Talmudic aphorisms on diet IV fasting--the lightest diet!
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Aphorisms and Proverbs as Topic↗
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[Chemically defined diets and diet formulas].
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Food, Formulated↗
Influence of diet on experimental swine dysentery. 1. Effects of a vitamin E and selenium deficient diet supplemented with 6.8% cod liver oil.
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Animal Nutritional Physiological Phenomena↗
[Relationship between diet-knowledge and diet-adherence (author's transl)].
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Adult↗
Simple, novel diets produce more weight loss than conventional diets
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Journal Article↗
Response of broiler chicks to threonine-supplemented diets to 4 weeks of age.
1. Two experiments were carried out to determine the response of broiler chicks to threonine-supplemented diets between 10 and 28 d and 7 and 21 d of age, respectively. 2. In the first experiment female broiler chicks were fed on 11 experimental diets. Two iso-energetic basal diets (diets 1 and 2) were prepared with 200 and 160 g CP/kg and 7.6 and 6.0 g threonine/kg respectively. Both diets contained 11.5 g lysine and 8.7 g sulphur-containing amino acids/kg. Diet 3 was composed of diet 2, supplemented with all essential and non-essential amino acids (EAA and NEAA, respectively) except threonine, to the concentrations of the amino acids in diet 1. The NEAA were added as a combination of glutamic acid and glycine. Diets 4 to 11 had the same compositions as diet 3, but contained increasing amounts of threonine. 3. For birds fed on diet 2, gain was significantly lower and food/gain ratio was significantly higher than for birds fed on diet 1. Supplementation with EAA, NEAA and threonine to the same concentrations in diet 1 resulted in a performance similar to that found on diet 1. 4. In experiment 2, male and female broiler chicks both received 10 experimental diets. Diet 1 contained 220 g CP/kg and 8.5 g threonine/kg, diet 2 contained 160 g CP/kg from natural raw materials and 6 g threonine/kg. Both diets contained 12.4 g lysine and 9.3 g sulphur-containing amino acids/kg. Basal diet 2 was supplemented with all EAA and NEAA to the concentrations of basal diet 1, except for threonine. Diets 3 to 10 had the same compositions as the supplemented diet 2, but contained increasing amounts of threonine. 5. For male and female chicks on diet 2, gain was significantly lower and food/gain ratio significantly higher than those on diet 1. Diet 10 (160 g CP/kg plus all EAA, including threonine, and NEAA supplemented to the concentrations of diet 1) resulted in the same performance as diet 1. 6. The results indicate that, when low protein maize-soyabean meal diets supplemented with EAA and NEAA with 13.31 MJ ME/kg were fed to male and female broiler chicks until 21 d of age, improvements in gain and food/gain ratio were obtained when the dietary threonine content was increased to 7.25 g/kg. When female chicks were fed threonine-supplemented diets to 28 d of age, improvement in gain and food/gain ratio was obtained when the threonine concentrations were increased to 6.32 g/kg diet.(ABSTRACT TRUNCATED AT 400 WORDS)
Analysis of Variance↗
Effect of feeding reduced protein, amino acid-supplemented diets on nitrogen and energy balance in grower pigs.
Two experiments were conducted to determine the effect of feeding reduced CP, amino acid (AA)-supplemented diets on the nitrogen (N) and energy (E) balance of grower pigs. In Exp. 1, 24 barrows (22.2 kg BW) were fed corn-soybean meal (C-SBM) diets containing either 16% CP, 12% CP, or 12% CP supplemented with lysine (LYS), tryptophan (TRP), and threonine (THR). After 6 d of adaptation to the diets and feeding frequency, a 5-d N and E balance trial was conducted. Supplementation of the 12% CP diet with LYS, TRP, and THR improved N retention ( P < .01) but failed to improve N retention to the level attained by pigs fed the 16% CP diet (P < .01). Efficiency of N retention was similar between pigs fed the AA-supplemented 12% CP diet and pigs fed the 16% CP diet (P > .10). Energy retention was increased by AA-supplementation of the 12% CP diet ( P < .10) to a level higher than that of pigs fed the 16% CP diet (P < .01). In Exp. 2, 60 barrows (21.7 kg BW) were fed one of the following diets: 16% CP; 12% CP diet supplemented with indispensable AA (IDAA) to simulate the 16% CP diet; 12% CP supplemented with LYS, TRP, THR, and dispensable AA N (DAAN); 12% CP supplemented with LYS, TRP, and THR; or a 12% CP negative control diet. After 6 d of adaptation to the diets and feeding frequency, a 5-d N and E balance trial was conducted. Nitrogen retention was improved (P < .01) by supplementing the 12% CP diet with LYS, TRP, and THR but remained inferior (P < .01) to that obtained when pigs were fed the other three diets. Pigs fed the 12% CP diet with LYS, TRP, THR, and DAAN supplementation retained less N (P < .07) than pigs fed the 16% CP but retained an amount similar (P > .10) to pigs fed the 12% CP diet with IDAA and DAAN supplementation. Pigs fed the 12% CP diet with LYS, TRP, and THR supplementation exhibited the highest efficiency of N retention (P < .01). Pigs fed the 12% CP diet supplemented with LYS, TRP, THR, and DAAN retained more (P < .01) E than pigs fed the 12% CP diet supplemented with IDAA and DAAN and more (P < .07) E than pigs fed either the 12% CP diet supplemented with LYS, TRP, and THR or the unsupplemented 12% CP diet. Pigs fed the 16% CP diet retained more (P < .06) E than pigs fed the 12% CP diet with IDAA and DAAN supplementation. Although the data show that the efficiency of N retention is greatest when LYS, TRP, and THR are supplemented to the 12% CP diet, maximal N retention is achieved only when the 12% CP diets are supplemented with both the deficient AA and a source of N for dispensable AA synthesis.
Amino Acids↗
Adding wheat middlings, microbial phytase, and citric acid to corn-soybean meal diets for growing pigs may replace inorganic phosphorus supplementation.
Three experiments were conducted with 96 growing Landrace x Yorkshire x Duroc crossbreds to determine the collective effectiveness of cereal phytase from wheat middlings, microbial phytase, and citric acid in improving phytate-P bioavailability in corn-soy diets. In Exp. 1, 40 gilts (7 wk old) were fed five diets for 8 wk. Diets 1, 2, and 3 were low-P, corn-soybean meal diets (CSB) + 0, .1, or .2% inorganic P (Pi) as calcium phosphate, respectively. Diet 4 was a similar corn-soy diet that included 15% wheat middlings (461 cereal phytase U/kg). Diet 5 was the CSB + microbial phytase (1,200 U/kg; Natuphos, BASF, Mount Olive, NJ). In Exp. 2, 16 barrows (8 wk old) were fed two diets for 6 wk. Diet 1 was the same as Diet 3 of Exp. 1 (.2% Pi). Diet 2 was Diet 4 of Exp. 1 + microbial phytase (300 U/kg). In Exp. 3, 40 barrows and gilts (6 wk old) were fed four diets for 6 wk. Diets 1 and 2 were the same as those in Exp. 2. Diet 3 was Diet 2 of Exp. 2 + 1.5% citric acid. Diet 4 was similar to Diet 3 but contained 10 instead of 15% wheat middlings. In Exp. 1, pigs fed the low-P, CSB (Diet 1) had lower (P < .05) ADG, ADFI, plasma Pi concentration, bone strength, and mobility score than pigs of the other four treatments. Measurements for pigs fed the 15% wheat middlings diet were not significantly different from those of pigs fed the CSB + .1% Pi or microbial phytase. In Exp. 2, ADG (P=.06) during wk 1 to 3 and gain:feed ratio (P < .02) and plasma Pi concentration (P < .005) during all weeks favored pigs fed the CSB + .2% Pi compared with the other diet including 15% wheat middlings. In Exp. 3, identical ADG during all weeks and similar plasma Pi concentrations at wk 4 and 6 were observed between pigs fed the two citric acid diets (Diets 3 and 4) and the CSB + .2% Pi (Diet 1). Pigs fed Diet 4 (10% wheat middlings) had even higher (P < .02) gain:feed ratio during wk 1 to 3 than those fed Diet 1. It seems feasible to completely replace calcium phosphate with 10 to 15% wheat middlings, 300 U microbial phytase/ kg, and 1.5% citric acid in the corn-soy diets for growing pigs.
6-Phytase↗
Influence of n-6 versus n-3 polyunsaturated fatty acids in diets low in saturated fatty acids on plasma lipoproteins and hemostatic factors.
Modification of dietary fat composition may influence hemostatic variables, which are associated with increased risk of coronary heart disease (CHD). To address this question, we performed a controlled feeding study on 26 healthy male nonsmoking subjects with diets of differing fat composition. For the first 3 weeks, the subjects were given a diet calculated to supply 30% energy as total fat: 8% as monounsaturated, 4% as polyunsaturated, and 16% energy as saturated fatty acids, respectively (saturated diet). This was followed immediately by two diets taken in random order, each of 3-week duration and separated by an 8-week washout period on the subject's usual diet. Both diets were calculated to supply 30% of energy as fat: 14% monounsaturated, 6% as polyunsaturated, and 8% energy as saturated fatty acids. They both provided 5 g (approximately 1.7% energy) more of polyunsaturated fatty acids than the saturated fat diet; in one diet as long-chain n-3 fatty acids (n-3 diet) and in the other as linoleic acid (n-6 diet). Fasting plasma lipids, lipoproteins, and hemostatic factors were measured on the final 3 days of each dietary period. In a subset of 9 subjects the postprandial responses to a test meal were studied on the penultimate day of each period, each meal having the fat composition of its parent diet. On the n-3 diet compared with the n-6 diet, plasma triglyceride, HDL3 cholesterol, apoprotein AII, and fibrinogen concentrations were lower and HDL2 cholesterol concentration was higher (P = .0001, P = .003, P = .0001, P = .004, and P = .001, respectively). On both the n-3 and n-6 diets compared with the saturated diet, fasting plasma total and LDL cholesterol, apoprotein B, beta-thromboglobulin concentrations, and platelet counts were lower (P < .0001, P < .0001, P < .001, P < .01, and P < .05 respectively) and plasma Lp(a) and von Willebrand factor concentrations were higher (P = .02 and P < .01, respectively). Fasting factor VII coagulant activity (VIIc) was increased and apoprotein AI concentration reduced following the n-3 diet (P = .004 and P = .01, respectively) compared with the saturated diet. Plasma fibrinogen concentration was significantly greater following the n-6 diet than on the saturated diet (P = .02). Postprandially, plasma triglyceridemia was greater on the n-6 diet and lowest on the n-3 diet (P < .001) with the saturated diet being intermediate. Plasma VIIc was increased at 4 hours following the standardized test meals on the n-3 and n-6 diets (both P < .05) but not on the saturated diet. An increased intake of long chain n-3 fatty acids decreases fasting plasma triglyceride and apoprotein AII concentrations and increases HDL2 cholesterol concentrations and results in less postprandial lipemia but leads to an increase in VIIc. An increased intake of linoleic acid may raise plasma fibrinogen concentration. Decreasing the intake of saturated fatty acids reduces plasma LDL cholesterol and apoprotein B without affecting HDL cholesterol concentration independent of the type of polyunsaturated fatty acids in the diet. When advice is given to reduce saturated fat intake, it is important to ensure an appropriate ratio of n-3/n-6 fatty acids in the diet.
Adult↗
Salvage of exogenous urea nitrogen enhances nitrogen balance in normal men consuming marginally inadequate protein diets.
1. Urea kinetics were measured in six healthy men using prime/intermittent oral doses of [15N15N] urea, after five days consuming one of four diets which varied in their nitrogen content: a reference diet (REF, 70 g of protein and 11.2 g of N); a low-protein diet (LP, 30 g of protein and 4.8 g of N); a low-protein diet with 6.9 g of urea added (LP-U1, 30 g of protein and 8 g of N); a low-protein diet with 13.7 g of urea added (LP-U2, 30 g of protein and 11.2 g of N). 2. Apparent nitrogen balance on the REF diet was significantly better than on the LP or the LP-U1 diets. The addition of the higher level of urea in the LP-U2 diet enhanced apparent nitrogen balance compared with the LP or LP-U1 diets, and was not different to apparent nitrogen balance on the REF diet. 3. On the LP, LP-U1 and LP-U2 diets, the rate of endogenous urea production was not different, and was about 60% of that on the REF diet, a statistically significant difference. The addition of a dietary supplement of urea increased the rate of urea appearance in the urea pool in direct relation to the dose of urea taken. There was no difference in the rate of appearance between the REF and LP-U2 diets, for both of which the rate of appearance was significantly greater than on the LP diet. 4. The excretion of urea in urine on the LP diet was 62% of that on the REF diet, a significant difference. There was no significant difference in the rate of urea excretion between the REF, LP-U1 and LP-U2 diets. 5. The rate of urea hydrolysis by the colonic microflora on the REF diet was more than twice that on the LP or LP-U1 diets. Supplementation with urea at the higher level, LP-U2, significantly increased hydrolysis to the same level as on the REF diet. Most of the nitrogen derived from urea hydrolysis was retained in the metabolic pool (> 80%), with no difference in the rate of retention between the REF and LP-U2 diets, both greater than the LP or LP-U1 diets. 6. The dietary supplements of urea increased the size of the body urea pool significantly. Renal clearance of urea was highest on the REF diet and decreased 13-29% on the low-protein diets. Bowel clearance was highest on the REF diet and decreased 46-55% on the low-protein diets. Neither urinary excretion of urea nor urea hydrolysis in the bowel were related simply to the concentration of urea in blood. Urea hydrolysis related most closely to the rate of appearance of urea in the urea pool. 7. The salvage of urea nitrogen was increased on the highest level of supplementation, but the overall sensitivity of the system was low, suggesting that other factors might be limiting for effective urea hydrolysis and the salvage of urea nitrogen.
Adult↗
The serum LDL/HDL cholesterol ratio is influenced more favorably by exchanging saturated with unsaturated fat than by reducing saturated fat in the diet of women.
We compared the effects of a high fat diet [38.4% of energy (E%) from fat; HSAFA diet, polyunsaturated/saturated fatty acid (P/S) ratio = 0.14], a low fat diet (19.7 E% from fat; LSAFA diet, P/S = 0.17), both based on coconut oil, and a diet with a high content of mono- and polyunsaturated fatty acids (PUFA; 38.2 E% from fat; HUFA diet, P/S = 1.9) on serum lipoproteins. The 25 women studied consumed each diet for 3-wk periods in a crossover design. The two high fat diets were identical except for the quality of the test fat. The LSAFA diet was identical to the HSAFA diet except that half the fat was replaced by carbohydrates. Serum total cholesterol, LDL cholesterol and apoB concentrations did not differ between the HSAFA and the LSAFA diet periods. Total cholesterol, LDL cholesterol and apoB were lower when women consumed the HUFA diet than when they consumed the other two diets. HDL cholesterol and apoA-I were 15 and 11%, respectively, higher when women consumed the HSAFA diet than when they consumed the LSAFA diet; HDL cholesterol and apoA-I were lower when women consumed the HUFA diet than when they consumed the HSAFA diet, but not the LSAFA diet. The LDL cholesterol/HDL cholesterol and apoB/apoA-I ratios were higher when women consumed the LSAFA diet than when they consumed the HSAFA diet. The LDL/HDL cholesterol ratio was higher when women consumed either the LSAFA or the HSAFA diet than when they consumed the HUFA diet, whereas apoB/apoA-I was higher when women consumed the LSAFA diet than when they consumed the HUFA diet. Triacylglycerol and VLDL cholesterol were higher when women consumed the LSAFA diet than when they consumed either the HSAFA or the HUFA diet. We conclude that, to influence the LDL/HDL cholesterol ratio, changing the proportions of dietary fatty acids may be more important than restricting the percentage of total or saturated fat energy, at least when derived mainly from lauric and myristic acids, both of which increase HDL cholesterol.
Adult↗
Hepatocarcinogenesis in rats fed methyl-deficient, amino acid-defined diets.
The ability of methyl-deficient, amino acid-defined diets to produce liver tumors was studied in rats treated both with and without initiating doses of diethylnitrosamine (DENA). Male, weanling F344 rats were fed a complete, amino acid-defined diet for one week. They were then injected once i.p. with one of 3 doses of DENA (20, 70 or 200 mg/kg body weight) and fed the complete diet for an additional week. Thirty animals from each dose group were then maintained for 76 weeks on the complete diet (Diet 1) or one of 4 methyl-deficient diets: Diet 2, devoid of methionine and choline; Diet 3, devoid of methionine only; Diet 4, devoid of choline only and Diet 5, devoid of methionine, choline, folic acid and vitamin B12. In Diets 2, 3 and 5 methionine was replaced by equimolar amounts of its metabolic precursor DL-homocystine. Control rats were injected i.p. with the saline vehicle and maintained for the 76-week period on Diets 1 and 2. Forty percent of the rats fed Diet 2, but receiving no DENA, developed hepatocellular carcinomas or cholangiomas. A 90-100% incidence of hepatocellular carcinomas was seen in all groups initiated with DENA and fed Diet 2. No malignant liver tumors developed in Diet 1 rats that had received 0 or 20 mg/kg DENA; however, hepatocellular carcinomas were noted in one-half of such animals receiving the 70 and 200 mg/kg doses. Liver metastases grew in the lungs of 60% of the tumor-bearing rats fed Diet 2; none were seen in the Diet 1-fed rats. The singly deficient Diets 3 and 4 enhanced liver tumor formation to DENA-initiated rats to a significantly lesser extent than did Diet 2. All DENA-initiated rats fed the severely deficient Diet 5, died within 23 experimental weeks with livers containing hepatocytes of atypical appearance and, particularly at the 2 higher dosages, a cirrhotic pseudonodular architecture. No hepatocellular carcinomas or cholangiomas were observed in Diet 5-fed rats. None of the diets tested appeared to enhance tumor formation in extrahepatic tissues. In fact, significant decreases were noted in the formation of spontaneous testicular interstitial cell tumors in Diet 2-fed rats and of pancreatic acinar tumors in rats fed Diets 2 and 3. Diet 2, devoid of both methionine and choline, also induced metaplasia of pancreatic acinar cells to hepatocyte-like cells and was associated with moderate to severe hyperplasia of the transitional epithelium lining the renal pelvis.(ABSTRACT TRUNCATED AT 400 WORDS)
Adenoma, Bile Duct↗
The effect of high-, moderate-, and low-fat diets on weight loss and cardiovascular disease risk factors.
Over 60% of Americans are overweight and a number of popular diets have been advocated, often without evidence, to alleviate this public health hazard. This study was designed to investigate the effects of several diets on weight loss, serum lipids, and other cardiovascular disease risk factors. One hundred men and women followed one of four dietary programs for 1 year: a moderate-fat (MF) program without calorie restriction (28 patients); a low-fat (LF) diet (phase I) (16) ; a MF, calorie-controlled (phase II) diet (38 patients); and a high-fat (HF) diet (18 subjects) [corrected]. Weight, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), homocysteine (Ho), and lipoprotein(a) [Lp(a)], were measured every 4th month. The TC/HDL-C ratio was calculated and fibrinogen levels were measured at baseline and after one year. The MF diet resulted in a 2.6% (NS) decrease in weight compared with 18.4% (p=0.045) decrease in patients on phase I, 12.6% (p=0.0085) decrease in patients on phase II, and 13.7% (p=0.025) decrease in those on the HF diet. TC was reduced by 5% (NS) in the MF group, 39.1% (p=0.0005) in the phase I group, and 30.4% (p=0.0001) in the phase II group. HF group had a 4.3% (NS) increase in TC. LDL-C was reduced by 6.1% (NS) on MF, 52.0% (p=0.0001) on phase I, and 38.8% (p=0.0001) on phase II. Patients on HF had a 6.0% (NS) increase in LDL-C. There were nonsignificant reductions in HDL-C in those on MF (-1.5%) and HF (-5.8%). Patients on phase I showed an increase in HDL-C of 9.0% (NS), while those on phase II diet had a 3.6% increase (NS) in HDL-C. TC/HDL-C increased (9.8%) only in patients following the high-fat diets (NS). Patients on MF had a 5.3% (NS) reduction in TC/HDL-C, while those on LF had significant reductions on the phase I ( -45.8%; p=0.0001) diet and phase II diet (-34.7%; p=0.0001). TG levels increased on both the MF (1.0%) and HF (5.5%) diets, although neither was statistically significant. People following the phase I and II diets showed reductions of 37.3% and 36.9%, respectively. Ho levels increased by 9.7% when people followed the MF diet and by 12.4% when they followed the HF diet. Patients following the phase I and phase II diets showed reductions of 13.6% and 14.6%, respectively. Only those following phase II diets showed a tendency toward significant improvement (p=0.061). Lp(a) levels increased by 4.7% following the MF (NS) diet and by 31.0% (NS) on the HF diet. Patients following phase I showed a 7.4% (NS) reduction and a 10.8% reduction (NS) following phase II. Fibrinogen levels increased only in individuals following HF diets (11.9%), while patients following MF (-0.6%), phase I (-11.0%), and phase II (-6.3%) diets showed nonsignificant reductions in fibrinogen. Patients on MF demonstrated nonsignificant reductions in weight, LDL-C, TC, HDL-C, TC/HDL-C ratios, and fibrinogen and nonsignificant increases in TGs, Lp(a), and homocysteine. There was significant weight loss in patients on phase I and II and HF diets after 1 year. Reductions in TC, LDL-C, TGs, and TC/HDL ratios were significant only in patients either following a LF diet or a MF, calorically reduced diet. Only patients following HF diets showed a worsening of each cardiovascular disease risk factor (LDL-C, TG, TC, HDL-C, TC/HDL ratio, Ho, Lp(a), and fibrinogen), despite achieving statistically significant weight loss.
Adult↗
Different origin of hypertriglyceridemia induced by a high-fat and a high-sucrose diet in ventromedial hypothalamic-lesioned obese and normal rats.
OBJECTIVE: To clarify the mechanism by which plasma triacylglycerol is affected by a high fat or a sucrose diet. DESIGN: Two sets of six groups each having six rats were prepared-(1) ventromedial hypothalamic (VMH)-lesioned rats fed a standard diet; (2) sham VMH-lesioned rats fed a standard diet; (3) VMH-lesioned rats fed a high-fat diet; (4) sham VMH-lesioned rats fed a high-fat diet; (5) VMH-lesioned rats fed a high-sucrose diet; and (6) sham VMH-lesioned rats fed a high-sucrose diet. After VMH lesions and sham operations, the rats were provided standard, high-fat and high sucrose diets for 2 weeks. Two weeks later, blood samples were collected after overnight fast to determine plasma triacylglycerol (TAG), hepatic triacylglycerol secretion rate (TGSR), fractional catabolic rate (FCR) of triacylglycerol and postheparin plasma lipoprotein lipase (LPL), plasma glucose, insulin and leptin. RESULTS: Values of TAG, TGSR, FCR and LPL in VMH-lesioned obese rats were all greater than those in sham-operated rats, regardless of the diet fed. In sham-operated rats, high-fat diet fed rats showed higher TAG with similar TGSR, higher LPL and lower FCR than those of standard diet fed rats. High-sucrose diet fed rats showed significantly higher TAG with higher TGSR, higher LPL and lower FCR than those of standard diet fed rats. Moreover, high-sucrose diet fed rats showed higher TAG with higher TGSR, lower LPL and higher FCR than those of high-fat diet fed rats. In VMH-lesioned rats, high-fat diet fed rats showed higher TAG with similar TGSR, higher LPL and lower FCR than those of standard diet fed rats. High-sucrose diet fed rats showed markedly higher TAG with notably higher TGSR, higher LPL and lower FCR than those of standard diet fed rats. High-sucrose diet fed rats showed still higher TAG with markedly higher TGSR, similar LPL and higher FCR than those of high-fat diet fed rats. CONCLUSIONS: The mechanism by which TAG metabolism is affected by a high-fat or a high-sucrose diet differed; a high-fat diet increased plasma TAG level by lowering removal of TAG without increase in hepatic TAG secretion in sham-operated (normal) rats. A high-sucrose diet, in contrast, induced much higher plasma TAG levels by both increased hepatic TAG secretion and decreased removal of TAG. The effects of a high-fat or a high-sucrose diet were similar but exaggerated in VMH lesioned animals.
Animals↗
Post-ingestive food-aversion learning to amino acid deficient diets by the terrestrial slug Limax maximus.
An agar-based artificial diet containing carbohydrates, fats and twenty amino acids was constructed. This diet is highly palatable and nutritionally complete for Limax maximus as demonstrated by significant ingestion on first encounter, consistent ingestion on subsequent days and good growth of young slugs fed this diet. Removing methionine, an essential amino acid, from the complete diet produces a food which is initially as palatable as the complete diet, but after one day's intake the amount of this deficient diet eaten is greatly reduced. Removing alanine, a nonessential amino acid, does not produce any decrement in feeding relative to the complete diet. A single meal can be sufficient for establishing the aversion to the deficient diet. Following seven days of feeding on the deficient diet the aversion is retained with little or no attenuation for at least 30 days and does not generalize to either a known 'safe' food or a novel food. Evidence of a mild neophobia towards the artificial diet which attenuated after one or two meals was seen. The learned aversion to the deficient diet is reversible if slugs are repeatedly fed the complete diet following feeding on the deficient diet. Also, slugs initially fed the complete diet will develop an aversion to the methionine-deficient diet after sampling it. Slugs readily ate the artificial diets when these were offered 7 days post-hatch. The methionine-deficient diet however was not eaten in large amounts after the first meals and did not support growth. Baby slugs fed the methionine-deficient diet for 10 days and then maintained on rat chow ate only small amounts when the deficient diet was presented again 126 days later, while baby slugs fed the complete diet or an alanine deficient diet for 10 days ate large amounts when these diets were presented 126 days later. Supplementing the methionine-deficient diet with an injection of methionine into the haemocoel one hour after the completion of a meal completely blocks the development of a learned aversion while injection of Limax saline does not. These results are best explained by the hypothesis that the slugs acquire, post-ingestively, an aversion to the taste and probably the odor of the diet as the result of associative learning.(ABSTRACT TRUNCATED AT 400 WORDS)
Amino Acids↗
Changes in glutathione peroxidase and tissue selenium concentrations of broilers after consuming a diet adequate in selenium.
Three experiments (EXP) were conducted with commercial broilers to develop a low-Se diet for comparing plasma glutathione peroxidase (pGPX3) concentrations and then to compare pGPX3 and plasma and tissue Se concentrations in broilers fed this low-Se diet after being supplemented with sodium selenite (SS) or Se-enriched yeast (SY). With the exception of Se, all diets were nutritionally adequate. The EXP lasted from 0 to 20 or 22 d posthatching, and treatments were replicated with 6 to 8 pens of 6 to 15 chicks per pen. The results of EXP 1 and 2 indicated that a cornstarch-dextrose diet containing 10% torula yeast and 31% soybean meal (SBM) resulted in similar gain as a corn-SBM (C-SBM) diet, but the cornstarch-dextrose-torula yeast-SBM diet with no added Se reduced pGPX3 activity 6-fold. In EXP 3, the treatments were a C-SBM diet with 0 or 0.30 ppm added Se from SS or SY. These diets were fed from 0 to 10 d posthatching. Beginning on d 10, all broilers were fed the cornstarch-dextrose-torula yeast-SBM, low-Se diet. On d 10, 13, 16, 19, and 22, three broilers per replicate were randomly selected for plasma and tissue collection. Treatment differences were significant at P < 0.05. Daily gain, daily feed intake, and gain:feed were not affected by diet during the 0-to-10-d or 0-to-22-d periods. Plasma GPX3 activity and plasma, liver, and breast Se concentrations were greater in broilers previously fed the diets with added Se, regardless of source, than in those fed the C-SBM diet, except for liver Se concentration on d 19 of broilers previously fed the SS diet. The pGPX3 concentrations were not different in broilers previously fed either Se diet on d 10 and 13 but were greater in broilers previously fed the SY diet on d 16, 19, and 22. Plasma Se concentrations were not different in broilers previously fed diets with SS or SY on d 10 and 22 but were greater in broilers previously fed the SY diet on d 13, 16, and 19. Breast Se concentrations were greater in broilers previously fed the SY diet than in those fed the SS diet on each day. Liver Se concentrations were not different in broilers previously fed SS or SY diets on d 19 and 22 but were greater in those previously fed the SY diet on d 10, 13, and 16. These results indicated that SY supplementation in broiler diets resulted in greater tissue Se concentrations than SS and that pGPX3 and tissue Se concentrations remained greater in birds previously fed a diet with SY than in those fed SS after being fed a low-Se diet.
Animal Feed↗
Effect of diet and housing on growth, body weight, survival and tumor incidences of B6C3F1 mice in chronic studies.
Diet is one of the most important environmental factors influencing growth, body weight, survival, and age-related diseases of rodents in chronic studies. NIH-07 open formula diet was the selected diet for the NTP studies from 1980 to 1994. A new diet designated as NTP-2000 diet is the current diet for mice in the NTP studies beginning in 1994. This report is a summary of results of untreated control groups of B6C3F1 mice fed NTP-2000 or NIH-07 diet from several retrospective 2-year dosed-feed and inhalation studies for differences in growth, body weight, survival, and tumor incidences. The dosed-feed studies were conducted in 3 different facilities located in the United States, and all the inhalation studies were conducted in 1 facility. During dosed-feed studies, male and female mice housed in polycarbonate cages and fed the NTP-2000 diet had lower maximum body weights than those fed NIH-07 diet. However, during inhalation studies, mice housed in wire mesh cages and fed the NTP-2000 diet had higher maximum body weights than the mice fed NIH-07 diet. Survival was higher in groups fed NTP-2000 diet irrespective of sex, housing conditions, or body weight compared to the corresponding groups fed NIH-07 diet. Survival was higher in mice housed in polycarbonate cages irrespective of diet and sex compared to the respective sex and diet groups housed in wire mesh cages. During inhalation studies, survival of male and female mice fed NTP-2000 diet was higher than that of the groups fed NIH-07 diet, although the body weights of NTP-2000 diet groups were higher than those of the groups fed NIH-07 diet. When the NTP-2000 diet was used, male and female mice in dosed-feed studies and male mice in inhalation studies had markedly lower incidences of liver tumors than the corresponding groups fed NIH-07 diet. Significant decreases in the incidences of lung tumors were observed only in the male groups fed NTP-2000 diet during dosed-feed studies. These results suggest that body weight may not be the major contributing factor for mortality and liver tumors and that an interaction between diet and housing conditions appears to affect the growth, survival and tumor incidences of B6C3F1 mice.
Animal Feed↗
Tissue levels of S-adenosylmethionine and S-adenosylhomocysteine in rats fed methyl-deficient, amino acid-defined diets for one to five weeks.
The levels of S-adenosylmethionine (AdoMet) and of S-adenosylhomocysteine (AdoHcy) as well as the ratio of AdoMet/AdoHcy were determined in the liver, lungs, testes and kidneys of weanling male rats fed a commercial chow diet or 5 different amino acid-defined diets for 1-5 weeks. The amino acid-defined diets used were as follows: diet 1, supplemented with methionine, choline, folic acid and vitamin B12; diet 2, deficient in methionine and choline; diet 3, deficient in methionine alone; diet 4, deficient in choline alone; diet 5, deficient in methionine, choline, folic acid and vitamin B12. All methionine-deficient diets were supplemented with an equimolar dose of its metabolic precursor, homocystine. The animals were sacrificed after 1, 3 and 5 weeks of treatment. In animals fed either the chow diet or diet 1, liver was the organ found to contain the highest levels of AdoMet and AdoHcy. Similarly, in animals fed diet 1 or chow, the testes and lungs contained the lowest level of AdoMet, while the lungs contained the lowest levels of AdoHcy. In general, the tissue levels of AdoHcy and AdoMet in rats fed diet 1 were very similar to the corresponding values found in chow-fed rats. Diet 1 feeding, however, led to higher hepatic levels of AdoMet than did the administration of the chow diet. The administration of the methyl-deficient diets generally led to decreased hepatic AdoMet contents at 3 and 5 weeks; the methyl-deficient diets also led to increased AdoHcy contents and decreased AdoMet:AdoHcy ratios when compared with diet 1. Linear regression analysis showed a significant direct correlation between the observed hepatic AdoMet levels and the methyl content of the diet as well as an inverse correlation between hepatic AdoHcy levels and dietary methyl contents. Unlike liver, the lung and testes did not show any decrease in AdoMet content following feeding of the methyl-deficient diets. These tissues did show, however, early significant increases in AdoHcy contents and corresponding decreases in the ratios of AdoMet:AdoHcy. These changes were found to be proportional to the dietary methyl content. The renal contents of AdoMet, AdoHcy and the ratio of AdoMet/AdoHcy were unaffected by any of the diets administered except for diet 5. The administration of diet 5 to rats for 5 weeks led to a significant increase in renal AdoHcy. These results provide evidence indicating that dietary methyl insufficiency may exert its role in carcinogenesis through a decreased availability of AdoMet in vivo.
Animals↗