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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?;Attachment Preview;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;Downloaded from jn.nutrition.org at BROOKLYN COLLEGE on October 1, 2014;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.;Downloaded from jn.nutrition.org at BROOKLYN COLLEGE on October 1, 2014;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.;Downloaded from jn.nutrition.org at BROOKLYN COLLEGE on October 1, 2014;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;Downloaded from jn.nutrition.org at BROOKLYN COLLEGE on October 1, 2014;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

 

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