereby becoming
oxidized (which are naturally not recognized by normal cell receptors molecules
for cholesterol but picked up by macrophages). In effect, there is dire need
for cholesterol in the cell leading to consequent increase in its production.
The other probable mechanism is that cholesterol production is a way of disposing
excess energy by the individual who consumes more than required energy.
LDL cholesterol was observed to increase as sucrose consumption increases in
a more profound manner. Intake at 10, 20, 30% energy supply from sucrose shows
increase in plasma LDL at about 100, 174 and 317%, respectively. This corroborates
the fact that plasma LDL cholesterol is influenced by high sucrose diet (Ryu
and Cha, 2003) and also clarifies that the fraction of cholesterol that
increased significantly is LDL cholesterol.
A similar trend was observed in plasma VLDL cholesterol. Increase VLDL cholesterol
has been implicated in cardiovascular risk (Rosenfeld et
al., 1987) and has also been reported to be influenced by high sucrose
diet (Frayn and Kingman, 1995).
On the other hand, a striking inverse relationship was observed in sucrose
in-take and HDL cholesterol. As sucrose supplies energy at 10, 20, 30%, HDL
cholesterol was observed to reduce by 18, 34 and 56%, respectively. This agrees
with previous studies of various investigators (US. USSR
Steering Committee, 1984; Archer et al., 1998;
Mensink et al., 2003; Appel
et al., 2005).
The result also indicates that as the concentration of sucrose increases, plasma
triglyceride also increases. This agrees with previous study (Frayn
and Kingman, 1995) and the report of Parks and Hellerstein
(2000) that a diet high in sucrose (>20%) of energy is associated with
an elevation of plasma triglycerides concentration. This could be as a result
of increase hepatic secretion of triglyceride and decreased clearance of plasma
triglyceride (Xve et al., 2001). It is important
to point out that it appears that increase in sucrose intake does not increase
triglycerides concentration proportionately. Ten percent of energy supply from
sucrose increases triglyceride by 10.21% while 20% sucrose intakes leads to
12.81% increase and 30% sucrose increased triglycerides by 17.16%.
Analysis shows that when sucrose supply 10% of energy, lipid profile risk was at 30.06% while at 20%, lipid profile risk rose to 52.41%. At 30% of energy supply from sucrose, lipid profile risk increased to 88.77%.
Atherogenic and coronary risk indices are ratios that can be used as quick
assessment of cardiovascular disease and have been shown to be influenced by
diet (Alam et al., 2011; Ibegbulem
and Chikezie, 2012). Increases in these indices are noticed as sucrose consumption
increased. Though, Ryu and Cha (2003) reported no significance
difference in the atherogenic index of sucrose diet and normal diet the difference
observed could be due to duration of feeding which was four weeks compared with
twelve weeks in our study.
The study demonstrated the relationship between intake of sucrose and cardiovascular risk factors (lipid profiles). Increase in sucrose consumption increased cardiovascular risk factors upsetting the balance between energy intakes and other nutrient. Consequently, it increases plasma triglycerides, total cholesterol, LDL cholesterol VLDL cholesterol, atherogenic and coronary risk indices, while decreasing HDL cholesterol. Our result corroborates the fact that energy supply from sucrose should not be more than 10% as stated by WHO/FAO at least for optimal cardiovascular health.
We acknowledge the assistance of messers Thomas Olayinka, Jimi Akinbolawa and Amos Olayinka during the laboratory work of this research. Also, Prof. O.A. Daini, Head of Biochemistry Department, Olabisi Onabanjo University for his moral support.
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