Dietary biotin requirement for maximum growth of juvenile grass shrimp, Penaeus monodon

A feeding trial was conducted to estimate the minimal dietary biotin requirement for juvenile grass shrimp, Penaeus monodon. Purified diets with eight levels (0, 0.2, 0.5, 1.0, 3.0, 6.0, 10.0 and 20.0 mg/kg) of supplemental biotin were fed to P. monodon (mean weight 0. 26 +/- 0.01 g) for 8 wk. Each diet was fed to three replicate groups of shrimp. Shrimp fed diets supplemented with biotin (0.2-20.0 mg/kg) had significantly (P < 0.05) higher weight gain, feed efficiency and protein efficiency ratio than those fed the unsupplemented control diet. Weight gain was high in shrimp fed 3. 0-10.0 mg biotin/kg diet and lowest in shrimp fed 相似文献   

Dose-titration to confirm the level of fenbendazole for control of Raillietina cesticillus in broiler chickens

A total of 452 broiler chickens, naturally infected with Raillietina cesticillus, were allotted into six treatment groups. One group was fed unmedicated broiler ration (Group 1), and the other five groups were fed broiler ration containing fenbendazole at 180 ppm for 3 days (38.5 mg/kg body weight [BW]), 240 ppm for 3 days (50.9 mg/kg BW), 120 ppm for 6 days (52.2 mg/kg BW), 180 ppm for 6 days (79.9 mg/kg BW), or 240 ppm for 6 days (104.3 mg/kg BW). Fenbendazole was 100.0% efficacious against R. cesticillus when administered in the diet at 240 ppm for 6 days; 99.9% at 240 ppm for 3 days and at 180 ppm for 6 days; 99.5% at 120 ppm for 6 days; and 96.9% at 180 ppm for 3 days. Fenbendazole treatment had no adverse effect on weight gain or feed intake.     

Cervicovaginal foetal fibronectin in the prediction of preterm labour in a low-risk population

Ten groups of 14 immunosuppressed NMRI-mice (nu/nu) were raised and kept under germ-reduced conditions. The control animals were fed a germ-reduced diet, nine other groups received the same diet with selegiline (CAS 14611-51-9, Deprenyl) or lipoic acid (thioctic acid, CAS 62-46-4) admixed at various amounts. The 50% survival rate, the total life span of each group and the areas under the curves were determined to evaluate life expectancy as compared to the controls. The racemate of lipoic acid at high dosage (350 mg/kg body weight) reduced the life span significantly. The S(-)-enantiomer of lipoic acid (75 mg/kg body weight) increased the 50% survival rate, whereas the physiologic R(+)-enantiomer (9 mg/kg body weight) expanded the total life span of its group. Alteration of only one out of three parameters was not considered significant. All other groups except for one did not differ from controls: only animals which obtained 75 micrograms selegiline per kg of body weight and per day exerted increased life expectancies by all three parameters. This group exhibited also in statistical evaluation a significantly (p < 0.05) prolongated survival time up to about 200% as compared to the control animals.     

Prevention of breast cancer in the rat with 9-cis-retinoic acid as a single agent and in combination with tamoxifen

We show that 9-cis-retinoic acid (9cRA) is a potent inhibitor of mammary carcinogenesis induced by N-nitroso-N-methylurea in Sprague-Dawley rats. Rats were first treated with a single dose of N-nitroso-N-methylurea (50 mg/kg body weight) and then fed non-toxic levels of 9cRA (120 or 60 mg/kg of diet). 9cRA was highly effective in reducing tumor incidence, average number of tumors per rat, and average tumor burden, as well as extending tumor latency. The combination of 9cRA with low levels of tamoxifen (TAM; fed at either 1.0 or 0.5 mg/kg of diet) was particularly effective; addition of 9cRA to a TAM regimen doubled the number of animals that were tumor-free at autopsy and significantly diminished tumor number and tumor burden. For suppression of carcinogenesis in vivo, 9cRA was much more potent than all-trans-retinoic acid, both as a single agent or in combination with TAM, although both retinoids had equivalent inhibitory effects on DNA synthesis in cultured human breast cancer cell lines. Both 9cRA and all-trans-retinoic acid induce the expression of the adhesion molecule, E-cadherin, in the SK-BR-3 cell line. We suggest that clinical evaluation of the combination of 9cRA and TAM, either for chemoprevention or for adjuvant therapy, should be considered.     

Influence of fumonisin B1, present in Fusarium moniliforme culture material, and T-2 toxin on turkey poults

Diets containing 300 mg fumonisin B1 (FB1)/kg of feed and 5 mg T-2 toxin/kg of feed singly or in combination were fed to female turkey poults (Nicholas Large White) from day of hatch to 21 d of age. When compared with controls, 21-d body weight gains were reduced 21% by FB1, 26% by T-2, and 47% by the combination. the efficiency of feed utilization was adversely affected by FB1 and the combination of FB1 and T-2. Relative weights (grams/100 g BW) of the liver and gizzard were increased in poults fed the FB1 and the combination diets; whereas, the relative weight of the pancreas was increased in all treated groups. All poults were scored for oral lesions using a scale of 1 to 4 (1 = no visible lesions, 4 = severe lesions). Oral lesions were present in all poults fed the T-2 diet (average score of 3.29) or the combination diet (average score of 3.54). Serum concentration of cholesterol was decreased and lactate dehydrogenase activity was increased in poults fed the FB1 and combination diets. The activity of aspartate aminotransferase and the values for red blood cells, hemoglobin, and hematocrit were increased only in poults fed the combination diet. Inorganic phosphorus concentration was decreased only in poults fed the combination diet. The increased toxicity in poults fed the combination diet for most variables can best be described as additive, although some variables not altered by FB1 or T-2 singly were significantly affected by the combination, indicating that the combination may pose a potentially greater problem to the turkey industry than either of the mycotoxins individually.     

Effects of rilmenidine on rats made insulin resistant and hypertensive by a high fructose diet

This study was aimed to determine the effects of rilmenidine, an hypertensive drug, in an animal model of hypertension associated with insulin resistance, i.e. rats fed on a high fructose diet. Wistar rats were fed during four weeks either on a standard diet (S) or on a high fructose diet (F, 34.5% de fructose). In half of the F groups, rilmenidine (1 mg/kg/day) was added to the drinking water during the two last weeks of the diet (FR). Arterial blood pressure as well as insulin efficiency were determined at the end of the four weeks. Body weight gain was higher in F than in S rats (66 +/- 8 g versus 45 +/- 8 g; p < 0.05), this was prevented by rilmenidine treatment (32 +/- 2 g). Arterial systolic blood pressure was increased in F rats (162 +/- 2 vs 155 +/- 2 mmHg; p < 0.05), rilmenidine brought this value back to normal (149 +/- 3 mmHg). During the euglycemic hyperinsulinemic clamp, glucose utilization was lower (10 +/- 1 vs 14 +/- 1.5 mg/min/kg; p < 0.05) and hepatic glucose production higher (1 +/- 0.01 vs 0 mg/min/kg; p < 0.01) in F than in S rats. These changes in insulin action were totally abolished by rilmenidine. These data demonstrate that rilmenidine can ameliorate the deleterious effects of a high fructose diet, i.e. weight gain, hypertension and resistance to the effects of insulin Rilmenidine could represent a potential therapeutic agent for the treatment of hypertension associated with metabolic disorders such as syndrom X and obesity.     

Body composition at farrowing and nutrition during lactation affect the performance of primiparous sows: II. Milk composition, milk yield, and pig growth

We used 35 primiparous sows to investigate the link between body fatness at farrowing and voluntary feed intake (VFI) during lactation. Two groups of sows were fed differently throughout gestation (either 2.3 kg/d of a diet containing 5.8% CP and 14.6 MJ DE/kg as fed or 1.7 kg/d of a diet containing 15.6% CP and 14.5 MJ DE/kg as fed) so that they commenced lactation at a similar body weight (158 to 152 kg) but with different body compositions: either 340 (fat) or 280 (lean) g of body fat/kg BW (P < .001). During lactation, sows were offered either a low-protein diet (7.9% CP and 15.5 MJ DE/kg as fed) or a high-protein diet (19.0% CP and 15.6 MJ DE/kg as fed) on an ad libitum basis. During lactation, VFI was measured daily, and sow body weight and backfat were measured weekly. Blood samples were collected from sows on d 110 of gestation and d 14 and 28 of lactation, and plasma was analyzed for NEFA, glycerol, insulin, glucose, and beta-hydroxybutyrate. Fat sows ate 30% less than their lean counterparts during lactation (P < .001), which corresponded to a 70% higher concentration of NEFA in plasma (P = .01) and a 30% higher concentration of glycerol (P = .15). The VFI during the first 2 wk of lactation was affected only by body fatness and not by the protein content of the lactation diet. The dietary supply of protein influenced VFI during wk 3 and 4 of lactation, possibly by affecting milk production and hence the drive to consume feed. Weight loss, particularly lean tissue loss, was minimized by feeding the high-protein diet during lactation (P < .002).     

Black tea and mammary gland carcinogenesis by 7,12-dimethylbenz[a]anthracene in rats fed control or high fat diets

Epidemiological studies suggest that tea may reduce cancer risk, and in laboratory rodents, chemopreventive effects of tea or purified extracts of tea have been demonstrated in lung, gastrointestinal tract and skin. There is some evidence of chemoprevention by tea in the mammary gland, but the data are not conclusive. In order to evaluate more fully the possible influence of black tea on 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary gland tumors in the female S-D (Sprague-Dawley) rat, three large studies were performed: experiment 1, tumorigenesis in rats fed AIN-76A diet and given 25 mg/kg DMBA and 1.25 or 2.5% whole tea extract or water to drink; experiment 2, tumorigenesis in rats given 15 mg/kg DMBA and the same diet and fluids as in experiment 1; experiment 3, tumorigenesis in rats fed control or HF (high fat, corn oil) diet and given 15 mg/kg DMBA and 2% tea or water to drink. Tea was given throughout the experiment; DMBA was given by gastric gavage at 8 weeks of age. There was no consistent effect of tea on tumorigenesis in rats fed AIN-76A diet; there was, however, evidence in experiment 3 of a reduction of tumorigenesis by tea in rats fed the HF diet. In experiment 3, rats fed the HF diet and given water showed the expected increase in tumor burden (number and weight) compared with rats fed control diet. However, rats fed the HF diet and given 2% tea showed no increase in tumor burden; their tumor burden was significantly lower than in rats fed the HF diet and given water (P < 0.01) and was not different from rats fed control diet and given water or tea. In addition, in experiment 3, the number of malignant tumors per tumor-bearing rat was increased by the HF diet in water-drinking rats (P < 0.01) but not in tea-drinking rats. Therefore, it appears that tea partially blocked the promotion of DMBA-induced mammary tumorigenesis by the HF diet.     

Toxicity and tissue residues from diphenylhydantoin fed to chickens

Within three experiments with broiler-type crossbred chickens, diphenlyhydantoin (DPH) was administered via the diet at levels ranging from 10 to 2500 mg./kg. Feed intake and body weight gain were adversely affected by levels of 100 mg./kg. or higher. A hemorrhagic syndrome occurred in 16 percent of the chickens fed 100-1000 mg./kg. and 33 percent of those fed 2500 mg./kg. Twenty percent of the chickens fed 1000 mg./kg. were anemic; none of those receiving 250 mg./kg. were anemic. Other toxic manifestations included neurological side effects of a lethargic stupor, excitability to a disturbance, or a characteristic condition referred to as "head under." Pair-feeding experiments revealed thatlowered feed intake was not responsible for any of the clinical signs. All of the toxicity signs were reversible in 3 to 4 weeks following withdrawal of DPH. Muscle samples contained 2.5 to 11.4 mcg. DPH/g. at drug levels of 1000 and 2500 mg. DPH/kg. diet. Dose-response curves revealed that plasma, adipose, kidney and liver had levels which were, respectively, 1.05, 1.51, 2.19, and 2.85 times those of muscle.     

Carry-over effects of dietary crude protein and triiodothyronine (T3) in broiler chickens

Indian River male broiler chickens growing from 7 to 30 d of age were fed on diets containing crude protein levels ranging from 120 to 300 g/kg plus 0 or 1 mg triiodothyronine (T3)/kg diet. The purpose of this study was to examine the effects of these treatments on lipogenesis after a common diet was fed (180 g crude protein/kg diet from 30 to 56 d of age). Dietary treatment groups were sampled at 30 and 56 d. In vitro lipogenesis was determined by incubating liver explants for 2 h at 37 degrees in Hanks' salts containing 25 mM-HEPES and 10 mM-[2-14C]acetate and then measuring acetate incorporation into total lipid. Growth and feed consumption from 7 to 30 d increased (P < 0.01) as dietary protein increased from 120 to 210 g/kg diet. Both measurements decreased as crude protein increased from 210 to 300 g/kg diet. T3 decreased (P < 0.01) growth and feed intake during this period. Low-protein (< 180 g/kg) diets increased (P < 0.05) and T3 decreased lipogenesis in 30-d-old chickens. Although birds given T3 from 7 to 30 d grew at the greatest rate from 30 to 56 d of age, the final body weight was still less than controls. In vitro lipogenesis at 56 d of age was not affected by either of the two dietary treatments. In contrast, the relative size of the abdominal fat pad (g/kg body weight) at 56 d was decreased by feeding T3 from 7 to 30 d. Any changes in metabolism elicited by either dietary protein levels or hormone treatments may be specific to the particular dosing interval and are not sustained when a common diet is fed during a repletion period.     

Postnatal patterns of fatty acids in brain of progeny from vitamin B-6 deficient rats before and after pyridoxine supplementation

The influence of deficient and adequate maternal intakes of pyridoxine on lipid profiles in brains of progeny at 5, 10, 15, 25 and 50 days of age was studied. The effects of supplementing deficient dams at two different times with pyridoxine on the brain development of progeny were also examined. Three groups of weanling, female rats were fed diets deficient in pyridoxine (1.2 mg pyridoxine-HC1/kg diet) and another group received a control diet (30.0 mg pyridoxine-HC1/kg diet). One deficient group and the control group were fed their diets throughout growth, gestation and lactation. Two groups of dams were fed the deficient diet through growth, gestation and until 5 or 10 days postpartum when pyridoxine was supplemented by feeding the control diet. Body and brain weights were significantly lower in 15, 25 and 50 day-old progeny of deficient dams and deficient dams supplemented at 10 days postpartum. Cerebroside content at 15 days and ganglioside content at 15 and 25 days were significantly lower in brains of pups from unsupplemented deficient dams and deficient dams supplemented at 10 days postpartum. The postnatal development of cerebroside and ganglioside levels in brain was delayed or retarded in brain of pups from unsupplemented deficient dams. Supplementation of dams fed a low level of pyridoxine (1.2 mg/kg diet) with the vitamin beginning at 5 days postpartum reversed all observed effects of the low vitamin intake on brain lipids in progeny.     

Results of antireflux surgery in infants with vesicoureteral reflux

The mechanism underlying the reduced Cu status in rats fed on a high-sulphide diet was investigated. Male rats aged 6 weeks were fed ad libitum on purified diets containing either 0 or 500 mg S2-/kg and demineralized water for a period of 2 weeks. The high-sulphide diet had no effect on feed intake, body-weight gain or weight of liver and kidney but significantly reduced Cu concentrations in plasma and kidney. Biliary Cu excretion was decreased significantly in rats fed on the high-sulphide diet. Apparent Cu absorption (Cu intake-faecal Cu) and true Cu absorption (Cu intake-(faecal Cu-biliary Cu)) were significantly lowered after sulphide feeding for 2 weeks. Rats fed on the high-sulphide diet excreted less Cu in urine than did the controls. We conclude that high sulphide intake reduces Cu status in rats through inhibition of Cu absorption which is reflected by a decrease in biliary Cu excretion as a secondary feature.     

True digestibility of amino acids and protein in pigs with 13C as a label to determine endogenous amino acid excretion

The objective of this study was to determine whether differential labeling of 13C occurs in pigs fed diets with different 13C abundances and, if so, to use 13C as a label to determine true amino acid digestibility. Forty-eight pigs averaging 10.5 kg BW were fed dietary treatments consisting of a corn-corn gluten meal-crystalline amino acid diet (C-CGM) and a wheat-soybean meal diet (W-SBM). The 13C abundance of the amino acid fraction (AAF) of the C-CGM and W-SBM diets averaged delta 13C -14.19 and -26.36/1000, respectively. Three pigs/treatment group were killed when groups averaged 10.5 (initial), 22.9, and 46.6 kg BW, and AAF of organs were analyzed for 13C abundance. Carbon 13 in empty body AAF increased (-18.14, -13.98, and -12.66/1000) with increasing body weight in pigs fed the C-CGM diet and decreased (-18.06, -22.78, and -24.76/1000) in pigs fed the W-SBM diet. Liver, small intestine, and longissimus muscle tissues showed similar trends. Each tissue had dietary treatment effects (P < .001) and dietary treatment x weight group (P < .001) interactions. Ten pigs averaging 55.0 kg BW from each treatment group were assigned to metabolism cages and fed at 0700 and 1900. Six of these pigs from each treatment group were implanted with T-cannulas in the ileum and given a 17-d recovery period. At 1900 on d 0 of the collection phase, pigs were switched to the opposite diet that contained chromic oxide.(ABSTRACT TRUNCATED AT 250 WORDS)     

Auditory function in 70- and 75-year-olds of four age cohorts. A cross-sectional and time-lag study of presbyacusis

Sucrose acetate isobutyrate (SAIB), a mixture of esters of sucrose with a composition approximating the name sucrose diacetate hexaisobutyrate, has been used for over 30 yr in many countries as a 'weighting' or 'density-adjusting' agent in non-alcoholic carbonated and non-carbonated beverages. As part of the demonstration of safety of SAIB as a direct food additive in human diets, a program of toxicity testing was started in the late 1950s that culminated in extensive studies of SAIB in rodents, monkeys and humans over the last decade. This review summarizes the toxicity data, accrued up until 1988, that precede the safety studies published elsewhere in this issue. SAIB has been shown to have very low acute and chronic toxicities in rats, monkeys, and, except for effects on the liver, in dogs at feeding levels of up to 10% in the diet. Slight effects seen in rats and monkeys at levels of 10% in the diet are unlikely to be directly caused by exposure to SAIB. In dogs, however, SAIB causes decreases in bromosulfophthalein (BSP) and indocyanine green (ICG) elimination from the serum immediately following a single dose, indicative of interference with biliary excretion. On repeated feeding in dogs, SAIB caused increases in serum alkaline phosphatase levels, but enzymes indicative of toxic effects on the liver were unaffected. On prolonged feeding to dogs, SAIB caused changes in liver morphology revealed by electron microscopy. All of these effects were reversed when SAIB was withdrawn from the diet. The no-effect level for these effects in dogs was near 5 mg/kg body weight, but these effects were not seen in rats fed up to 4 g/kg body weight/day, monkeys fed up to 10 g/kg body weight/day, or humans fed up to 20 mg/kg body weight/day. The toxicity and pharmacological studies in dogs, rats and monkeys suggest that the effect of SAIB on biliary excretion and liver morphology in dogs is essentially pharmacological rather than toxicological in nature and that the difference between the effects in dogs at levels as low as 5 mg/kg body weight/day, and the lack of effects in rats or monkeys at levels up to 10 g/kg/day is not merely a quantitative difference between species, but an absolute qualitative difference.     

Dietary components modify the ability of garlic to suppress 7,12-dimethylbenz(a)anthracene-induced mammary DNA adducts

Various dietary components were evaluated as factors influencing garlic's ability to depress rat mammary cell DNA adducts resulting from 7,12-dimethylbenz(a)anthracene (DMBA) treatment. Diets with or without garlic powder (20 g/kg) were provided for 2 wk before DMBA treatment (25 mg/kg body weight). Rats fed diets containing 36 g casein/100 g diet had 31% fewer (P < 0.05) mammary cell DNA adducts than those fed 12 g/100 g. Garlic supplementation significantly (P < 0.05) reduced DNA adducts in rats fed either 12 or 36 g casein/100 g by 35 and 32% respectively. In the absence of dietary garlic, DNA adducts were 23% lower (P < 0.05) in rats provided a diet containing supplemental L-methionine at 0.9 g/100 g than at 0.3 g/100 g. However, adduct inhibition by garlic supplementation was greater in rats fed the lower (P < 0.05) amount of methionine (54 vs. 26% inhibition). Adduct levels in rats fed diets with 20 g corn oil/100 g were twice those occurring in rats fed 5 g/100 g (P < 0.05), regardless of adjustment for energy density. Garlic supplementation prevented the increase in DNA adducts caused by increasing dietary corn oil. Combining dietary supplements of garlic, selenite (0.5 mg/kg diet) and retinyl acetate (328 mg/kg diet) inhibited the occurrence of DNA adducts to a greater degree than when each was supplied individually. These studies demonstrate that while dietary garlic can reduce DNA adduct formation in mammary tissue caused by DMBA, this protection is influenced by several dietary components.     

Effects of dietary copper and molybdenum on copper status, cytokine production, and humoral immune response of calves

Twenty-four male Holstein calves were used to determine the effects of dietary Cu and Mo on performance, Cu status, and immune function of calves. Calves were fed a milk replacer that was deficient in Cu for 8 wk and then were randomly assigned after weaning to one of four treatments: 1) control (no supplemental Cu or Mo), 2) 10 mg of Cu (from CuSO4)/kg of dry matter (DM) (Cu diet), 3) 5 mg of Mo (from Na2MoO4)/kg of DM (Mo diet), or 4) 5 mg of Cu (from CuSO4) and 5 mg of Mo (from Na2MoO4)/kg of DM (Cu + Mo diet). The basal diet was a semipurified diet that contained approximately 1.1 mg of Cu and 1.1 mg of Mo/kg of DM. Calves fed the Cu and Mo diets gained weight more efficiently than those fed the control and Cu + Mo diets during the 112-d study. By d 84 of the study, calves fed the Cu diet had higher plasma Cu concentrations and plasma ceruloplasmin activities than did calves fed the other three diets and had higher liver Cu concentrations on d 136. Plasma and liver Cu concentrations did not differ among calves fed the control, Mo, and Cu + Mo diets. At d 112, activity of Cu-Zn superoxide dismutase was lower in calves fed the Mo diet than in calves fed the Cu diet. Serum total antibodies to porcine erythrocytes (primary response) were lower in calves fed the Mo diet than in calves fed the Cu diet at 7, 14, and 21 d postinoculation. Production of tumor necrosis factor and interleukin-1 by isolated peripheral blood monocytes was not significantly affected by treatment. Although no differences were apparent in plasma or liver Cu concentrations among calves fed the control, Mo, and Cu + Mo diets, calves fed the Mo diet had a more severe Cu deficiency based on depressed humoral immune response and superoxide dismutase activity.     

Prenatal cocaine but not prenatal malnutrition affects foster mother-pup interactions in rats

The separate and combined effects of prenatal cocaine exposure and malnutrition on mother-pup interactions in rats were assessed daily from postnatal day 2 to day 21. Sprague-Dawley dams were fed a diet of low protein content (6% casein), an isocaloric diet of adequate protein content (25% casein, control), or a laboratory chow diet prior to mating and throughout pregnancy. Within each diet group, rats received either cocaine injections (30 mg/kg IP two times per week prior to mating and then 30 mg/kg SC daily from days 3 to 18 of pregnancy) or saline injections. Litters were fostered on the day of birth to control mothers (i.e., nondrug-exposed dams fed the control or chow diet). Foster mothers fed the 25% casein diet showed increased contact with cocaine-exposed pups compared with nondrug-exposed pups in the second postnatal week but lower levels as the pups approached weaning. Passive nursing was increased in dams caring for prenatally malnourished, cocaine-exposed pups compared with those caring for similar pups with no drug exposure. Chow-fed mothers did not differ in their behavior towards pups with or without prenatal cocaine treatment. Prenatal cocaine and malnutrition independently compromised birth weight and various reflexive milestones but the attainment of physical milestones was affected only by prenatal cocaine. There were no additive effects of the two prenatal insults on any measure of mother-pup interaction or pup development.     

Dehydroepiandrosterone-sulfate (DHEAS) reduces adipocyte hyperplasia associated with feeding rats a high-fat diet

OBJECTIVE: To determine if chronic administration of a low level of dehydroepiandrosterone-sulfate (DHEAS) (10 micrograms/ml drinking water) attenuates adiposity in male Osborne-Mendel rats fed low-fat (11% of kcals) vs high fat (46% of kcals) diets. DESIGN: Rats were randomly assigned to one of four treatment groups for 6 wk in this 2 x 2 factorial study. The main effects tested were diet (low vs high fat) and DHEAS (- or +). SUBJECTS: Male Osborne-Mendel rats (initial body wt approximately 265 g). MEASUREMENTS: Adipocyte mass, size and number from two major fat depots (retroperitoneal, epididymal); mass of one subcutaneous adipose depot (inguinal); serum levels of triglycerides, insulin, glucose and DHEAS; brown adipose tissue (BAT) mass; body weight gain, food and water consumption, and residual carcass composition. RESULTS: DHEAS treatment had no effect on weight gain, food consumption or water intake. DHEAS-treated rats fed the high-fat diet had smaller fat pads containing fewer adipocytes and less carcass lipid than the non DHEAS-treated rats fed the high-fat diet. In contrast, DHEAS-treated rats fed the low-fat diet had similar levels of adipose tissue mass and cellularity compared to control animals fed the low-fat diet. CONCLUSION: Administration of a low dose of DHEAS (10 micrograms/ml or 0.8 mg/kg body wt/d) in the drinking water of young male Osborne-Mendel rats fed a high-fat diet for 6 wk reduced carcass lipid, fat depot mass and retroperitoneal and epididymal adipocyte number compared to their high-fat-fed cohorts. In this study, the antiobesity effects of DHEAS were specific to the level of dietary fat used.     

Dose- and time-dependent effects of ethanol on functional and structural aspects of the liver sinusoid in the mouse

Two experiments were conducted to investigate the factors responsible for the adverse effects of guanidinated proteins on feed intake in chickens. In Experiment 1, male broiler chicks were fed one of five purified diets containing casein or guanidinated casein (G-casein) as the sole source of protein (230 g crude protein/kg diet) from d 6 to 13 post-hatching. A casein-based diet containing 17.2 g lysine/kg, served as the control. In the experimental diets, casein was substituted by G-casein and lysine was added at 0, 5.6, 11.4 and 17.0 g/kg diet, respectively. Feed intake and weight gains of chicks fed the G-casein diet without added lysine were markedly depressed (P < 0.05), but this depression was largely overcome by additional lysine. The intake and gains of chicks fed the G-casein diet plus 17.0 g lysine/kg were lower (P < 0.05) than those fed the G-casein diet plus 11.4 g lysine/kg and this was associated with a higher plasma lysine:arginine ratio. Tissue analysis showed that homoarginine is distributed throughout body tissues following absorption. Brain lysine concentrations were lower (P < 0.05) in chicks fed diets containing G-casein without added lysine, but increased (P < 0.05) with supplemental lysine. In Experiment 2, the effect of homoarginine per se on feed intake was investigated in two short-term intake studies using 5-wk-old broiler chickens. Significant (P < 0.05) depressions in feed intake were observed within the first hour after oral administration of 400 mg homoarginine-HCl. The results suggest that both lysine deficiency and homoarginine per se were responsible for the adverse effects of guanidinated proteins on feed intake in chickens.