Effect of diet supplementation with glutamine, dihydroxyacetone, and leucine on food intake, weight gain, and postprandial glycogen metabolism of rats

OBJECTIVE: We tested the hypothesis that increasing the rate of postprandial hepatic glycogen synthesis would decrease food intake and growth rate in normal rats. METHODS: Diets supplemented with glutamine, glutamine plus dihydroxyacetone, and glutamine plus dihydroxyacetone plus leucine were administered to male Sprague-Dawley rats for 1 wk. These are combinations that have been shown to stimulate hepatic glycogen synthesis in vitro. Food intake and body weight were monitored throughout the experiment. At the end of the feeding period, rats were fed a test meal and injected with 3H2O to measure in vivo rates of glycogen and lipid synthesis. Positional analysis of the 3H incorporated into glycogen was used to determine the proportion of glycogen synthesized via pyruvate. Final levels of plasma glucose and triacylglycerol and hepatic glycogen were also measured. RESULTS: Dietary glutamine increased hepatic glycogen synthesis. Addition of dihydroxyacetone, with or without additional leucine, caused an additional increase in hepatic glycogen synthesis and increased the proportion of glycogen synthesized via pyruvate. Lipogenesis was not altered in the liver or adipose tissue. None of the dietary treatments had any effect on food intake, but the diets that contained dihydroxyacetone decreased the rate of weight gain. CONCLUSIONS: Increasing glycogen synthesis had no effect on food intake. Increasing the proportion of glycogen synthesized by the indirect pathway through pyruvate was associated with a decrease in weight gain.     

Neuropeptide Y fails to normalize food intake in zinc-deficient rats

Zinc deprivation results in decreased and cyclic food intake in rats. We determined the response of zinc-deprived rats to neuropeptide Y (NPY). In a preliminary experiment, rats were fed a low (-Zn; <1 mg/kg) or adequate zinc diet (+Zn; 100 mg/kg) for 4 days. NPY (5 or 10 microg) was then administered via an intracerebroventricular (ICV) cannula and food intake measured for 4 h. NPY stimulated food intake in all rats, but the difference in food intake due to zinc deprivation persisted. In a subsequent experiment, rats were fed the low zinc and adequate zinc diets for 4, 5 or 6 days. Food intake was suppressed in rats fed the low zinc compared to the adequate zinc diet on all of these days. When NPY (10 microg) was administered at the onset of the light cycle, the food intake was approximately 2.5-fold greater regardless of dietary zinc status, but the amount of food consumed by rats fed low zinc was approximately one-half the quantity consumed by NPY-stimulated zinc-adequate rats. NPY administered at the onset of dark failed to stimulate food intake in either dietary group although the total intake difference due to zinc status persisted. ICV administration of 5 nmol of zinc prior to NPY injection failed to correct the food intake response of the zinc-deficient rats. We conclude that the basis of the reduced food intake of zinc-deficient rats does not relate to NPY quantity or release, or to impairment of its signal transduction. There appears to be another undefined factor that limits food intake in zinc deficiency.     

Effects of the beta-agonist, cimaterol, on growth, body composition and energy expenditure in rats

1. Male Sprague-Dawley rats weighing 146.5 (SE 4.3) g were fed on a semi-synthetic diet containing 0, 25 or 150 mg cimaterol/kg for 12 d. Net changes in weight and composition of carcass, liver, heart, gastrointestinal tract, gastrocnemius plus plantaris muscles, skin and remainder were estimated by comparative slaughter. 2. Cimaterol increased protein gains in gastrocnemius plus plantaris muscles from 0.09 g in controls to 0.14 and 0.12 g in 25 and 150 mg cimaterol/kg groups respectively. Carcass protein gains increased from 6.27 g in controls to 8.00 and 7.05 g in 25 and 150 mg cimaterol/kg groups respectively. 3. Rats treated with cimaterol either gained less fat or actually lost fat from all tissues studied, whilst control rats gained fat. These changes were reflected in lower energy retention in cimaterol-fed rats. 4. Energy intake was not affected by treatment. Cimaterol increased heat production from 776 kJ/kg body-weight0.75 in controls to 863 kJ/kg body-weight0.75 in both treated groups. Gross efficiency was reduced from 17.4% in controls to 8.0 and 7.7% in rats fed on 25 and 150 mg cimaterol/kg diets respectively. 5. These results indicate that cimaterol increases protein gain at the expense of fat in rats. In addition, subcutaneous adipose tissue appears to be more sensitive than abdominal fat, whilst protein gains are particularly enhanced in skeletal muscle relative to other body tissues.     

Effects of pyruvate and dihydroxyacetone consumption on the growth and metabolic state of obese Zucker rats

Female obese Zucker rats (aged 6 wk) were randomly assigned to one of two control or one of three experimental-diet groups. Experimental diets contained 6% pyruvate (Pyr). 6% dihydroxyacetone (Dha), or 3% each pyruvate and dihydroxyacetone (Pyr-Dha). Control-group 1 was fed a normal diet ad libitum and control-group 2 was pair fed according to the experimental group with the lowest consumption. After 5 wk the rats receiving Pyr (357.5 +/- 12.7 g) were significantly lighter than pair-fed (385.9 +/- 4.9 g) and ad libitum-fed (404.3 +/- 10.1) controls. Resting oxygen consumption (mL.min-1.kg0.65) was significantly higher in Pyr-fed rats than in pair-fed controls and food-conversion efficiency was significantly decreased. Rats fed Pyr had a lower resting respiratory-exchange ratio than did ad libitum- and pair-fed controls (0.81 +/- 0.01 vs 0.88 +/- 0.01 and 0.87 +/- 0.01, respectively). Results suggest that pyruvate consumption reduced the weight gain and food-conversion efficiency of obese Zucker rats, in part by increasing resting metabolic rate and fatty acid oxidation.     

Zinc-deficient rats are insensitive to glucoprivation caused by 2-deoxy-D-glucose

Three-choice macronutrient intake studies indicate that zinc-deficient (Zn-) rats selectively decrease intake of carbohydrate. Because glucoprivic stimuli increase food intake and selection for carbohydrate, the ability of Zn- rats to respond to glucoprivation induced by 2-deoxy-D-glucose (2-DG) was tested. Rats were fed a Zn-adequate (Zn+) or Zn- diet. In part 1, rats were challenged with 0, 250, or 400 mg 2-DG/kg BW (i.p.) after zinc deficiency was established. In part 2, rats received saline or 2-DG while zinc deficiency was being induced and then after deficiency was established. Food intake was increased after injection of 2-DG to Zn+ rats; however, food intake was not higher after 2-DG administration to Zn- rats. A dose-response test for 2-DG further confirmed these results. In part 2, it was found that Zn- rats lose the response to 2-DG administration when zinc deficiency-induced anorexia begins, after 3 days of consuming a zinc-deficient diet. It appears that the ability to sense blood glucose concentrations may be impaired during zinc deficiency, and this impairment could be a part of the anorexia that develops during zinc deficiency in the rat.     

Metabolic studies in rats under glucose and glycerol loading

It has been found in rats that 40% glycerol, when added to standard diet, reduces the food intake and thus prevents weight gain. The subcutaneous application (40 mg/kg three times daily) has no effect. Under pair feeding conditions the oxygen consumption, the RQ value and body weight remain unaffected as compared with controls receiving glucose. It is concluded that reduction of body weight induced by glycerol feeding is due to reduced amount of food intake and not due to any alterations of energy metabolism.     

An interaction between hypothalamic glucagon-like peptide-1 and macronutrient composition determines food intake in rats

Glucagon-like peptide-1 (GLP-1) release in response to food ingestion has been associated with decreased food intake. In the present study, we tested the hypothesis that the feeding response to GLP-1 injection into the hypothalamic paraventricular nucleus (PVN) is influenced by the macronutrient composition of the food consumed. In the first experiment, rats were injected with GLP-1 (0.2 microg) or saline (0.5 microL) in the PVN at dark onset (1800 h), and food intake from a maintenance diet (18% protein) was measured at 1, 2 and 14 h. In Experiment 2, after GLP-1 injection, rats were fed a carbohydrate (protein-free) diet for the first 2 h or gavaged with glucose (1.4 g/5 mL). In Experiment 3, after GLP-1 injection, rats were fed a protein (50%) diet for the first 2 h, or were preloaded with egg albumin (1.0 g). In the last experiment, GLP-1 was given after corn oil gavage (2.4 g). GLP-1 injection resulted in a reduced consumption of the maintenance diet from 2 to 14 h. The decreased food intake from 2 to 14 h after GLP-1 administration occurred after carbohydrate intake, either by meal or preloads, but not after protein intake, either as a meal or preload. A transient interaction of GLP-1 with a corn oil gavage was detected but only in early feeding (0-2 h). We conclude that the effect of GLP-1 injected in the PVN on food intake is influenced by the macronutrient composition of the food consumed. Carbohydrate enhances, protein blocks and corn oil has a transient effect on the suppression of food intake caused by GLP-1 in the PVN.     

The effect of glutamine and dihydroxyacetone supplementation on food intake, weight gain, and postprandial glycogen synthesis in female Zucker rats

OBJECTIVE: We sought to test the hypothesis that increasing postprandial hepatic glycogen synthesis rate would decrease food intake and growth rate in obese Zucker rats. DESIGN: Supplements of glutamine, with and without dihydroxyacetone (DHA), which have previously been shown to stimulate hepatic glycogen synthesis, were administered in the diet of obese Zucker rats for periods of 1 and 3 wk. MEASUREMENTS: Food intake and body weight were monitored throughout the experiments. At the end of the feeding period the rats were fed a test meal and injected with (3)H(2)O to measure in vivo rates of glycogen and lipid synthesis. Final plasma glucose and triacylglycerol and hepatic glycogen content were also determined. Carcass fat and water contents were also measured in the 3-wk study. RESULTS: Dietary glutamine had no effect on food intake, weight gain, or body composition. Addition of DHA caused a reduction in food intake and weight gain and a stimulation of in vivo hepatic glycogen synthesis after 1 wk, but these changes were abolished by the end of 3 wk. Hepatic lipogenesis in vivo was increased by DHA treatment for 1 and 3 wk. CONCLUSIONS: Stimulation of hepatic glycogen synthesis by DHA treatment was associated with a reduction in food intake. However, the effect of DHA on glycogen synthesis and food intake disappeared after 3 wk of supplementation.     

Adaptation to a high-fat diet leads to hyperphagia and diminished sensitivity to cholecystokinin in rats

Rats fed high-fat (HF) diets exhibit reduced sensitivity to some peptide satiety signals. We hypothesized that reduced sensitivity to satiety signals might contribute to overconsumption of a high-energy food after adaptation to HF diets. To test this, we measured daily, 3-h intake of a high-energy, high-fat (HHF, 22.3 kJ/g) test food in rats fed either low-fat (LF) or HF, isoenergetic (16.2 kJ/g) diets. During testing, half of each group received the HHF test food (LF/HHF; HF/HHF), whereas the other half received their respective maintenance diet (LF/LF; HF/HF). Rats fed a HF diet ate more of the HHF food during the 3-h testing period than LF-fed rats (HF/HHF = 7.7 +/- 0.3 g vs. LF/HHF = 5.5 +/- 0.2 g; P = 0.003). Rats tested on their own maintenance diets had similar intakes (HF/HF = 3.2 +/- 0.2 g vs. LF/LF = 3.7 +/- 0.3 g), which were lower (P < or = 0.008) than intakes of rats tested on HHF. HHF-tested rats did not differ in body weight by the end of wk 2 of testing. In a subsequent short-term choice preference test, rats exhibited an equal relative preference for HHF irrespective of their maintenance diets (HF = 63.1%, LF = 68.1%, P = 0.29). Finally, we examined the effect of intraperitoneal NaCl or cholecystokinin (CCK)-8 (100 and 250 ng/kg) injection on 1-h food intake. Both doses of CCK significantly suppressed food intake in LF-fed rats but not HF-fed rats. These results demonstrate that chronic ingestion of a HF diet leads to short-term overconsumption of a high-energy, high-fat food compared with LF-fed cohorts, which is associated with a decreased sensitivity to CCK.     

Iron supplementation increases gentamicin nephrotoxicity in rats

Gentamicin (GM), an aminoglycoside antibiotic, can cause acute renal failure in humans and experimental animals. It has been proposed that lipid peroxidation may play a role in GM nephrotoxicity. Nutrients such as copper, selenium or iron that influence lipid peroxidation may also be a factor in toxicity. This study investigated the effect of supplemental dietary iron on the nephrotoxicity of GM. Weanling male Sprague-Dawley rats were fed control [0.75 mmol (42 mg) iron/kg] or iron-supplemented [4.32 mmol (242 mg) iron/kg] diets for 3 wk. Rats were subsequently injected intraperitoneally with GM (50 or 100 mg.kg body wt-1.d-1) or saline for 8 d. High dietary iron resulted in greater sensitivity to GM (100 mg/kg body wt) toxicity in terms of elevated urinary excretion of n-acetyl-beta-glucosaminidase (NAG) and increased mineralization, casts and megalocytes in renal tubules. After GM treatment was terminated, NAG excretion decreased with both dietary treatments. However, renal tubular cell damage, due to GM, remained higher than in saline-treated controls in rats fed 4.32 mmol iron/kg diet.     

Cadmium absorption and retention by rats fed durum wheat (Triticum turgidum L. var. durum) grain

A whole-body radioassay procedure was used to assess the retention and apparent absorption by rats of Cd in kernels of durum wheat (Triticum turgidum L. var. durum) harvested from plants grown hydroponically in 109Cd-labelled nutrient solution. Wholegrain wheat, containing 5 micromol Cd (570 microg)/kg dry weight labelled intrinsically with 109Cd, was incorporated into test meals fed to rats that had been maintained on diets containing marginally adequate, adequate or surplus levels of Zn (0.12 mmol (8 mg), 0.43 mmol (28 mg) or 1.55 mmol (101 mg) Zn/kg respectively), and either 0 or 50 g durum wheat/kg. Regardless of diet, all rats consumed about 99 % of the test meal offered. In rats fed diets without wheat, initial Cd absorption averaged 7.7, 4.6 and 2.4 % of the dose when the diet contained 0.12 mmol (8 mg), 0.43 mmol (28 mg) or 1.55 mmol (101 mg) Zn/kg diet respectively. In rats fed wheat-containing diets, initial Cd absorption averaged 3.8 and 2.6 % of the dose when dietary Zn concentration was 0.12 mmol (8 mg) and 0.43 mmol (28 mg)/kg diet respectively. The amount of Cd retained in the body at 15 d postprandial was <2 % of the dose in all rats, and decreased as Zn in the diet increased. Even at 15 d postprandial, 32 to 44 % of the Cd retained in the body was still in the gastrointestinal tract. The results show that: (1) the bioavailability to rats of Cd in wholegrain durum wheat was depressed when wholegrain wheat was part of the regular diet; (2) increased intake of dietary Zn lowered Cd absorption and retention; (3) retention of Cd in the body at 15 d postprandial from diets containing adequate Zn was <1.3 %.     

Energy metabolism in the liver of rats fed a diet contaminated with dithiocarbamates]

Young male rats, Wistar CF strain, weighing about 100 g, were fed during 14 days with a well-balanced diet, but containing either 275 p.p.m. nabame, either 600 p.p.m. thirame or 3 600 p.p.m. zinebe. The animals given the non-contaminated diet were the controls. On the evening before the experiment, they were all fasted and some of them, forced to walk during 18 hours in a restraint wheel. On the morning of the experiment, some of the rats which have not been working were placed in a cold room at + 4 degrees C, and some others were given an i.p. injection of 2,6 g glucose per kg body weight. The animals were then killed, those that received the glucose treatment 30 mn after the injection, the cold-exposed rats 90 mn after the beginning of their exposure. The redox and energy potentials of the liver tissue were determined after the enzymatic assay of the following liver metabolites : lactate, pyruvate, beta-hydroxybutyrate, acetoacetate, ATP, ADP, AMP, inorganic phosphate. The thirame group rats had the smallest body weight and the lowest food intake. All the pesticides-exposed animals has a higher liver weight than predicted by their body weight. The pesticides-containing diets decreased liver lactate concentration and the lac/pyr ratio. Thirame was the more efficient and it partly impaired the glucose induced increase of the cytoplasmic redox potential, as estimated from the variation of the lac/pyr ratio. The pesticide-containing diets also lowered the liver concentrations of beta-hydroxybutyrate, acetoacetate, and their ratio. Last the pesticides, which but slightly modified the liver contents in adenine nucleotides and inorganic phosphate in the fasting state, increased the ATP fall following cold exposure and decreased the net ATP synthesis produced by glucose administration. The thirame diet was the more efficient in our experimental conditions, the zinebe diet the least one. It was concluded in our discussion that dietary dithiocarbamates either induced a hyperthyroidic status in the animal, or acted themselves as thyroxin-like compounds, because the liver metabolism was more directed towards heat production than towards that of chemical energy available for syntheses.     

Effect of abomasal glucose infusion on alanine metabolism and urea production in sheep

The effect of abomasal infusion of glucose (120 kJ/d per kg body weight (BW)0.75, 758 mmol/d) on urea production, plasma alanine-N flux rate and the conversion of alanine-N to urea was studied in sheep offered a low-N diet at limited energy intake (500 kJ/d per kg BW0.75), based on hay and grass pellets. Glucose provision reduced urinary N (P = 0.040) and urea (P = 0.009) elimination but this was offset by poorer N digestibility. Urea-N production was significantly reduced (822 v. 619 mmol/d, P = 0.024) by glucose while plasma alanine-N flux rate was elevated (295 v. 342 mmol/d, P = 0.011). The quantity of urea-N derived from alanine tended to be decreased by glucose (127 v. 95 mmol/d) but the fraction of urea production from alanine was unaltered (15%). Plasma urea and alanine concentrations (plus those of the branched chain amino acids) decreased in response to exogenous glucose, an effect probably related to enhanced anabolic usage of amino acids and lowered urea production.     

The effect of dietary protein content and feeding level on the rate of protein deposition and energy utilization in growing Iberian pigs from 15 to 50 kg body weight

The effects of dietary protein content and feeding level on the utilization of metabolizable energy (ME) and on the rates of gain, protein and fat deposition have been studied in seventy-two Iberian pigs growing from 15 to 50 kg body weight (BW) by means of comparative slaughter experiments. The animals were fed on six diets providing 223, 192, 175, 156, 129 and 101 g crude ideal protein ( CP)/kg DM and 14.64, 14.14, 14.37, 14.80, 15.36 and 15.53 MJ ME/kg DM respectively. Each diet was offered at three levels of feeding: 0.60, 0.80 and 0.95xad libitum intake. Protein deposition (PD) increased significantly (P<0.01) with each decrease in dietary CP content and reached a maximum value (74.0 g) when the diet providing 129 g CP/kg DM (6.86 g digestible ideal protein/MJ ME) was offered at the highest feeding level. This feeding regimen resulted in average values for live-weight gain and retained energy (RE) of 559 g/d and 10.9 MJ/d respectively. RE increased significantly (P<0.001) from 480 to 626 kJ/kg BW0.75 with each decrease in dietary CP content from 192 to 129 g/kg DM. Raising the level of feed intake led to significant linear increases in PD and RE irrespective of the diet fed (P<0.001). When diets approaching an adequate supply of CP were given, the net efficiency of use of ME for growth (kw) and the maintenance energy requirements were 58.2 % and 422 kJ/kg BW0.75 per d respectively.     

Whole-body protein turnover of a carnivore,Felis silvestris catus

The cat (Felis silvestris catus) has a higher dietary protein requirement than omnivores and herbivores, thought to be due to metabolic inflexibility. An aspect of metabolic flexibility was examined with studies of whole-body protein turnover at two levels of dietary protein energy, moderate protein (MP; 20 %) and high protein (HP; 70 %), in five adult cats in a crossover design. Following a 14 d pre-feed period, a single intravenous dose of [15N]glycine was administered and cumulative excretion of the isotope in urine and faeces determined over 48 h. N flux increased (P<0.005) with dietary protein, being 56 (se 5) mmol N/kg body weight (BW) per d for cats fed the MP diet and 146 (se 8) mmol N/kg BW per d for cats fed the HP diet. Protein synthesis was higher (P<0.05) on the HP diet (75 (se 10) mmol N/kg BW per d; 6.6 (se 1) g protein/kg BW per d) than the MP diet (38 (se 5) mmol N/kg BW per d; 3.4 (se 0.4) g protein/kg BW per d). Protein breakdown was higher (P<0.05) on the HP diet (72 (se 8) mmol N/kg BW per d; 6.3 (se 0.7) g protein/kg BW per d) than the MP diet (44 (se 3) mmol N/kg BW per d; 3.9 (se 0.3) g protein/kg BW per d). Compared with other species the rate of whole-body protein synthesis in the well-nourished cat (9.7 (se 1.3) g protein/kg BW0.75 per d) is at the lower end of the range. These results show that feline protein turnover adapts to dietary protein as has been shown in other species and demonstrates metabolic flexibility. Further work is required to determine exactly why cats have such a high protein requirement.     

Previous feeding level influences plateau heat production following a 24 h fast in growing pigs

Factorial approaches to estimate energy requirements of growing pigs require estimation of maintenance energy requirements. Heat production (HP) during fasting (FHP) may provide an estimate of maintenance energy requirements. Six barrows were used to determine effects of feeding level on components of HP, including extrapolated plateau HP following a 24 h fast (FHPp). Based on a cross-over design, each pig was exposed to three feeding levels (1.55, 2.05 and 2.54 MJ metabolisable energy/kg body weight (BW)(0.60) per d) between 30 and 90 kg BW. Following a 14 d adaptation period, HP was estimated using indirect calorimetry on pigs housed individually. Dynamics of HP were recorded in pigs for 5 d during the fed state and during a subsequent 24 h fast. Metabolisable energy intake was partitioned between thermal effect of feeding (HPf), activity HP (HPa), FHPp and energy retention. Feeding level influenced (P<0.05) total HP during the fed state, HPf and activity-free FHPp (609, 644 and 729 (SE 31) kJ/kg BW(0.60) per d for low, medium and high ME intakes, respectively). The value of FHPp when expressed per kg BW(0.60) did not differ (P=0.34) between the three subsequent experimental periods. Feeding level did not (P=0.75) influence HPa. Regression of total HP during the fed state to zero metabolisable energy intake yielded a value of 489 (SE 69) kJ/kg BW(0.60) per d, which is a lower estimate of maintenance energy requirement than FHPp. Duration of adaptation of pigs to changes in feeding level and calculation methods should be considered when measuring or estimating FHPp, maintenance energy requirements and diet net energy content.     

Dietary sesame oils inhibits iron-induced oxidative stress in rats [corrected

The high stability of sesame oil against oxidative deterioration is attributed to lignans in its non-glycerol fraction. The present study evaluates the effects of feeding sesame lignans (sesamin and sesamolin) on Fe2+-induced oxidative stress in rats. Three groups, each of sixteen male weanling WNIN rats, were fed diets containing 200 g casein/kg and l00 g oil/kg (group 1, groundnut oil; group 2, sesame oil; group 3,sesame oil + sesamin (0.4 g/kg). After 45 d of feeding, eight rats from each group were injected with saline (9 g Na Cl/l, controls) intraperitoneally while the remaining eight rats were injected with 30 mg Fe2+/kg body weight as ferrous sulfate in normal saline. The animals were killed after 90 min to evaluate hepatic function and antioxidant status. Compared with those fed groundnut oil (group 1), sesame oil-fed rats(groups 2 and 3) had lower levels of hepatic thiobarbituric acid-reactive substances, serum glutamate:oxaloacetate transaminase activities and serum glutamate pyruvate transaminase activities, indicating protection against Fe-induced oxidative stress. Despite similar tocopherol levels in the three diets, hepatic a-tocopherol levels were higher in rats fed the sesame-oil diets (groups 2 and 3) compared with controls (group 1).However, activities of hepatic antioxidant enzymes (superoxide dismutase and glutathione peroxidase) were significantly (P< 0-05) increased only in rats fed higher levels of lignans (group 3). These observations suggest that sesame lignans may have sparing effects on tocopherols. The increased bioavailability of tocopherols in the presence of dietary lignans might be due to the regeneration of oxidized tocopherols. The synergistic effects of lignans with tocols has nutritional and therapeutic implications.     

Soy protein-based compared with casein-based diets fed during pregnancy and lactation increase food intake and characteristics of metabolic syndrome less in female than male rat offspring

We hypothesized that soy protein (S)-based diets fed during pregnancy and lactation increase food intake and the presence of characteristics of the metabolic syndrome to a lesser extent in female than in male rats. Soy protein- and casein (C)-based American Institute of Nutrition-93G diets were fed to 2 groups (n = 12 per group) of pregnant Wistar rats from day 3 of gestation and throughout lactation. Their effects on characteristics of metabolic syndrome and food intake regulation in female pups maintained for 15 weeks on the C diet were compared. Body weight (BW) and food intake (FI) were measured weekly. Fat pad mass was measured at birth, at weaning, and at week 15. Glucose and insulin tolerance tests were conducted at weeks 8 and 12; and systolic and diastolic blood pressures were measured at weeks 4, 8, and 12. Plasma was collected at weaning and at the end of the studies for glucose, insulin, glucagon-like peptide 1, peptide YY, and ghrelin. Food intake in response to protein preloads was measured at week 7. Feeding the S diet throughout gestation and lactation resulted in higher systolic blood pressure (P < .005), FI (P < .05), and glucagon-like peptide 1 and lower peptide YY at weaning and higher BW during weeks 11 to 15 and fat pad mass at week 15 (all Ps < .05). However, no sign of insulin resistance was found; nor was short-term FI in response to protein preloads affected. In conclusion, S- compared with C-based American Institute of Nutrition-93 G diets consumed throughout gestation and lactation increased BW and FI later and resulted in fewer characteristics of metabolic syndrome in female than in male offspring.     

Angiotensin II reduces alcohol intake and choice in water- or food-restricted rats

Two experiments were conducted to assess the effects of administration of the neuropeptide and hormone angiotensin II (AII) on ethanol intake and choice. First, 18 male Wistar rats were water deprived for 23 h and given access to 5% w/v ethanol for 30 min, followed by 30 min of access to water; food was ad lib. Following adaptation to this schedule, rats were randomly assigned to receive an IP injection of 0, 100, or 200 μg/kg of AII at either −30 or 0 min prior to ethanol access. Each AII injection decreased ethanol intake only if injected immediately before access; water and food intake were unaffected. Secondly, rats were given food daily at 2% of body weight with ad lib water and randomly assigned to receive either only water or 4% w/v ethanol ad lib on alternate days. Following adaptation, rats were randomly assigned to receive IP saline or 200 μg/kg of AII prior to presentation of a choice of ethanol or water for 1 h. AII reduced ethanol intake and increased water intake at 0–30 min after injection. Results confirm previous reports of inhibition of alcohol consumption by peripheral AII, and indicate a temporal constraint on AII's effect, which is consistent with a role as a short-term satiety factor.     

Curcumin-supplemented yoghurt improves physiological and biochemical markers of experimental diabetes

We investigated the effects of prolonged treatment of diabetic rats with curcumin-supplemented yoghurt on the physiological and biochemical changes associated with diabetes mellitus. An established metabolic cage model was used to assess these changes in three groups of streptozotocin-diabetic rats which had been administered, by gavage, curcumin blended into yoghurt in the doses of 30, 60 and 90?mg/kg body weight (BW) per d (groups DC30, DC60, DC90) for 31?d. One group of non-diabetic rats was also treated with 90?mg/kg BW per d curcumin (NDC90). Three control groups of diabetic animals received water (DW), yoghurt (DY) and insulin at 27·78?μmol/d by subcutaneous injection (DI). Also, two groups of non-diabetic animals received water (NDW) and yoghurt (NDY). Groups DI and DC90 exhibited significant falls, relative to DW and DY, in food and water intake, urine volume, glycaemia, urinary urea and glucose, proteinuria, serum TAG and activities of aspartate and alanine aminotransferases, and higher hepatic glycogen and BW. These improvements were greater in DI than in DC90. No difference was observed in the serum levels of total cholesterol or HDL-cholesterol, or in the masses of adipose and muscular tissues, between DC90 and DW or DY. Moreover, the improvements in curcumin-treated rats, relative to DW and DY, were significant and dose-dependent. The NDC90 group also showed no difference from the NDW or NDY groups, in any of the markers for diabetes. In conclusion, curcumin mixed into yoghurt at the highest dose tested exhibited anti-diabetic activity, improving significantly most of the markers assessed in this study.