Anthropometrical parameters and markers of

obesity in rats
E L B Novelli1, Y S Diniz1, C M Galhardi2, G M X Ebaid1, H G Rodrigues2,
F Mani1, A A H Fernandes1, A C Cicogna2 and J L V B Novelli Filho3
1

Department of Chemistry and Biochemistry, Institute of Biological Sciences, University of Sao Paulo
State, UNESP, 18618-000 Botucatu; 2Post Graduation Course, Department of Clinical Cardiology,
Faculty of Medicine, UNESP, Botucatu; 3Department of Orthopaedic Surgery, Faculty of Medicine,
UNESP, Botucatu, Sao Paulo, Brazil

Summary
The present study was undertaken to determine anthropometrical parameters in male adult
Wistar rats. We tested the hypothesis that the anthropometrical index may identify obesity
and may predict its adverse effects on lipid profile and oxidative stress in rats. Two
experimental protocols were performed. In the first experiment, 50 male Wistar rats, 21 days
old and fed a control chow were studied up to 150 days of age. In the second experiment,
male Wistar rats, 60 days old, were divided into three groups (n 8): control (C) given free
access to a control chow; (S) receiving the control chow and drinking 30% sucrose ad
libitum and (HC) fed a high-carbohydrate diet ad libitum. The first experiment showed that
food consumption, energy intake and body weight increased with increasing age, while
specific rate of body mass gain was significantly decreased. There were no significant
differences in body length and thoracic circumference of rats from 60 days of age. The
abdominal circumference (AC) and body mass index (BMI) significantly increased with
enhancing age in rats up to 90 days of age and remained constant thereafter. In the second
experiment, after 30 days of dietary treatment, the final body weight, body mass gain, carcass
fat and BMI were higher in S and HC rats than in C. There were no significant alterations in
body length and carcass protein among the groups. Triacylglycerol (TG), total cholesterol
(CT), low-density lipoprotein cholesterol (LDL-C) and lipid hydroperoxide (LH) were higher
in S and HC rats than in C. High-density lipoprotein cholesterol (HDL-C) decreased in HC
rats and total antioxidant substances (TAS) decreased in S and HC rats. There were positive
correlations between BMI with carcass fat, BMI with LH and BMI and serum TG
concentration. In conclusion, the BMI for male adult Wistar rats ranged between 0.45 and
0.68 g/cm2. Obesity may be easily estimated from the BMI in rats. Alterations in BMI were
associated with dyslipidemic profile and oxidative stress in serum of rats and BMI may
predict these adverse consequences of the obesity in rats.
Keywords Obesity; body mass index; lipid profile; oxidative stress

Obesity has been considered an emerging

health problem (Acheson 2004) and in spite
of the number of studies to prevent or treat
obesity, its prevalence continues to rise.
Correspondence: Dr E L B Novelli. Email: drno@uol.com.br
Accepted 14 March 2006

Diet is certainly of importance to obesity

incidence and to its negative consequences,
such as cancer (Bianchini et al. 2002), aging
(Hart et al. 1999), cardiovascular disease
(Novelli et al. 2002, Diniz et al. 2004) and
a number of other pathological conditions

r Laboratory
Animals
Laboratory
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Animals (2007) 41, 111119

112

E L B Novelli et al.

(Rolandsson et al. 2001, Peltonen et al.

2003), but the mechanisms responsible for
these pathological changes are not yet
clearly elucidated.
Rats are frequently used as animal models
for studying adverse effects of obesity (Iossa
et al. 1999). Both humans and rodents tend
to gain weight with high-caloric intake
(Chicco et al. 1999). However, under ad
libitum feeding conditions, obesity occurs in
some but not in all experimental rats
(Commerford et al. 2000).
There is a lack of information on
anthropometrical parameters in laboratory
rodents, and there is no definition of obesity
in laboratory rats. Obesity is usually taken as
any significant increase in body weight or
energy content relative to control animals
(Rothwell & Stock 1981). This definition of
obesity relies on the assumption that all
control animals maintained in the laboratory
are both lean and normal. Therefore, many
experimental bioassays have shown a steady
variability in the incidence, onset time and
severity of degenerative diseases. These
adverse changes have all been associated with
different patterns of voluntary food intake, or
ad libitum overfeeding of food and calories
(Faine et al. 2002), and might influence the
accuracy of the experimental results.
Thus, the purpose of the present study was
to determine anthropometrical parameters
to identify obesity in male adult Wistar rats.
We tested the hypothesis that the anthropometrical index may define the threshold
for obesity and may predict its adverse effects
on lipid profile and oxidative stress in rats.

both experimental protocols were

individually housed in polypropylene cages
in an environmentally controlled clean air
room, with a temperature of 22731C, a 12 h
light/12 h dark cycle and a relative humidity
of 6075%.

Experiment 1
Animals and diet

Fifty male Wistar rats, weighing 6075 g at

21 days of age, were given water ad libitum
and were fed a standard chow (3074 SIF,
Purina Ltd, Campinas, SP, Brazil) with
26.5% protein, 3.8% fat, 40% carbohydrate,
4.5% crude fibre in 100 g of chow, and
12.56 kJ/g metabolizable energy, during 150
days of the experimental period. Food and
water consumption were measured daily at
the same time (09:00 to 10:00 h) and body
weights were determined once a week.
Anthropometrical and nutritional
determinations

The abdominal circumference (AC)

(immediately anterior to the forefoot),
thoracic circumference (immediately behind
the foreleg), body length (nose-to-anus or
noseanus length) were determined in all
rats at 30, 60, 90, 120 and 150 days of
age. The measurements were made in
anaesthetized rats (0.1 mL intraperitoneally
of 1% sodium barbiturate).
The body weight and body length were
used to determine the following anthropometrical parameters:

Body mass index (BMI) body weight

Materials and methods

Animals and housing conditions

The Ethical Committee for Conduction of

Animal Studies at the Institute of Biological
Sciences, Sao Paulo State University
(UNESP) approved the experimental protocol
and all animals were cared for in accordance
with the principles and guidelines of the
Canadian Council on Animal Care as
outlined in the Guide to the Care and Use of
Experimental Animals. Two experimental
protocols were performed. The animals in
Laboratory Animals (2007) 41

(g)/length2 (cm2)
Lee index cube root of body weight (g) /
nose-to-anus length (cm) (Bernardis 1970)
Specific rate of body mass gain (g/kg)
dM/M dt, where dM represents the gain
of body weight during dt t2t1 and M is
the rat body weight at t1

Based on food and caloric intake (Diniz

et al. 2005), the following nutritional
parameters were calculated:

Energy intake (kJ/day) mean food consumption x dietary metabolizable energy

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Index of obesity in rats

113

Feed efficiency (FE; %) (mean body

weight gain  100)/energy intake

Experiment 2
Animals and diet

In order to more appropriately study the

effects of obesity on anthropometrical
measures, nutritional parameters and the
association of anthropometrical parameters
with changes in lipid profile and oxidative
stress, in a separate experiment 24 male
Wistar rats, weighing 210.775.3 g at 60 days
of age were randomly assigned to one of
three groups (n 8/group). Rats in the
control group (C) were given free access
to a standard Purina rodent chow, as in
experiment 1. The (S) group was fed ad
libitum standard Purina chow and received
ad libitum 30% sucrose in its drinking
water. The (HC) group was fed ad libitum, a
high-carbohydrate diet with 19.93% protein,
15.39% fat, 57.50% carbohydrate, 2.81%
dietary fibre in 100 g of chow, and 18.84 kJ/g
metabolizable energy. For inclusion in the
chow of the HC group, we tested 10
palatable foods such as, potato crisps, milk
chocolate, chocolate cookies, corn flakes,
cheese biscuits, puffed wheat, salami,
toasted peanuts, almonds and maize
crackers (Barber et al. 1985). The animals
were placed in a rectangular box and the
various types of foods were appropriately
mixed into the chow. Each animal was
submitted to one day of each food
component and the number of ingested
pellets was measured. The three more
palatable food components were offered to
the animals until the end of the experiment.
The high-carbohydrate diet (HC) was
formulated by mixing 100 g of toasted
peanut, 100 g of milk chocolate and 50 g of
maize cracker to 150 g of the Purina chow
(Novelli et al. 2002, Diniz et al. 2004).
Therefore, all diets provided sufficient
amounts of vitamins, minerals and essential
lipids. The diets contained 2025% total
protein to provide essential amino acids,
according to the recommendation of the
American Institute of Nutrition (Bieri et al.
1977). The dietary ingredients were
homogenized in distilled water at 601C and

the homogenate was used to prepare the

pellets. Diets were given fresh each day as
dry pellets; therefore there was no spillage.
Food consumption was measured daily at
the same time (09:00 to 10:00 h). The body
weights were determined once a week. The
nutritional and anthropometrical parameters
were determined as in experiment 1. After
four weeks of treatment, rats were fasted
overnight (1214 h) and killed by
decapitation.
Biochemical determinations

Blood was placed in a centrifuge tube and

allowed to clot to obtain the serum. Serum
was separated by centrifugation at 1400 g
for 10 min. The triacylglycerol (TG), total
cholesterol (CT) and high-density
lipoprotein cholesterol (HDL-C) were
assayed in serum by enzymatic method (test
kit CELM diagnosis, Modern Laboratory
Equipment Company, Sao Paulo, SP, Brazil).
Low-density lipoprotein cholesterol (LDLC) was selectively precipitated from 60 mL of
serum by adding 1 mL of phosphotungstic
acid and MgCl2 precipitating reagents
(CELM diagnosis), vortex-mixed and
separation by centrifugation carried out at
1400 g for 10 min. The LDL-C pellet was
dissolved in 600 mL of 0.015 mM NaOH,
which did not contain interfering
substances; therefore dialysis was not
needed. The cholesterol concentrations in
the dissolved LDL-C pellet were measured
by enzymatic method (CELM diagnosis)
(Scoccia et al. 2001).
Total protein (Lowry et al. 1951), lipid
hydroperoxide (LH) and total antioxidant
substances (TAS; test kit Randox Ltd,
Crumlin, County Antrim, UK) were also
determined in serum. Spectrophotometric
determinations were performed in a
Pharmacia Biotech spectrophotometer with
temperature-controlled cuvette chamber
(model 974213, UV/visible Ultrospec 5000
with Swift II Applications software to
computer system control, Cambridge, UK).
LH was measured through hydroperoxidemediated oxidation of Fe2 , with 100 mL of
sample and 900 mL of a reaction mixture
containing 250 mM of FeSO4, 25 mM of

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Laboratory Animals (2007) 41

E L B Novelli et al.

Statistics

The results are presented as means7

standard deviations. Significance of
difference was tested using analysis of
variance in conjunction with Tukeys test.
A probability of 0.05 was chosen as the
significant level. Correlations analyses
were determined by the Pearsons linear
correlation test (Curi 1997).

Results

Body weight

21

30

45

60 75 90
Age (days)

105 120 150

Figure 1 Body weight (g) of male Wistar rats during

150 days of age

Specific rate of body mass gain

80
70
60
50
40
30
20
10
0
45

60

75

90
105
Age (days)

120

150

Figure 2 Specific rate of body mass gain of male

Wistar rats during 150 days of age

days of age and remained constant thereafter.

No significant differences were observed in
the AC/TC ratio or in the Lee index (Table 1).
Experiment 2

Experiment 1

Body weights of developing rats, from 21 to

150 days of age, are shown in Figure 1. The
body weight gain by the rats over the study
enhanced with increasing age with no
significant differences in body weight of rats
between 120 and 150 days. Before 60 days of
age, an initial rapid growth period occurred,
and then the gain slowed. The specific rate of
body mass gain was significantly decreased
with increasing age (Figure 2).
The food consumption, energy intake and
AC significantly increased in rats up to 90
days of age and remained constant thereafter.
The FE significantly decreased with
enhancing age. The FE exhibited the highest
values in rats at 30 and 60 days of age. The
body length and TC were lowest in rats at 30
days. BMI was lower in 30-day-old rats and
increased with enhancing age in rats up to 90
Laboratory Animals (2007) 41

500
450
400
350
300
250
200
150
100
50
0

Specific rate of body mass

gain (g/kg)

H2SO4, 100 mM of xylenol orange and 4 mM

of butylated hydroxytoluene in 90% (v/v)
methanol (Jiang et al. 1991). LH was analysed
using a micro plate reader (mQuant-MQX 200
with Kcjunior software to computer system
control, Bio-Tech Instruments, Inc, Winooski,
VT, USA). All reagents were from Sigma
(St Louis, MO, USA).
The body composition was analysed from
the carcass. Carcasses were weighed,
chopped into small pieces and finally
homogenized with distilled water (volumes
equal to twice the carcass weight) (Iossa
et al. 1999) in an ultraturrax homogenizer
(IKA Works, Inc, Wilmington, NC, USA).
Aliquots of the homogenate were analysed
for lipid (Bligh & Dyer 1959) and protein
content (Lowry et al. 1951).

Body weight (g)

114

S rats had significantly higher final body

weight, body weight gain and specific rate of
body mass gain than did HC rats from
the controls. The food consumption was
significantly decreased in S and in HC rats
from the controls. S animals had the highest
energy intake, since the energy was from
food and sucrose aqueous solution intake in
these animals. The FE was higher in S and in
HC rats than in C (Table 2).
The body length, Lee index and carcass
protein were comparable in all three groups.
The AC and TC were higher in S and HC rats
than in C, whereas S rats had significantly
higher AC/TC ratio than the others. BMI
was higher in S than in HC and C groups.
HC rats had higher BMI than C. The carcass
fat was increased in S and HC groups. S rats
had the highest values of carcass fat
(Table 2). The analyses of lipid from the

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Index of obesity in rats

115

Table 1 Food consumption, energy intake, feed efficiency (FE), body length, abdominal circumference (AC),
thoracic circumference (TC), AC/TC ratio, body mass index (BMI) and Lee index in control rats at 30, 60, 90, 120
and 150 days of age
Days of age
Parameters
Food consumption (g/day)
Energy intake (kJ/day)
FE (%)
Body length (cm)
AC (cm)
TC (cm)
AC/TC
BMI (g/cm2)
Lee index

30

60
a

23.072.1
288.8726.3a
7.471.5c
16.570.4a
11.470.1a
10.170.2a
1.170.02a
0.3870.03a
0.2870.03a

90
a

120
b

25.371.2
317.7715.1a
6.570.9c
23.970.3b
14.970.2b
13.270.4b
1.170.03a
0.4570.02b
0.2670.03a

38.676.2
484.8718.3b
2.870.4b
24.070.3b
16.170.4c
15.770.5b
1.070.06a
0.6170.03c
0.3070.02a

150
b

31.273.9
391.8746b
3.270.6b
25.570.5b
17.570.7c
16.270.3b
1.170.04a
0.6870.02c
0.3070.01a

30.972.9b
386.2736.7b
0.0370.001a
25.570.6b
17.270.3c
16.870.2b
1.170.06a
0.6870.05c
0.3070.03a

Values are mean7standard deviation of the mean

Means with different superscripts differ significantly, Po0.05

Table 2 Initial body weight, final body weight, body weight gain, specific rate of body mass gain, food
consumption, energy intake and feed efficiency (FE), body length, abdominal circumference (AC), thoracic
circumference (TC), AC/TC ratio, body mass index (BMI), Lee index, carcass protein and carcass fat in control
rats (C), rats drinking sucrose solution (S) and rats fed a high-carbohydrate diet (HC) during 30 days
Groups
Parameters

Initial body weight (g)

Final body weight (g)
Body weight gain (g/day)
Specific rate of body mass gain (g/kg)
Food consumption (g/day)
Energy intake (kJ/day)
FE (%)
Body length (cm)
AC (cm)
TC (cm)
AC/TC
BMI (g/cm2)
Lee index
Carcass protein (g/100 g)
Carcass fat (g/100 g)

S
a

210.172.7
337.472.9a
3.970.3a
20.171.1a
31.771.2c
398.1715.6a
4.170.2a
23.670.3a
11.470.7a
10.170.2a
1.170.01a
0.6070.01a
0.2970.01a
61.674.8a
19.771.6a

HC
a

211.171.9
445.778.7c
7.870.1c
37.174.2c
20.773.8b 
549.2745.1c
5.970.2b
23.270.1a
20.771.4b
17.970.9b
1.270.05b
0.8270.01c
0.3370.01a
69.675.8a
38.773.8c

210.8711.4a
394.9714.6b
6.170.6b
29.173.1b
24.973.6b
469.1716.6b
5.470.8b
23.570.6a
18.770.6b
17.270.8b
1.170.04a
0.7270.02b
0.3170.02a
65.273.3a
29.672.1b

Values are mean7standard deviation of the mean

Means with different superscripts differ significantly, Po0.05
Energy intake from food and water sucrose intake

carcass were positively correlated with BMI

(r 0.9496; P 0.0005) (Figure 3).
Table 3 shows that S rats had significantly
higher TG, than HC rats and controls. CT
and LDL-C serum concentrations were
higher in HC than in S and in C animals.
S rats had increased CT and LDL-C in
relation to C animals. HDL-C was lower in
HC rats than in S and C. TAS concentrations
were reduced in S and HC rats, while LH was
increased in these groups from the C. The
TAS/LH ratio was significantly lower in S

and HC groups than in C. There were

positive correlations between BMI and TG
levels (r 0.9691; P 0.0001) (Figure 4), and
between serum LH concentrations and BMI
(r 0.8155; P 0.0001) (Figure 5).

Discussion
The adverse effects of obesity have been
extensively studied in experimental animals.
Interestingly, little information is available
on the relationships between obesity and

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Laboratory Animals (2007) 41

116

E L B Novelli et al.

energy intake (Thomas et al. 2002).

Therefore, the increase in food consumption
and energy intake in rats from 90 days of age
were associated with reduced FE. Note that
in Table 1 there were no significant changes

TG

1.4
1.3
1.2
1.1
1
0.9
0.8
0.7
0.6
0.5
0.55

r =0.9691

0.65

0.75

Figure 4 Correlations between body mass index

(BMI, g/cm2) and serum triacylglycerol concentration
(TG, mmol/L) of control rats (~), rats fed a highcarbohydrate diet () and rats drinking sucrose
solution (m), during 30 days

50.00

10.00

40.00

9.00
8.00

30.00

7.00

r =0.9496

20.00

6.00

10.00
0.55

0.85

BMI

LH

Carcass fat

anthropometrical parameters in laboratory

rodents, as well as on anthropometrical
measures, lipid profile and oxidative stress
in rats.
Figure 1 shows that a rapid increase in
body weight was coupled with a significant
increased rate of body mass gain at 60 days of
age, and was followed by a lower rate of body
mass gain (Figure 2). Eating behaviour is an
integral part of nutritional research (Diniz
et al. 2005), and coordinating energy intake
and energy expenditure is involved in the
regulation of body weight (Commerford
et al. 2000).
Food consumption and energy intake
were increased in rats up to 90 days
of age, indicating that from this age
intakeexpenditure adjustments were
delayed. Rat maturation was characterized
by variations in food consumption and

0.65

0.75

r =0.8155

5.00
0.55

0.85

BMI

Figure 3 Correlations between body mass index

(BMI, g/cm2) and serum carcass fat (g/100 g) of
control rats (E), rats fed a high-carbohydrate diet
() and rats drinking sucrose solution (m), during 30
days

0.65

BMI

0.75

0.85

Figure 5 Correlations between body mass index

(BMI, g/cm2) and serum lipid hydroperoxide concentration (LH, nmol/mL) of control rats (~), rats fed a
high-carbohydrate diet () and rats drinking sucrose
solution (m), during 30 days

Table 3 Triacylglycerol (TG), total cholesterol (CT), high-density lipoprotein cholesterol (HDL-C), low-density
lipoprotein cholesterol (LDL-C), lipid hydroperoxide (LH), total antioxidant substances (TAS) and TAS/LH ratio
in control rats (C), rats drinking sucrose solution (S) and rats fed a hypercaloric diet (HC) during 30 days
Groups
Biochemical determinations
TG (nmol/L)
CT (nmol/L)
HDL-C (nmol/L)
LDL-C (nmol/L)
LH (nmol/mL)
TAS (nmol/mL)
TAS/LH

S
a

0.8770.02
1.977 0.07a
0.7770.03b
0.8170.05a
5.670.9a
68.172.1b
12.271.2b

1.3170.03
2.6370.16b
0.8870.08b
1.1570.04b
7.270.6b
60.771.3a
8.470.9a

Values are mean7standard deviation of the mean

Means with different superscripts differ significantly, Po0.05

Laboratory Animals (2007) 41

HC
c

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1.1970.01b
3.3170.15c
0.6770.01a
2.1070.11c
7.570.5b
59.872.5a
7.970.6a

Index of obesity in rats

117

in body length and TC of rats from 60 days of

age, and there were no significant changes in
the Lee index and AC/TC ratio during the
entire experimental period. However, AC
was significantly enhanced in rats at 90 days
of age and it remained constant thereafter.
These observations indicated that from 90
days of age there was fat accumulation in the
abdominal region and that AC for adult male
rats ranged between 14.970.2 and
17.270.3 cm.
It has previously been shown that adult
rats (age 60 days) are characterized by the
cessation of growth and development
(Bernardis 1970, Thomas et al. 2002). Since
the BMI increased in rats up to 90 days of age
and remained constant thereafter, we can
affirm that the BMI for normal adult rats
ranged between the values observed at 60
and 90 days of age (0.4570.02 to 0.687
0.05 g/cm2).
Table 2 shows that S and HC rats had
reduced food consumption, while final body
weight, body weight gain and specific rate of
body mass gain were increased in these
animals. This is in agreement with previous
reports (Novelli et al. 2002). Several factors
may contribute to differential patterns of
food intake. The hypophagia (defined as an
individual food intake score lower than
2 standard deviations above the mean for the
control rats) was partly due to the energy of
HC (average 18.84 kJ/g) compared with C
(12.56 kJ/g), and related to sucrose intake
from drinking water in S rats. The energy
intake is an important factor in the
regulation of body weight (Chicco et al.
1999). Note that in Table 2 the total energy
intake was higher in S and HC than in C
animals, confirming that obesity was the
result of energy intake exceeding energy
expenditure (Acheson 2004).
Despite the higher energy intake in S than
in HC rats, no significant differences were
observed in body length and carcass protein
among the groups indicating that the
increased body weight due to excessive
energy intake was adipose tissue. Table 2
shows that carcass fat was higher in S than
in HC rats from the controls. Considering
that there were no significant differences in
FE of S and HC rats, the excess of energy

intake that was higher in S than in HC was

responsible for increased carcass fat in S rats
from HC. It has been reported that sucrose
can increase the body weight when given
separately from chow in a solution, or as a
supplement (Goodson et al. 2001). In both
these cases, the animal can modulate the
intake of sucrose relative to the intake of
other energy sources.
There were positive correlations between
BMI and carcass fat (Figure 3) demonstrating
that BMI is a simple reliable estimate of
body fat in rats. BMI, body weight and
carcass fat were higher in S than in HC rats.
On the other hand, although S and HC rats
had a higher Lee index than C, no significant
differences were observed in the Lee index
of S and HC rats indicating that BMI had
advantage over the Lee index as an estimate
of body fat and obesity in rats. Since the BMI
for normal rats ranged between 0.45 and
0.68 g/cm2 (experiment 1), both S and HC
rats had obesity, but obesity was significantly higher in S than in HC rats, and this
was reflected in a BMI value that was higher
in S than in HC (Table 2).
The AC and TC were also increased in S
and HC rats. Since no significant differences
were observed in TC and AC between S and
HC groups, and S rats had higher final body
weight than HC, we can affirm that these
anthropometrical parameters were not
accurate as markers of increased body weight
and obesity in rats. In the same way, AC/TC
ratio was only enhanced in S rats and was
not changed with the increased body weight
observed in HC rats (Table 2).
Interestingly, S rats had the highest TG
serum concentrations (Table 3). It has been
reported that the increased amount of
fructose in the diets increases the fructosephosphate aldolase activity resulting in
increased glycerol-phosphate and acetyl
coenzyme-A, so providing more TG
precursors (Hallfrish 1990). During periods
of high-carbohydrate intake, the hepatic
tissue can convert glucose into fatty acids,
from which TGs are made, transported to
the blood stream as very low-density
lipoprotein cholesterol (VLDL-C) and
stored as fat in the adipose tissue (Colette
et al. 2003). Delayed lipolysis of VLDL-C

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Laboratory Animals (2007) 41

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E L B Novelli et al.

because of the competition for the site of

lipoprotein lipase between VLDL-C from
hepatic origin and chylomicrons from
intestinal origin could lead to the formation of TG-rich lipoprotein remnants
(Raveh et al. 2001).
S and HC rats had increased CT and
LDL-C compared with controls, with HC
rats having the highest LDL-C concentrations. This fact was explained by
the decreased HDL-C observed in HC rats,
thus decreasing the reverse cholesterol
transport from the blood stream to the liver
(Raveh et al. 2001).
Oxidative stress was associated with
obesity in S and HC rats. There is a growing
awareness that obesity is a prime risk factor
for the development of dyslipidemic profile
and that oxidative stress may play a role in
various adverse effects of obesity (Diniz
et al. 2005). The use of oxygen to oxidative
metabolism of fuel results in free radical, or
reactive oxygen species (ROS) production
(Feuers 1998). Increased caloric intake
is an important factor in decreasing the
mitochondrial membrane fluidity and
increasing the generation of ROS (Esposito
et al. 1999). Therefore, although ROS are
essential for certain physiological processes,
when that concentration is raised, the
bodys antioxidant defences may be unable
to cope. The result is a condition called
oxidative stress, an imbalance between the
oxidants and antioxidants systems
(Nishiyama et al. 1998).
The LH levels were significantly increased
in S and in HC rats, and TAS concentrations
were decreased in these animals (Table 3).
Although the role of oxidative stress is well
established, lipid peroxidation products,
such as LH, should not represent the only
component that is important in oxidative
stress. The emerging view of free radicals as
modulators in several signal transduction
pathways (Astley 2003) brought new insights
into oxidative stress theories and questions
concerning their influence on lipid profile.
Free radicals react with protein thiol
moieties to produce a variety of sulphur
oxidation states, thus diminishing the
cellular uptake of lipids from the blood
(Chen et al. 2003). Note that S and HC rats
Laboratory Animals (2007) 41

had oxidative stress and although these

groups had different changes in serum lipids,
both S and HC animals had dyslipidemic
profiles (Table 3). There were positive
correlations between BMI and TG levels
(Figure 4) indicating that BMI may predict
this adverse consequence of obesity.
On the other hand, increased serum TG
concentrations have been associated with
decreased LDL-C, which becomes more
susceptible to oxidative modification (Brizzi
et al. 2003). It is widely accepted that
atherogenesis is initiated by oxidation of the
lipids in LDL-C (Chen et al. 2003). Figure 5
shows positive correlations between BMI
and LH concentrations. Therefore, a
threshold BMI is indicative of obesity, and
its severity is indicated by how high the BMI
is past this threshold.
In conclusion, the BMI for male adult
Wistar rats ranged between 0.45 and 0.68 g/
cm2. The results show the effectiveness
of BMI as a threshold of increased body
weight in rats and should be taken into
consideration in future studies dealing with
obesity in rats. Alterations in BMI were
associated with dyslipidemic profile and
oxidative stress in serum of rats; therefore,
BMI may predict these adverse consequences
of the obesity in rats.
Acknowledgements This research was supported by
FAPESP and CNPq.

References
Acheson KJ (2004) Carbohydrate and weight control:
where do we stand? Current Opinion in Clinical
Nutritional Metabolism Care 7, 48592
Astley SB (2003) Dietary antioxidants past, present
and future? Trends in Food Science and Technology
14, 938
Barber T, Vina J, Cabo J (1985) Decreased urea
synthesis in cafeteria-diet-induced obesity in the
rat. Biochemical Journal 230, 67581
Bernardis LL (1970) Prediction of carcass fat, water
and lean body mass from Lees nutritive ratio in
rats with hypothalamic obesity. Experientia 26,
78990
Bianchini F, Kaaks R, Vainiuo H (2002) Overweight, obesity and cancer risk. Lancet Oncology
3, 56574
Bieri JG, Stoenband GS, Briggs GM, Phillips RW,
Woodand JC, Knpha JJ (1977) American Institute of

Downloaded from lan.sagepub.com by guest on December 30, 2015

Index of obesity in rats

119

Nutrition. Report of the American Institute of

Nutrition Ad Hoc Committee on Standards for
Nutritional Studies. Journal of Nutrition 107,
134051
Bligh E, Dyer W (1959) A rapid method of total lipid
extraction and purification. Canadian Journal of
Biochemical Physiology 37, 91119
Brizzi P, Tonolo G, Carusillo F, Malaguarnera M,
Maioli M, Musumeci S (2003) Plasma lipid composition and LDL oxidation. Clinical Chemistry
and Laboratory Medicine 41, 5660
Chen K, Thomas SR, Keaney JF (2003) Beyond
LDL oxidation: ROS in vascular signal transduction. Free Radical Biology and Medicine 35,
11723
Chicco A, Bernal C, Soria A, Giangrossi BS, Lombardo
Y (1999) Dietary effects of partial or total substitution of sucrose for starch on glucose and
lipid metabolism in dyslipidemic rats. Nutrition
Research 19, 28193
Colette C, Percheron C, Herbute N, Michel F, Pham T
(2003) Exchanging carbohydrates for monounsaturated fats in energy restricted diets. International
Journal of Obesity 27, 64856
Commerford SR, Pagliassotti MJ, Melby CL, Wei Y,
Gayles EC, Hill JO (2000) Fat oxidation, lipolysis
and free fatty acid cycling in obesity-prone and
obesity-resistant rats. American Journal of
Physiology Endocrinology and Metabolism 279,
87585
Curi PR (1997) Metodologia e Analise da Pesquisa em
Ciencias Biologicas. 1st edn. Botucatu, SP: Editora
Tipomic, 263pp
Diniz YS, Cicogna A, Padovani C, Santana L, Faine L,
Novelli ELB (2004) Diets rich in saturated and
polyunsaturated fatty acids: metabolic shifting and
cardiac health. Nutrition 20, 2304
Diniz YS, Faine LA, Galhardi CM, et al. (2005)
Monosodium glutamate in standard and high-fiber
diets: metabolic syndrome and oxidative stress in
rats. Nutrition 21, 74955
Esposito LA, Melov S, Panov A (1999) Mitochondrial
disease in mouse results in increased oxidative
stress. Proceedings of the National Academy of
Sciences 96, 48205
Faine L, Diniz YS, Almeida J, Novelli ELB, Ribas BO
(2002) Toxicity of ad lib overfeeding. Food and
Chemical Toxicology 40, 6638
Feuers RJ (1998) The effects of dietary restriction
on mitochondrial dysfunction in aging. Annals
of the New York Academy of Sciences 125,
192201
Goodson G, Halford JCG, Javkson HC, Blundell JE
(2001) Paradoxial effects of a high sucrose diet: high

energy intake and reduced body weight gain.

Appetite 37, 2534
Hallfrish J (1990) Metabolic effects of dietary fructose.
FASEB Journal 4, 265260
Hart RW, Dixit R, Seng J, et al. (1999) Adaptive role of
caloric intake on degenerative disease process.
Toxicological Sciences 52, 312
Iossa S, Lionetti L, Mollica M, Barletta A, Liverini G
(1999) Energy intake and utilization vary during
development in rats. Journal of Nutrition 129,
15968
Jiang Z, Woollard A, Wolff S (1991) Lipid hydroperoxide measurement by oxidation of Fe2+ in the
presence of xylenol orange. Comparison with the
TBA assay and on iodometric method. Lipids 26,
8537
Lowry DH, Rosembrough N, Farr A (1951) Protein
measurement with folinphenol reagent. Journal of
Biological Chemistry 193, 26575
Nishiyama Y, Ikeda H, Haramaki N, Yoshida N,
Imaizumi T (1998) Oxidative stress is related to
exercise intolerance in patients with heart failure.
American Heart Journal 135, 11520
Novelli ELB, Fernandes A, Campos K, Diniz Y,
Almeida J, Ribas BO (2002) The adverse effects
of a high-energy dense diet on cardiac tissue.
Journal of Nutritional and Environmental
Medicine 12, 28790
Peltonen M, Lindroos AK, Torgerson JS (2003) Musculoskeletal pain in the obese: a comparison with a
general population and long-term changes after
conventional and surgical obesity treatment. Pain
104, 54957
Raveh O, Pinchuk I, Fainaru M, Lichtenberg D (2001)
Kinetics of lipid peroxidation in mixture of HDL
and LDL, mutual effects. Free Radical Biology and
Medicine 31, 148697
Rolandsson O, Hagg E, Nilsson M, Hallmans G,
Mincheva-Nilsson L, Lernmark A (2001) Prediction
of diabetes with body mass index, oral glucose
tolerance test and islet cell autoantibodies in a
regional population. Journal of Internal Medicine
249, 27988
Rothwell NJ, Stock MJ (1981) Regulation of
energy balance. Annual Review of Nutrition 1,
23556
Scoccia AE, Molinuevo MS, McCarthy AD, Cortizo
AM (2001) A simple method to assess the oxidative
susceptibility of low density lipoproteins. Clinical
Pathology 1, 112
Thomas MA, Rice HB, Weinstock D, Corwin RL
(2002) Effects of aging on food intake and body
composition in rats. Physiology and Behavior 76,
487500

Downloaded from lan.sagepub.com by guest on December 30, 2015

Laboratory Animals (2007) 41