What is the hypothesis of the experiment...

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hey for the reading attached to this i need these answers
1. What is the hypothesis of the experiment?
2. Describe each graph in detail, making sure to discuss how each graph relates to the hypothesis of the paper.
3. a. What is the conclusion of the study?
3. b. What will the researchers do next, based on the current results of this study?
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J. Nutr.-2003-Axen-2244-9.pdf Download Attachment
Nutrient Metabolism
High Dietary Fat Promotes Syndrome X in Nonobese Rats1,2
Kathleen V. Axen,*3 Aphrodite Dikeakos* and Anthony Sclafani
*Department of Health and Nutrition Sciences and Department of Psychology, Brooklyn College of the City
University of New York, Brooklyn, NY 11210
KEY WORDS
dietary fat
obesity
energy restriction
Syndrome X
Although high fat, low carbohydrate diets, without restriction of energy intake, are promoted as weight loss regimens
rats that consume high fat, low carbohydrate diets ad libitum
generally become obese (13,14). Therefore, to evaluate the
effect of such a diet on Syndome X in rats, we restricted intake
of a high fat (60% of energy), low carbohydrate (15% of
energy) diet, in lean and obese rats, to a level that would
prevent excessive weight gain. The level of energy restriction
was designed to support normal weight gain in growing rats
not to produce weight loss, so that the effects of diet composition could be examined apart from those of weight loss. This
design mimics the use of high fat, low carbohydrate diets to
slow weight gain by growing obese or nonobese adolescents.
As a control for the effects of low energy intake, comparisons
were made using lean rats that consumed restricted amounts of
a low fat, high carbohydrate diet. An essential feature of the
study was the constancy of the type of fat and the protein
level, as well as the virtual absence of sucrose in the diets, to
control for their effects on blood levels of insulin and lipids
(15) and glucose tolerance (16).
Diets with very low carbohydrate (20% of energy), and
therefore high fat, contents are advertised to the public, commercially and through mass media, for loss of body weight and
improvement in health. Although high fat, low carbohydrate
diets are claimed to lower risk factors for cardiovascular disease
and type 2 diabetes (1,2), the American Diabetes Association (3)
and the American Heart Association (4) recommend low fat
high complex carbohydrate intakes. Despite their contraindication for individuals at risk for obesity-related diseases, the use of
high fat, low carbohydrate diets is widespread. Furthermore, there
is lack of agreement on the effects of such diets on insulin
resistance and dyslipidemia (5 8). These conditions, along with
hypertension and abdominal obesity, are included in an aggregate
of metabolic risk factors for cardiovascular disease and type 2
diabetes, known as metabolic Syndrome X (9,10).
Adherence to a high fat, low carbohydrate diet, like any
dietary change, may affect physiologic function and health
through a variety of alterations in an individuals nutritional
state. These alterations may include a decrease in energy
intake, a decrease in sucrose intake, an increase in protein
intake, and a change in the amounts and/or ratios of saturated
monounsaturated, and (n-3) and (n-6) PUFA. Furthermore
weight loss itself, independent of diet composition, has an
effect on disease risk (11). Any of these changes, alone or in
combination, can potentially alter biomarkers of diabetes and
cardiovascular disease (12).
MATERIALS AND METHODS
Animals and diets. Phase 1. Male Sprague-Dawley rats (n 24
age 6 7 wk, Charles River Laboratories, Wilmington MA) were
individually housed in mesh-bottomed cages at 20 22C, with a 12-h
light:dark cycle. Rats were separated into two weight-matched groups
one group was fed a low fat (LF4, 45 g fat/kg of diet, Table 1) high
carbohydrate diet (13.8 kJ/g, 3.3 kcal/g) of Purina 5001 pellets (PMI
Feeds, St. Louis, MO), and the other group was fed a high fat (HF
1
Presented in part in abstract form [Axen, K.V., Dikeakos, A., Nicolaides, I.
and Dunbar, C. (1999) High fat, energy-restricted diet increases diabetes risk
factors in rats. Diabetes 48 (suppl 1.): A1351 (abs.)].
2
Supported by PSC-CUNY Research Award 669238.
3
To whom correspondence should be addressed.
E-mail: kaxen@brooklyn.cuny.edu.
4
Abbreviations used: HF, high fat, HFa, high fat consumed ad libitum, HFr
high fat consumed in restricted amounts, ip, intraperitoneal, LF, low fat, LFa, low
fat consumed ad libitum, LFr, low fat consumed in restricted amounts.
0022-3166/03 $3.00 2003 American Society for Nutritional Sciences.
Manuscript received 1 November 2002. Initial review completed 2 January 2003. Revision accepted 12 March 2003.
2244
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ABSTRACT High fat, low carbohydrate diets are popularly advocated for weight loss and improvement in
metabolic Syndrome X, a constellation of risk factors for type 2 diabetes mellitus and cardiovascular disease. The
effects of an energy-restricted (to prevent weight gain in excess of normal growth) high fat (60% of energy), low
carbohydrate (15%) diet were assessed in both lean rats and in rats previously rendered obese through ad libitum
consumption of the same high fat diet. In obese rats, restriction of intake failed to improve impaired glucose
tolerance, hyperinsulinemia, and hypertriglyceridemia, although it lowered visceral fat mass, liver lipid content and
in vitro insulin hypersecretion compared with rats continuing to consume the high fat diet ad libitum. In lean rats
restricted intake of the high fat diet impaired glucose tolerance and increased visceral fat mass and liver lipid
content. These ndings support the conclusion that, in the absence of weight loss, a high fat, low carbohydrate diet
not only may be ineffective in decreasing risk factors for cardiovascular disease and type 2 diabetes but may
promote the development of disease in previously lower risk, nonobese individuals. J. Nutr. 133: 2244 2249, 2003.
HIGH DIETARY FAT AND SYNDROME X
TABLE 1
Composition of the diets
Low fat
diet
High fat
diet
g/kg diet
Ingredient
PMI 5001
Hydrogenated vegetable fat
Casein
L-Methionine
AIN-93 Vitamin mix1
AIN-93 Mineral mix1
Energy, kJ/g
Protein, % of energy
Carbohydrate, % of energy
Fat, % of energy
Fiber,2 g/kg diet
1000
13.8
28
60
12
143
411.3
329.0
231.5
2.8
19.7
5.6
22.6
25
15
60
60
nation of plasma insulin and triglyceride levels, anesthetized rats were
killed by exsanguination. Livers were excised and samples were stored
at 80C for later lipid measurement. Fat pads from three visceral fat
regions (epidydimal, retroperitoneal perirenal, and mesenteric
omental) were dissected from the rats. The mean age was the same for
all groups at the end of the experiment.
In vitro measurements. Pancreatic islets (50/chamber) were preincubated for 30 min at 3 mmol/L glucose in Krebs-Ringer bicarbonate buffer under 95% O2:5% CO2 at 37C. Islets were perifused at a
rate of 1 mL/min with 3 mmol/L glucose for 20 min. Samples of
efuent were collected each minute and stored at 80C for insulin
assay.
Analyses. Plasma insulin was measured using a double antibody
RIA kit specic for rat insulin (Linco, St. Charles MO), a kit with
human standard was used for perifusate samples (DPC, Los Angeles
CA). Plasma free fatty acid concentration was assayed using a NEFA
C kit (Wako, Richmond VA), plasma triglyceride level was measured
using a GPO-Trinder kit (Sigma, St. Louis MO), plasma glucose
levels were measured utilizing a YSI Biochemistry Analyzer (YSI
Yellow Springs OH), and liver lipid was extracted with chloroformmethanol (19). Statistical analyses were performed by ANOVA and
the Newman-Keuls post-hoc test (Crunch 4, Crunch Software, Oakland, CA), differences were considered signicant at P 0.05.
RESULTS
347 g fat/kg diet) low carbohydrate diet (22.6 kJ/g, 5.4 kcal/g). The
HF diet was comprised of powdered Purina 5001 and hydrogenated
vegetable fat (Proctor & Gamble, Cincinnati OH), with casein
L-methionine, AIN vitamin mix, and AIN mineral mix (Bio-serv
Frenchtown, NJ) (17) added to provide equivalent protein concentrations (LF, 234 g/kg diet, HF, 331 g/kg diet) and equivalent vitamin
and mineral contents for the two diets. The hydrogenated vegetable
fat contained 25% long-chain saturated, 44% monounsaturated
and 28% PUFA, with 17% of total fat as trans fatty acids (manufacturers communication). This high fat, low carbohydrate diet was
used because of the more pronounced obesity it has produced in rats
in our laboratory than have several commercial high fat diets. Food
and water were consumed ad libitum by all rats for 4 wk in Phase 1.
Phase 2. Each diet group was then divided into two weightmatched subgroups (each n 6), resulting in a total of four groups.
One HF subgroup (HFa-HFa) continued to consume the HF diet ad
libitum for the rest of the study, whereas the other HF subgroup
(HFa-HFr) received sufcient amounts of HF each day to provide
90% of the energy consumed ad libitum by the original LF rats during
Phase 1. The LF rats were divided so that half of the rats (LFa-HFr)
consumed the same restricted ration of the HF diet as did the
HFa-HFr, whereas the other LF subgroup (LFa-LFr) continued to
consume the LF diet but in powdered form (to better match the
consistency of the other diets) given at the same energy-restricted
level as the HFa-HFr and LFa-HFr groups. Phase 2 of the study
continued until wk 10 12 of the experiment, rats were used as islet
donors for incubation experiments performed over the course of 2 wk
at the end. The protocol was approved by the Brooklyn College
Institutional Animal Care and Use Committee.
In vivo measurements. Food intakes, corrected for spillage, were
measured twice a week, body weights were recorded once a week.
During wk 4 of Phase 1, 6 HF and 6 LF rats were deprived of food for
16 h overnight before blood sampling, in Phase 2, these rats were
evenly distributed among the four groups. Plasma samples, obtained
from the tail, were analyzed for glucose, insulin and free fatty acid
concentrations. These 12 rats, after overnight food deprivation on a
separate day, were given an intraperitoneal (ip) injection of glucose
(1 g/kg body weight, 50 g/100 mL solution), plasma was obtained
preinjection and 15, 30 and 90 min postinjection for glucose determination. During wk 9 of the study (Phase 2), all 24 rats were
subjected to collection of plasma in the food-deprived state as well as
during an ip glucose tolerance test.
At the end of Phase 2 (wk 10 12 of the study), fed rats were
anesthetized by ip injection with a mixture of ketamine (63 mg/kg)
and xylazine (9.4 mg/kg) (Butler, Columbus OH). Pancreases were
removed for isolation of islets by collagenase (Sigma, St. Louis MO)
digestion (18). Blood obtained from the aorta was used for determi-
Food intake and body weight. During Phase 1, rats consumed more energy from the HF than the LF diet (Fig. 1, P
0.001), resulting in higher body weights in HF rats by wk 3
(Fig. 2, P 0.002). During Phase 2, the food intake of rats
continuing to consume HF ad libitum was highest, whereas
intakes of the two groups consuming restricted amounts of HF
(HFa-HFr and LFa-HFr) did not differ from one another but
by design, were lower than HFa-HFa, that of the LF rats
consuming restricted amounts of LF (LFa-LFr) was lowest (P
0.001). Although all groups of energy-restricted rats were
FIGURE 1 Energy intakes of rats consuming high fat (HF) or low
fat (LF) diets ad libitum in Phase 1, followed in Phase 2 by either
continued ad libitum consumption of HF (HFa-HFa) or intakes of HF
(HFa-HFa, LFa-HFr) or LF (LFa-LFr) restricted to 90% of the previous
energy intake of LF-fed rats during wk 2. Values are means SEM, n
6. Data for wk 1 are omitted due to an error in data collection. Means
without a common letter differ, P 0.001. ANOVA: Effect of group, P
0.001, effect of time, P 0.02, interaction between group and time
P 0.05.
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1 AIN (17).
2 Neutral detergent ber from PMI 5001 diet.
2245
2246
AXEN ET AL.
given an amount of food providing the same amount of energy
per day (equal to 90% of ad libitum LF consumption in Phase
1), the LFa-LFr group did not nish its daily ration. During
Phase 2, rats in all groups continued to grow, and in the early
part of Phase 2 (until wk 7 of the study), body weights
generally reected the previous diet (Fig. 2, effect of group
according to Phase 1 diet, P 0.01). However, by wk 9 of the
study, body weights of the four groups paralleled the relationship for food intake (P 0.01).
Dietary ber intakes, based on the neutral detergent ber
content of the diet (Table 1) differed among groups in Phase
2 (P 0.0001). LFa-LFr rats had higher (two- to threefold, P
0.002) ber intakes than all other groups, and HFa-HFa rats
had higher (30 40%, P 0.002) intakes than that of either
of the restricted HF groups, LFa-HFr and HFa-HFr.
Fat pad weight. Visceral fat pad weights, analyzed either
as individual pads or as the sum of the pads, were highest in
HFa-HFa rats, intermediate and equivalent in the two groups
consuming restricted HF intakes (HFa-HFr and LFa-HFr) despite different diets in Phase 1, and lowest in the group
consuming restricted LF intake (P 0.001, Fig. 3). The
percentage of carcass weight due to these visceral pads followed the same pattern among groups (P 0.001), with 9% of
total body weight represented as dissected visceral fat mass in
HFa-HFa, 6% in either HFa-HFr or LFa-HFr and 3% in
LFa-LFr. The relationship among the weights of the individual
pads was consistent among diet groups, with retroperitonealperirenal epididymal mesenteric-omental (P 0.0001).
Indices of glycemic control. Plasma glucose and insulin
levels did not differ at wk 4 (end of Phase 1) between HF and
LF rats in the fed or food-deprived states (Table 2). Plasma
glucose levels in the fed or food-deprived states did not differ
among the four groups at wk 9 (end of Phase 2). In the subset
of rats for which samples were taken for glucose measurement
in both Phases 1 and 2 (3 rats/Phase 2 group), plasma glucose
FIGURE 3 Mass of fat pads of rats consuming high fat (HF) or low
fat (LF) diets ad libitum in Phase 1, followed in Phase 2 by either
continued ad libitum consumption of HF (HFa-HFa) or intakes of HF
(HFa-HF, LFa-HFr) or LF (LFa-LFr) restricted to 90% of the previous
energy intake of LF-fed rats during wk 4. Fat pads were dissected at wk
10 12 of the experiment (mean ages were the same for all groups).
Values are means SEM, n 6. Means without a common letter differ
P 0.001. ANOVA: Effect of group, P 0.0001, effect of fat pad
location, P 0.0001, interaction between group and fat pad location, P
0.0001.
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FIGURE 2 Body weights of rats consuming high fat (HF) or low fat
(LF) diets ad libitum in Phase 1, followed in Phase 2 by either continued
ad libitum consumption of HF (HFa-HFa) or intakes of HF (HFa-HFr
LFa-HFr) or LF (LFa-LFr) restricted to 90% of the previous energy intake
of LF-fed rats during wk 4. Values are means SEM, n 6. Means
without a common letter differ, P 0.001. ANOVA: Effect of group, P
0.01, effect of time, P 0.0001, interaction between group and time
P 0.05.
levels in food-deprived rats did not change with time. However, plasma glucose levels of fed rats decreased (P 0.05)
from Phase 1 to Phase 2 in all groups except the lean group
that consumed the energy-restricted, high fat diet in Phase 2
(LFa-HFr). Although plasma insulin levels in the fed state did
not differ signicantly among the four groups at the end of
Phase 2, rats that had consumed HF during Phase 1 (HFa-HFa
and HFa-HFr) had higher plasma insulin levels in the fooddeprived state than did rats that had consumed LF (LFa-HFr
and LFa-LFr) during Phase 1 (P 0.02). Restriction of intake
of the HF diet in obese rats did not lower their hyperinsulinemia in the fed or food-deprived state.
Plasma glucose response to an ip glucose tolerance test
differed signicantly only at 30 min after glucose injection
between HF and LF rats in Phase 1 (P 0.05), there was a
group time interaction (P 0.0233, Fig. 4, upper panel). In
Phase 2, plasma glucose levels at 15 and 30 min after an ip
injection of glucose were elevated in all groups that were fed
HF during Phase 2 (HFa-HFa, HFa-HFr, and LFa-HFr) compared with the group fed LF (LFa-LFr) (P 0.001, Fig. 4, lower
panel), demonstrating impaired glucose tolerance in all HF-fed
groups. At 30 min after glucose injection, plasma glucose
concentrations were higher in HFa-HFr than in HFa-HFa rats
(P 0.05), indicating poorer glycemic control in the restricted HF rats than in rats consuming HF ad libitum. The
plasma glucose vs. time curve for LFa-LFr rats at the end of
Phase 2 remained similar to that of the LF rats at the end of
Phase 1, indicating that energy restriction did not affect their
glycemic control. Plasma insulin levels measured before (Table
2) and 15 min (data not shown) after glucose injection did not
differ among groups in either Phase 1 or Phase 2 of the study.
Lipid levels. Plasma free fatty acid concentration, measured after 16 h of food deprivation, did not differ among
groups in either Phase 1 or Phase 2. Although plasma triglyceride levels of fed rats did not differ among the four diet groups
HIGH DIETARY FAT AND SYNDROME X
2247
TABLE 2
Plasma concentrations of glucose, insulin, triglyceride and free fatty acids in rats consuming high (HF)
or low fat (LF) diets with or without energy restriction1
Phase 1
Phase 2
HF
Fed rats
Glucose, mmol/L
Insulin, pmol/L
Triglyceride,2 mmol/L
Food-deprived rats3
Glucose, mmol/L
Insulin, pmol/L
Free fatty acids, mol/L
LF
HFa-HFa
HFa-HFr
LFa-HFr
LFa-LFr
9.2 0.6
362 276
8.6 0.4
362 121
7.0 0.3
310 34
1.94 0.44a
6.7 0.4
276 52
1.74 0.81a
7.2 0.3
241 34
0.76 0.32b
7.0 0.4
224 34
0.47 0.02b
6.0 0.4
155 34
853 188
6.6 0.6
121 34
881 113
6.4 0.2
241 86a
640 75
7.1 0.6
190 17a
630 76
6.6 0.4
103 34b
649 104
5.9 0.2
103 34b
791 116
at the end of Phase 2 (Table 2), when rats were grouped by
their Phase 1 diet, plasma triglyceride levels were higher in rats
fed HF (HFa-HFa and HFa-HFr) than in those fed LF (LFaHFr and LFa-LFr) during Phase 1 (P 0.03).
Total liver lipid content was higher in HFa-HFa and LFaHFr rats (1.64 0.19 and 1.57 0.29 g, means SEM)
compared with LFa-LFr (0.76 0.07 g, P 0.05), but liver
lipid content of HFa-HFr (1.13 0.23 g) did not differ from
that of any other group. Liver lipid concentrations did not
differ between HFa-HFa and LFa-HFr rats (0.10 0.01 and
0.11 0.02 mg/mg of liver) but were higher than those in
HFa-HFr and LFa-LFr rats (0.08 0.01 and 0.06 0.01
mg/mg liver) (P 0.01), livers of HFa-HFa rats were also
heavier than those of LFa-LFr rats (17.03 1.03 vs. 13.39
0.64 g, P 0.05).
In vitro insulin release. Basal (3 mmol/L glucose) insulin
release of isolated islets differed among groups (P 0.002).
Islets of HFa-HFa rats had higher secretion (295 64 pmol/L
mean SEM) than those of LFa-HFr (172 33 pmol/L) or
LFa-LFr (102 33 pmol/L) rats (P 0.05), insulin release by
HFa-HFr islets (185 30 pmol/L) did not differ from that of
any other group.
DISCUSSION
Effect of HF diet. Ad libitum consumption of the high fat
low carbohydrate (HF) diet produced obesity during Phase 1
rats that continued to consume the HF diet ad libitum
throughout the study had the greatest visceral fat pad mass
largest livers, highest liver lipid content, and the highest basal
insulin release by their isolated islets. Similar high fat, low
carbohydrate, sucrose-free diets have been shown to produce
obesity (13,14) and insulin resistance (20) and in vitro basal
hypersecretion of insulin (21) in rodents.
Human subjects consuming 20% of their energy intake as
trans fatty acids have been shown to exhibit insulin resistance
(22). Because 10% of the energy of the HF diet used in the
present study was provided by trans fatty acids, they may have
contributed to the diets effect on Syndrome X. It has been
estimated that trans fatty acid intakes in the general population range from 3 to 7% of total fat intake (23) compared with
17% for rats consuming the HF diet. Although the actual trans
fatty acid intake of people consuming high fat, low carbohy-
drate diets is not known, the shortening, oils, peanut butter
and a variety of prepared foods that are permitted by these
regimens would be expected to contribute to trans fatty acid
intake.
The ratio of polyunsaturated to saturated fatty acids (P/S)
in the HF diet was 1, a ratio that is recommended by the
American Heart Association (4) for moderate (30% of energy)
fat intakes. The P/S ratio of the HF diet matches (24) or
exceeds (1) that reported for popular high fat, low carbohydrates diets. Like these diets, the total saturated fat content of
the HF diet exceeded the recommended 10% of total energy
intake. The HF diet was low in (n-3) PUFA, which may
mitigate the atherogenic effects of a high fat diet (25).
Effect of energy-restricted HF diet on obese rats. Compared with ad libitum HF intake, restriction of HF intake
slowed the rate of weight gain by 30%. The mean weight gain
of the rats was reduced from 31 to 24 g/wk. This latter
rate of gain agrees with that predicted by the supplier for male
rats of the same age and strain consuming a standard diet
(Charles River Laboratories), indicating that the dietary restriction prevented weight gain in excess of normal growth.
Restriction of HF intake in rats previously consuming HF
ad libitum decreased visceral fat mass, liver lipid content, and
basal in vitro hypersecretion of insulin compared with that of
rats continuing to consume the HF diet ad libitum. However
restriction of intake of the HF diet in rats failed to lower their
elevated plasma insulin levels in the food-deprived state or
plasma triglyceride levels in the fed state, or to diminish
glucose intolerance, all of which are major features of Syndrome X. Although dietary ber intake was higher in HFa-HFa
rats compared with that of rats with restricted HF intake
(HFa-HFr), it could not offset the effects of greater fat or
energy intake, a high ber diet has been reported to lower
plasma insulin and postprandial glucose levels in obese
rats (26).
Energy-restricted high fat, low carbohydrate diets that cause
body weight loss have been reported to lower plasma glucose in
food-deprived obese mice (27), as well as insulin (14) and
triglyceride (28) levels, although these results are not observed
consistently (14,27,29). At the same level of weight loss
however, a low fat diet has been shown to have a greater effect
than a high fat diet in improving features of Syndrome X in
Downloaded from jn.nutrition.org at BROOKLYN COLLEGE on October 1, 2014
1 Values are means SEM, n 6. Means in a row without a common superscript differ, P 0.05. Phase 1: wk 1 4, Phase 2: wk 510/12 of
experiment. Rats consumed 60% (HF) or 12% (LF) of energy as fat ad libitum in Phase 1. In Phase 2, HFa-HFa continued to consume HF ad libitum
HFa-HFr and LFa-HFr consumed HF restricted to 90% of LF energy intake in Phase 1, LFa-LFr consumed LF diet at 90% energy level.
2 Values are expressed as triolein.
3 Food was removed 16 h before blood samples were taken.
2248
AXEN ET AL.
rats (27). In human subjects, isoenergetic high fat diets have
been reported to promote hyperinsulinemia (7) and insulin
resistance (5), a high fat diet that yielded weight loss was
reported to lower plasma insulin and triglyceride levels (6).
These studies collectively support the importance of weight
loss and not a high fat diet in lowering risk factors associated
with Syndrome X.
In the present study, a mildly restricted level of intake
(90% of previous ad libitum consumption of LF) of the high
fat, low carbohydrate, sucrose-free (2% of energy) diet by
growing rats failed to produce the improvements in Syndrome
X promised in the popular literature (1,2). The percentage of
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FIGURE 4 Plasma glucose responses to an intraperitoneal injection of glucose (1 g/kg) after 16 h of food deprivation at wk 4 (upper
panel) and wk 9 (lower panel) in lean and obese rats fed high (HF) and
low fat (LF) diets with and without food restriction. Values are means
SEM. Upper panel: Response at wk 4 (end of Phase1) of rats consuming LF or HF diets ad libitum, n 6. Due to loss of samples in
centrifuge, one LF rats data were omitted and ANOVA was performed
using only 0-, 15- and 30-min data. ANOVA: effect of group, P 0.4
effect of time, P 0.01, interaction between group and time, P 0.05.
Means without a common letter differ, P 0.05. Lower panel: Response at wk 9 (end of Phase 2) of rats continuing to consume the HF
diet ad libitum (HFa-HFa) or consume HF (HFa-HFr, LFa-HFr) or LF
(LFa-LFr) diets at energy intakes restricted to 90% of that of LF-fed rats
during wk 4. ANOVA: Effect of group, P 0.01, effect of time, P
0.001, interaction between group and time, P 0.001. Means
without a common letter differ, P 0.001.
energy consumed as fat was within the range of 50 66%
reported for people self-selecting such diets (1,8,24). A 4- to
6-wk period of dietary change (Phase 2) represents 4% of the
rats 2.5 y life-span and thus would correspond to a substantial period of dieting in humans.
Effect of the energy-restricted HF diet on lean rats. Consumption of the energy-restricted HF diet during Phase 2 by
either obese (HFa-HFr) or lean (LFa-HFr) rats resulted in the
same visceral fat pad mass, which was greater than that of the
lean rats consuming the energy-restricted LF diet (LFa-LFr).
Although LFa-HFr rats initially gained weight at a slower rate
than did HFa-HFr for the rst half of Phase 2, they had an
increased rate of weight gain later in Phase 2 (Fig. 2). Because
visceral fat pad weights of the two groups were similar at the
end of the experiment, there appears to have been an adaptation to the diet. Lean rats fed high fat (48% of energy)
sucrose-containing diets for 6 wk in an amount restricted to
match that of low fatfed controls have been shown to have
increased visceral adiposity vs. lower fatfed rats (30), supporting the idea that diet composition and not simply energy
intake inuences fat deposition. Plasma glucose and insulin
levels of fed rats in that study did not differ among groups with
differing visceral fat mass. In the present study, LFa-HFr rats
were the only group that did not have a signicant decrease in
plasma glucose level in the fed state between Phases 1 and 2
this decrease could have been an effect of age or handling. The
lack of such an effect in LFa-HFr rats in the fed state suggests
that despite lower carbohydrate intake, their increased fat
intake during Phase 2 may have made this group more insulin
resistant.
Rats consuming the LF diet during Phase 1 (LFa-HFr and
LFa-LFr) did not differ in body weight until wk 8 when the
glucose tolerance test was administered, thus, they received
the same amount of glucose. All rats consuming HF diets in
Phase 2, including LFa-HFr, had elevated plasma glucose levels 15 and 30 min after the glucose load compared with
LFa-LFr and with their own Phase 1 results, whereas the
plasma glucose response of the LFa-LFr group did not differ
from the LF response in Phase 1. These ndings indicate that
even a restricted intake of the high fat, low carbohydrate diet
impairs glucose tolerance in lean rats. Because insulin levels
among groups did not differ at 15 min, all three groups of
HF-fed rats, including lean rats fed the energy-restricted HF
diet, were relatively insulin resistant.
Regardless of diet or body weight in Phase 1, consumption
of the HF diet in Phase 2 was associated with a higher liver
lipid content. The group originally consuming the LF diet in
Phase 1 but fed the restricted HF diet in Phase 2 (LFa-HFr)
had a high liver lipid concentration similar to that of HFa-HFa
rats at the end of the study. In contrast, fed LFa-HFr rats had
lower plasma triglyceride levels than those of HFa-HFa rats.
These observations suggest that there is a period of adaptation
to the HF diet, even at restricted intake, in which uptake of
dietary fat from the blood is still high (providing lower plasma
triglyceride levels in fed rats), whereas export or suppression of
hepatic triglyceride synthesis still may be low, thereby elevating hepatic lipid concentration.
Effect of fat content of energy-restricted diet on lean rats.
Restricted feeding of the LF diet to rats previously consuming
the LF diet ad libitum produced the lowest body weights at the
end of the study and the lowest fat pad masses. This group
(LFa-LFr) consumed less food than the other diet-restricted
groups, although they were provided with the same amount of
energy, apparently because of their lower acceptance of the
powdered version of the LF diet.
Consumption of the LF diet during Phase 2 permitted lean

 

Solution ID:350939 | This paper was updated on 26-Nov-2015

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