Health benefits of dietary fat reduction by a novel fat replacer: Mimix

The primary goals of this study were to identify any health benefits of the replacement of dietary fat with a novel fat replacer, Mimix, and to assure that the consumption of this fat replacer did not convey any deleterious health effects. Male, weanling, Fischer 344 rats were fed one of six diets containing between 5 and 20% w/w as fat for 8 weeks. These diets included two high fat diets (safflower oil or lard), a low fat diet and three diets where 15% of the fat in the high fat diets was replaced with various amounts of Mimix. When animals were fed a diet rich in saturated fat they consumed significantly more energy than other diet groups. When 15% saturated fat (lard) was replaced with safflower oil animals adjusted their food intake so that no difference in energy intake was observed between the high safflower diet and the low fat and Mimix diets. When the various Mimix fat replacements were compared to animals fed a high fat lard diet there was incomplete compensation of energy intake. Animals fed the high fat lard diet also had higher glucose and total serum cholesterol than their low fat and fat replacement counterparts. Feeding a high fat safflower oil diet to rats resulted in a significantly lower total serum cholesterol and serum triglyceride than all other diets. Replacement of dietary fat with Mimix demonstrated no deleterious effects on the heart, liver and intestinal tract that were all of normal weight, morphology and colour compared to other diet groups. Body composition analysis demonstrated that animals fed high fat diets had higher body fat mass at the expense of lean body mass. This was most obvious for animals fed high fat lard diets who had heavier epididymal fat pads. These data demonstrate that the replacement of dietary fat with the novel fat replacer Mimix can convey a number of health benefits in the absence of any deleterious effects.     

Fat Quality Influences the Obesogenic Effect of High Fat Diets

High fat and/or carbohydrate intake are associated with an elevated risk for obesity and chronic diseases such as diabetes and cardiovascular diseases. The harmful effects of a high fat diet could be different, depending on dietary fat quality. In fact, high fat diets rich in unsaturated fatty acids are considered less deleterious for human health than those rich in saturated fat. In our previous studies, we have shown that rats fed a high fat diet developed obesity and exhibited a decrease in oxidative capacity and an increase in oxidative stress in liver mitochondria. To investigate whether polyunsaturated fats could attenuate the above deleterious effects of high fat diets, energy balance and body composition were assessed after two weeks in rats fed isocaloric amounts of a high-fat diet (58.2% by energy) rich either in lard or safflower/linseed oil. Hepatic functionality, plasma parameters, and oxidative status were also measured. The results show that feeding on safflower/linseed oil diet attenuates the obesogenic effect of high fat diets and ameliorates the blood lipid profile. Conversely, hepatic steatosis and mitochondrial oxidative stress appear to be negatively affected by a diet rich in unsaturated fatty acids.     

Adaptive response of rat pancreatic lipase to dietary fat: effects of amount and type of fat

Pancreatic lipase adapts to changes in dietary fat by parallel changes in synthesis. The adaptation to changes in type of dietary fat (saturation or chain length) is unclear. The effects of changes in amount and type of dietary fat were examined in weanling rats fed for 1 wk diets low in fat (LF) with 10% kcal as corn oil, moderate in fat (MF) with 40% kcal as fat (corn oil, lard, safflower oil, butter, olive oil or coconut oil), or high in fat (HF) with 67% kcal as fat (as for MF). Growth was comparable among rats fed these diets. Pancreatic lipase activity increased in all HF diets (180%) compared to the LF diet. In MF diets, only the highly unsaturated safflower oil increased pancreatic lipase (162%) compared to the LF diet. Food consumption varied, but was not related to the response of pancreatic lipase. When weanling rats were fed diets with 11, 40, 47, 54, 67 and 75% kcal as corn oil, pancreatic lipase activity was not stimulated at or below 47% kcal fat, but was maximally stimulated (twofold) by 54 or 67% fat. These findings suggest that pancreatic lipase activity adapts primarily to the amount of dietary fat and responds to the type of fat only below the threshold level of dietary fat (47% kcal).     

The influence of dietary isomeric and saturated fatty acids on atherosclerosis and eicosanoid synthesis in swine

Weanling swine were fed for 6 months high fat diets containing as fat source, a high oleic acid safflower oil, lard, or a partially hydrogenated soybean oil blended with soybean oil. The extent of atherosclerosis in left coronary arteries and the ability of vascular components to synthesize eicosanoids important for blood clotting were determined. There was no significant difference (p greater than 0.05) in the extent of atherosclerosis or the synthesis of thromboxane A2. Significant effects were observed on serum cholesterol, which was elevated in the lard fed group, serum triacylglycerol, which was highest in the safflower oil group, and prostacyclin synthesis, which was depressed in both the lard and hydrogenated soybean oil diets compared to the safflower oil diet. No unique effect on the development of heart disease appears to be attributable to hydrogenated fats. The hydrogenated fat was similar to lard in decreasing prostacyclin synthesis, suggesting that the saturation of dietary fatty acids may be a contributory factor in the development of heart disease, through its effect on thrombotic processes.     

Physiological response of mature rats to replacement of dietary fat with a fat substitute

The effects of replacing dietary fat with a fat substitute on food intake, body composition and lipid metabolism were examined in rats. Female Sprague-Dawley rats (250 g) were fed diets containing between 2 and 63% of energy as fat for 64 d. Inclusion of a substitute resulted in diets of different fat content but similar texture. When 10% corn oil (21% kJ-fat diet) was replaced with the substitute supplemented with linoleic acid (2% kJ-fat diet), rats increased food intake so that there was no effect on energy intake, body weight, body composition or serum lipid profile. Rats fed a diet containing 10% corn oil and 30% Crisco vegetable shortening (63% kJ-fat diet) became obese and hyperinsulinemic. When half (51% kJ-fat diet) or all (30% kJ-fat diet) of the Crisco was replaced with the fat substitute, the rats increased food intake and were fatter than controls but less obese than rats fed the 63% kJ-fat diet. Hepatic lipid oxidation and ketone synthesis were proportional to the percentage of dietary energy as fat. Adipocyte de novo lipid synthesis was inhibited by 51% kJ-fat and 63% kJ-fat diets. Partial or total replacement of Crisco prevented the hyperinsulinemia observed in 63% kJ-fat rats, suggesting a protective effect against the development of insulin resistance with diet-induced obesity.     

合成油的营养评价——(二)合成油饲料对实验性高胆固醇血症大鼠体重、血脂和肝脂成分的影响

在88g基础饲料中加入12g不同种类的油脂(合成油、猪油和豆油)和1％胆固醇喂养大鼠5周以诱导动物产生高脂血症,并以不加入胆固醇的豆油饲料作为正常对照。比较各组动物在实验期内的生长、血清脂质、肝脏脂质和某些内脏器官重量的改变。结果如下: (1)大鼠摄食含不同油脂的致高胆固醇血症饲料5周后,各组雄鼠的体重增加无明显的不同,雌鼠的体重增加则有显著的差别,即合成油组动物的增重显著较猪油组和对照组的为低。 (2)在各种油脂饲料中加入胆固醇都可使动物的肝重增大。猪油组和豆油组动物的肝脏有明显的脂肪肝病变。肝脂含量增加,肝胆固醇和甘油三酯大量积存(分别约为对照组的9-10倍和2-3倍)。而合成油组动物的肝脏外观表现正常,肝脂含量、肝胆固醇和甘油三酯水平则接近对照组的正常水平。 (3)在各种油脂饲料中加入胆固醇喂养大鼠,对雄鼠血清胆固醇水平的影响不明显,但引起雌鼠血清胆固醇的改变和对照组比较,猪油饲料使动物的血清胆固醇含量明显增高,豆 油和合成油饲料则可维持动物的血胆固醇含量于正常水平。血清甘油三酯水平则以合成油饲料组动物的为最高。 (4)在各种饲料中加入胆固醇除增大肝脏重量外,也使雌鼠的主动脉重量增高,但饲料油脂种类对其重量的影响不明显。 上述结果表明,当饲料中含有高水?     

Effect of types and amount of dietary fat during the initiation phase of hepatocarcinogenesis.

The effects of various levels of corn oil and lard fed during the initiation stage of azoxymethane (AOM)-induced hepatocarcinogenesis were studied in male Fischer 344 rats. The animals were fed diets containing 5%, 13.6%, and 23.5% corn oil or lard two weeks before, during, and until one week after injections of AOM (15 mg/kg body wt s.c.) once weekly for two weeks. One week after AOM treatment, groups of animals fed the 13.6% and 23.5% corn oil or lard diet were transferred to their respective 5% corn oil or lard diet and fed these diets until the termination of the study (34 wk). Immunohistochemical staining of glutathione S-transferase placental form was performed in the liver, and the number of glutathione S-transferase placental form-positive foci was determined. Density, average area, and unit area of foci were significantly inhibited in the animals fed the 13.6% and 23.5% lard diets compared with those fed the 13.6% and 23.5% corn oil diets. These results indicate that the effect of dietary fat during the initiation phase of AOM-induced hepatocarcinogenesis depends on the type of fat and its fatty acid composition. Additionally, the enhancing effect of a corn oil diet in hepatocarcinogenesis is mainly present during the initiation phase of carcinogenesis compared with a lard diet.     

Dietary fat and colon cancer: animal models

During the past 15 years, human and animal model studies performed in our laboratory indicate that dietary fat plays an important role in the etiology of colon cancer. The effect of dietary fat during the stages of initiation and postinitiation of colon carcinogenesis depends on not only the amount of fat but also the type of fat and its fatty acid composition. Studies conducted in animal models have shown that high intake of dietary corn oil, beef fat, safflower oil, and lard increases colon carcinogenesis, whereas diets high in olive oil, coconut oil, and fish oil are without enhancing effect. The mechanisms by which various types of fat increase colon carcinogenesis are not fully understood; however, in most instances, the high-fat diet seems to enhance colon carcinogenesis through its elevation of agents that act as promoters of tumor development.     

Dietary fat dependence of intestinal 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity in rats

The effects of dietary fats on intestinal 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity were studied in rats. Animals were fed experimental diets ad libitum for 7-13 d then killed in the morning for the determination of the reductase activity in an epithelial cell homogenate. When corn oil was the source of dietary fat, the specific activity of jejunal reductase depicted a biphasic pattern in response to dietary fat level with a peak activity when the diet contained 10% fat (by weight) whereas the specific activity of ileal reductase was independent of the fat level. Reductase activities were apparently independent of the degree of saturation of dietary fat (safflower oil, olive oil, lard and tallow) when each was fed as 10% of the diet. Both jejunal and ileal reductase activities were higher when trilaurin was fed than when other saturated fats (tricaprylin, trimyristin, tripalmitin and tristearin) were fed. The jejunum synthesized more cholesterol than the ileum. There was no significant correlation among the reductase activity, cholesterol content of the epithelial cells and the rate of fat absorption, suggesting a complex regulatory mechanism.     

Effect of dietary cholesterol with or without saturated fat on plasma lipoprotein cholesterol levels in the laboratory opossum (Monodelphis domestica) model for diet-induced hyperlipidaemia

Laboratory opossums (Monodelphis domestica) show extreme genetic variability in their responsiveness to dietary lipids; a great proportion of the genetic variability in responsiveness is due to a single major gene. To determine whether the major gene for dietary response detected by genetic analysis in opossums is responsive to dietary cholesterol or dietary saturated fat, or a combination of both, we used males and females of susceptible and resistant lines of laboratory opossums that were 5 to 7 months old. The animals were challenged with three different experimental diets (high-cholesterol diets with or without high saturated fat from lard or coconut oil) and plasma lipoproteins were measured. Plasma and VLDL+LDL-cholesterol concentrations increased several-fold when the animals were fed the diet containing elevated cholesterol (P<0.001) or elevated cholesterol and fat (P<0.001) and differed between the two lines when they were fed high-cholesterol diets with or without fat (P<0.001). Plasma HDL-cholesterol concentrations were higher (P<0.05) in animals of the resistant line than in the susceptible line when they were fed the basal diet (550 (SEM 30) v. 440 (SEM 20) mg/l) and when they were fed the low-cholesterol and high-fat diet (600 (SEM 30) v. 490 (SEM 30) mg/l). Dietary coconut oil and lard had similar effects on plasma lipoprotein cholesterol concentrations in the susceptible line of opossums. A reduction in dietary cholesterol by 50 % with either the lard or coconut oil blunted the plasma cholesterol response. The results from the present studies suggest that the major gene for dietary response previously detected by genetic analysis in laboratory opossums affects the response to dietary cholesterol but not to saturated fat.     

Regulation of cholesterol and lipoprotein metabolism in guinea pigs mediated by dietary fat quality and quantity.

The effects of dietary fat quality and quantity on regulation of cholesterol and lipoprotein metabolism were measured in guinea pigs. The animals were fed 7.5 or 15% (wt/wt) fat diets containing either polyunsaturated corn oil (CO), monounsaturated olive oil (OL) or saturated lard as the fat source. Dietary fat quality had a number of significant effects: animals fed the CO-based diet had lower plasma LDL levels and LDL particles of higher density with decreased ratios of core-to-surface components. Apoprotein B/E receptor-mediated binding of LDL to hepatic membranes was twofold higher for animals fed the CO-based diet. Animals fed the OL-based diet had lower hepatic 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase activity and increased levels of hepatic cholesterol. Hepatic cholesteryl ester levels were lowest for animals fed the lard-based diet. Increasing dietary fat quantity resulted in increased plasma LDL levels and hepatic cholesterol, HMG-CoA reductase activity and receptor affinity for LDL. No changes were observed in LDL binding. These data demonstrate that, independent of dietary fat quantity, CO-based diets lower plasma LDL levels, modify LDL composition and increase hepatic apoprotein B/E receptor number.     

Reversal of the promotional effect of high-fat diet on mammary tumorigenesis by subsequent lowering of dietary fat

Female Sprague-Dawley rats were given 7,12-dimethylbenz(a)anthracene at 50 days of age to induce mammary tumors, and beginning one week later were fed a high-fat, semipurified diet containing 20% sunflowerseed oil to promote tumor development. After another 7 weeks, when one third of the rats had palpable mammary tumors, the rats were randomly assigned to five groups of 31 animals each, with the same number of tumor-bearers in each group. One group was continued on the high-fat diet, another was given a fat-free diet, and the three remaining groups were fed diets containing 10% lard, butter, or coconut oil, respectively. During the next 29 weeks, rats fed the diets containing 0% or 10% fat developed significantly fewer tumors than those continued on the 20% fat diet. The diets containing 10% fat suppressed tumorigenesis at least as effectively as the fat-free diet. Rats fed the 10% butter and 10% lard diets had growth rates comparable to those fed the 20% sunflowerseed-oil diet throughout, and evidence of essential fatty acid deficiency was seen only in rats on the fat-free diet. These results provide additional evidence that high-fat diets promote development of mammary cancer and suggest that reducing the level of dietary fat might help to prevent the development and recurrence of breast cancer in humans.     

Serum aminopeptidase A activity of mice is related to dietary fat saturation

A high intake of monounsaturated fat has been proposed to be a dietary factor that can decrease the incidence of cardiovascular disease and hypertension. In addition, increasing dietary fat saturation has been shown to increase plasma total cholesterol and elevate systolic and diastolic blood pressures. We demonstrated previously that cholesterol selectively increases in vitro aminopeptidase A activity, which is related to angiotensin metabolism. In this study, we investigated the effect of different degrees of dietary fatty acid saturation on serum aminopeptidase activities in vivo. Serum total cholesterol concentrations were also measured. Five groups of male Balb/C mice were fed for 10 wk diets containing 2.4 g/100 g of sunflower oil, fish oil, olive oil, lard or coconut oil. We measured alanyl-, arginyl-, cystinyl-, pyroglutamyl-, aspartyl- and glutamyl-specific aminopeptidase activities using arylamides as substrates. Serum total cholesterol levels were higher in mice fed diets containing saturated oils (lard and coconut) than in those consuming sunflower oil, which is unsaturated. Two of the serum aminopeptidase A activities (aspartyl and glutamyl aminopeptidase) increased progressively with the degree of saturation of the dietary fatty acids; activities were significantly greater in mice fed coconut oil than in those fed sunflower or fish oil. Therefore, the substrates hydrolyzed by this activity as well as their functions may be similarly affected. These results may have some implication for the treatment of cardiovascular disease.     

Effect of dietary saturated fatty acids on intracellular free fatty acids and kinetic properties of hormone-sensitive lipase of rat adipocytes

Experiments were conducted to examine the effects of dietary saturated fatty acids on the intracellular free fatty acid concentration and composition and on the kinetic parameters of hormone-sensitive lipase of rat adipocytes. Animals were fed for 4 wk 14% coconut oil, beef fat or safflower oil and 2% corn oil in a purified diet. Adipocytes of animals fed the coconut oil diet contained higher basal level of intracellular free fatty acids than those of animals fed other beef fat or safflower oil diets. Norepinephrine (10(-5) M) stimulated the basal intracellular free fatty acid concentration by 2.3-3.4-fold in adipocytes from animals fed saturated fatty acids, compared with 6.4-fold in those of animals fed the safflower oil diet. The concentrations of intracellular free fatty acids in adipocytes of experimental animals after stimulation with 10(-5) M norepinephrine, however, were not significantly different. The intracellular free fatty acid pool of adipocytes of animals fed the saturated fatty acids had more palmitic acid and less linoleic acid than those of safflower oil-fed animals. The results indicate that type of dietary fat had no effect on kinetic properties of hormone-sensitive lipase.     

不同膳食脂肪对糖耐量及胰岛素敏感性的影响

目的:比较4种膳食脂肪对大鼠糖耐量及胰岛素敏感性的影响。方法:将50只SD大鼠随机分为5组,分别为紫苏油组、葵花籽油组、橄榄油组、猪油组和基础饲料组。各膳食脂肪组大鼠的脂肪摄入量占总能量的30.4%。喂养6 w后,进行口服葡萄糖耐量试验(OGTT),测定血清胰岛素、甘油三酯、总胆固醇等指标,并计算胰岛素敏感指数(ISI)。同时分离附睾脂肪垫并称重。结果:与基础饲料组相比,猪油组大鼠葡萄糖餐后2 h血糖及胰岛素显著升高,ISI显著降低;葵花籽油组和橄榄油组大鼠的餐后2 h血糖显著低于猪油组,ISI显著高于猪油组;紫苏油组大鼠空腹及餐后2h血糖、胰岛素水平均显著低于猪油组,ISI高于猪油组,其中空腹血糖还低于葵花籽油组、橄榄油组和基础饲料组,ISI高于上述组。紫苏油组血清甘油三酯、总胆固醇水平显著低于猪油组和基础饲料组,大鼠附睾脂肪垫相对重量显著低于猪油组。结论:猪油可促使胰岛素抵抗及高血糖的发生,而紫苏油可提高大鼠胰岛素敏感性、改善糖代谢;葵花籽油和橄榄油对胰岛素敏感性和糖耐量的作用介于紫苏油和猪油之间。紫苏油对糖代谢的有利作用可能与其降低血中甘油三酯水平、减少体内脂肪堆积有关。     

Regulation of hepatic microsomal cytochrome P450IIE1 level by dietary lipids and carbohydrates in rats

The present work tests the hypothesis that high fat/low carbohydrate diets elevate the level of liver microsomal cytochrome P450IIE1. Male Sprague-Dawley rats were fed liquid diets containing varied ratios of corn oil/carbohydrate for 4 d. Rats fed diets with higher fat/carbohydrate ratios produced higher serum acetone levels and higher hepatic microsomal P450IIE1 content and N-nitrosodimethylamine demethylase activity than those fed diets with lower fat/carbohydrate ratios. This dietary fat/carbohydrate effect on P450IIE1 also was observed with modified semipurified AIN-76A diets. In addition, both the quantity and the extent of unsaturation of dietary lipids affected P450IIE1 regulation. At moderate fat levels (5 and 20% diet), rats fed corn oil and menhaden oil diets produced higher P450IIE1 activity than those fed lard and olive oil diets. Rats fed a diet containing 20% corn oil or an amount of linoleic acid equivalent to the 20% corn oil diet showed twofold to threefold increases in the level of P450IIE1 over those fed a fat-free diet. Rats fed a 25% corn oil diet showed twofold higher enflurane metabolism in vivo than those fed a 0.5% corn oil diet. The present results suggest that the constitutive P450 enzyme level is regulated by dietary fat/carbohydrate ratios.     

Dietary fatty acids temporarily alter liver very long-chain fatty acid composition in mice.

To determine the influence of dietary fatty acids on tissue very long-chain fatty acid (VLFA) composition, mice were fed four diets containing 15 g fat/100 g diet derived largely from either safflower oil, peanut oil, olive oil or glycerol trioleate oil. The diets varied widely in the composition of VLFA and other fatty acids. Digestibility of total dietary VLFA ranged from 84.6% in mice fed the glycerol trioleate diet to 96.7% in those fed the safflower oil diet. After 3 mo, the saturated VLFA composition of liver total lipids and sphingomyelin was lower in animals fed the glycerol trioleate oil diet than in mice fed most other diets. Although the saturated VLFA content of the peanut oil diet was more than 15-fold greater than that of the other diets, animals fed the peanut oil diet showed little or no selective increase in liver saturated VLFA. The VLFA composition of brain was comparable in all dietary groups. After 8 mo of feeding, the liver saturated VLFA composition tended to increase and differences between groups disappeared. Liver peroxisomal beta-oxidation of lignocerate (24:0) was similar among all dietary groups. These results demonstrate that dietary fatty acids shorter than VLFA temporarily influence the saturated VLFA composition of liver.     

Fat and endocrine-responsive cancer in animals

Studies using the N-nitrosomethylurea mammary tumor model indicate that the tumor-promoting effect of dietary fat is dependent on both qualitative and quantitative factors. Rats were fed diets containing either safflower, corn, or olive oil at either 23 (HF) or 5% (LF) in the diet (w/w). Coconut oil was fed to one group at 23% (w/w). It was found that animals fed HF diets rich in linoleic acid, such as safflower and corn oil, exhibited increased incidence and decreased latent period compared with either their LF counterparts or animals fed HF diets rich in oleic acid (olive oil) or medium-chain saturated fatty acids (coconut oil). Analysis of tumor lipid fatty acid content indicated that tumor-neutral lipids reflected the diet whereas tumor phospholipids did not. Moreover, tumor prostaglandins (PGE2) were high in the two high-incidence groups (HF safflower and corn) and low in the two low-incidence groups (HF olive and coconut). These results indicate that HF intake is a necessary, but not a sufficient, condition for mammary tumor promotion, and that the proportion of essential polyunsaturates vis a vis monounsaturates and saturates is a critical determinant of the fat effect. In addition, our studies suggest that alterations in the metabolism of linoleic acid to (prosta . . .) prostaglandins may underlie the fat effect. Dose-response studies in the same model, using four different levels of corn oil, suggest that instead of a linear relationship with respect to tumor incidence, there appears to be a threshold lying between 20 and 33% fat as calories, above which tumor promotion is manifested and below which it is not.     

Dietary calcium phosphate promotes Listeria monocytogenes colonization and translocation in rats fed diets containing corn oil but not milk fat

Most Gram-positive bacteria are susceptible to the bactericidal action of fatty acids and bile acids. Because dietary calcium phosphate (CaP(i)) lowers the intestinal concentration of these antimicrobial agents, high CaP(i) intake may enhance intestinal colonization of Gram-positive pathogens and the subsequent pathogenesis. In this study, we tested this hypothesis in a rat model using Listeria monocytogenes. Rats were fed diets containing low (20 micromol/g diet) or high (160 micromol/g diet) amounts of CaP(i). Dietary fat was provided as corn oil or milk fat. Rats were orally inoculated with L. monocytogenes. When rats consumed diets containing corn oil, high CaP(i) intake indeed stimulated colonization of L. monocytogenes and increased L. monocytogenes translocation and diarrhea. In addition, supplemental CaP(i) enhanced ex vivo growth of L. monocytogenes in fecal extracts of rats fed corn oil diets, suggesting that high CaP(i) intake decreased a luminal inhibitory factor. The concentrations of bile salts and fatty acids, which were highly listericidal in vitro, were indeed considerably decreased in fecal water of rats in the high calcium corn oil group. Surprisingly, dietary CaP(i) did not affect colonization and translocation of L. monocytogenes in rats fed the milk fat diet, nor did CaP(i) enhance ex vivo growth in fecal extracts. This absence of Listeria stimulation was associated with a lack of effect of dietary CaP(i) on fecal soluble fatty acids. In addition, residual soluble bile salts were higher in rats fed the high CaP(i) milk fat diet compared with the high CaP(i) corn oil diet. These results suggest that the stimulating effect of CaP(i) on L. monocytogenes infection depends on the type of dietary fat consumed.     

Effect of the fat/carbohydrate ratio in the diet on obesity and oral glucose tolerance in C57BL/6J mice

To study whether consumed dietary fat has a linear relationship or a threshold with glycemic controls, female C57BL/6J mice were fed different levels of a safflower oil (10, 20, 30, 40, 50, and 60% of total energy) diet ad libitum for 15 wk. Food intake, body weight, parametrial white adipose tissue (WAT) and liver weight were measured, and oral glucose tolerance tests were conducted. Although there was no significant difference in average energy intake, graded increments of safflower oil resulted in graded deterioration of glucose tolerance during 5 and 12-wk feeding, and deterioration of glucose tolerance was more manifested after 12-wk feeding as compared to 5-wk feeding. After 12-wk feeding, a significant deterioration of glucose tolerance was observed in diets of more than 40% fat. Graded increments of body weight and WAT weight were observed, and their weight increases were manifested in diets of more than 30% fat. These data indicated that the amount of dietary fat had an almost linear relationship with glucose tolerance, and significant differences were observed in mice fed diets more of than 40% fat.