High beta-hydroxybutyrate concentration in liver and skeletal muscle of newly hatched chicks

Characteristic changes in ketone body concentrations in blood, liver, and skeletal muscle were investigated in detail in newly hatched chicks. The concentration of beta-hydroxybutyrate in the blood was maximal at hatch (0 day), markedly decreased to 3 days, then maintained at low levels, up to 14 days of age. The concentration of acetoacetate in blood, on the other hand, did not change after hatching but remained lower than that of beta-hydroxybutyrate at all ages. In liver and muscles, the concentration of beta-hydroxybutyrate changed in a manner similar to that in the blood. The muscle to blood ratio of the beta-hydroxybutyrate concentration on days -1 and 0 was significantly higher than those at 1 through 14 days post-hatch. These results show that newly hatched chicks have the same high ketone body concentrations in the skeletal muscle, blood and liver. It is, hence, suggested that uptake of beta-hydroxybutyrate by muscles is substantial or that ketogenesis, if any, occurs in muscles immediately before and after hatching of chicks.     

A comparative study of aldolase from human muscle and liver

Aldolase was purified from human skeletal muscle and human liver by techniques capable of processing large quantities (10-20kg) of tissue. The methods used also proved convenient for isolating aldolase on a large scale from other mammalian and avian sources. Aldolase from both human liver and muscle was crystallized; each gave two crystalline forms, depending on the conditions of crystallization. X-ray studies on the muscle aldolase crystals suggest a close structural similarity between human and rabbit muscle aldolase. Aldolases from human muscle and liver have similar pH optima and pH stability but their stability to heat treatment differs. The effect of heat on the enzymes may therefore provide an easy means of distinguishing them. The kinetic constants K(m) and k(cat.) for these aldolases are similar to other mammalian aldolases. Amino acid analyses and tryptic peptide ;mapping' show that the primary structures of the two aldolases differ greatly.     

Interindividual variations in feeding and growth in rainbow trout during restricted feeding and in a subsequent period of compensatory growth

Compensatory growth responses of rainbow trout Oncorhynchus mykiss were studied by examining food intake and growth of individual fish held within groups that were switched between regimes that involved full and restricted feeding. Restricted feeding led to marked interindividual variability in food intake, probably as a result of the establishment of feeding hierarchies. This disparity in food acquisition was reflected in highly heterogeneous growth amongst the fish fed low rations. When fish were transferred from restricted to full rations, they became hyperphagic and displayed high rates of growth. Growth compensation was most marked amongst those fish which had shown the poorest growth during the period of feed restriction. These results suggest that the feeding hierarchies established under feed restriction did not persist, but were rapidly broken down when food became increasingly available, enabling the previously suppressed fish to gain access to food and to display rapid growth.     

Anesthetic effects on liver and muscle glycogen concentrations: rest and postexercise

We compared the effects of three different anesthetics (halothane, ketamine-xylazine, and diethyl ether) on arterial blood gases, acid-base status, and tissue glycogen concentrations in rats subjected to 20 min of rest or treadmill exercise (10% grade, 28 m/min). Results demonstrated that exercise produced significant increases in arterial lactate concentrations along with reductions in arterial Pco2 (PaCO2) and bicarbonate concentrations in all rats compared with resting values. Furthermore, exercise produced significant reductions in the glycogen concentrations in the liver and soleus and plantaris muscles, whereas the glycogen concentrations found in the diaphragm and white gastrocnemius muscles were similar to those found at rest. Rats that received halothane and ketamine-xylazine anesthesia demonstrated an increase in Paco2 and a respiratory acidosis compared with rats that received either anesthesia. These differences in arterial blood gases and acid-base status did not appear to have any effect on tissue glycogen concentrations, because the glycogen contents found in liver and different skeletal muscles were similar to one another cross all three anesthetic groups. These data suggest that even though halothane and ketamine-xylazine anesthesia will produce a significant amount of ventilatory depression in the rat, both anesthetics may be used in studies where changes in tissue glycogen concentrations are being measured and where adequate general anesthesia is required.     

A comparative study of the central effects of melanocortin peptides on food intake in broiler and layer chicks

Broiler chicks eat more food than layer chicks. However, the causes of the difference in food intake in the neonatal period between these strains are not clear. In this study, we examined the involvement of proopiomelanocortin (POMC)-derived melanocortin peptides α-, β- and γ-melanocyte-stimulating hormones (MSHs) in the difference in food intake between broiler and layer chicks. First, we compared the hypothalamic mRNA levels of POMC between these strains and found that there was no significant difference in these levels between broiler and layer chicks. Next, we examined the effects of central administration of MSHs on food intake in these strains. Central administration of α-MSH significantly suppressed food intake in both strains. Central administration of β-MSH significantly suppressed food intake in layer chicks, but not in broiler chicks, while central administration of γ-MSH did not influence food intake in either strain. It is therefore likely that the absence of the anorexigenic effect of β-MSH might be related to the increased food intake in broiler chicks.     

Regulation of glycogen concentration and glycogen synthase activity in skeletal muscle of insulin-resistant rats

The aim of this study was to investigate the effect of insulin resistance on glycogen concentration and glycogen synthase activity in the red and white gastrocnemius muscles and to determine whether the inverse relationship existing between glycogen concentration and enzyme activity is maintained in insulin resistant state. These questions were addressed using 3 models that induce various degrees of insulin resistance: sucrose feeding, dexamethasone administration, and a combination of both treatments (dex+sucrose). Sucrose feeding raised triglyceride levels without affecting plasma glucose or insulin concentrations whereas dexamethasone and dex+sucrose provoked severe hyperinsulinemia, hyperglycemia and hypertriglyceridemia. Sucrose feeding did not alter muscle glycogen concentration but provoked a small reduction in the glycogen synthase activity ratio (-/+ glucose-6-phosphate) in red but not in white gastrocnemius. Dexamethasone administration augmented glycogen concentration and reduced glycogen synthase activity ratio in both muscle fiber types. In contrast, dex+sucrose animals showed decreased muscle glycogen concentration compared to dexamethasone group, leading to levels similar to those of control animals. This was associated with lower glycogen synthase activity compared to control animals leading to levels comparable to those of dexamethasone-treated animals. Thus, in dex+sucrose animals, the inverse relationship observed between glycogen levels and glycogen synthase activity was not maintained, suggesting that factors other than the glycogen concentration modulate the enzyme's activity. In conclusion, while insulin resistance was associated with a reduced glycogen synthase activity ratio, we found no correlation between muscle glycogen concentration and insulin resistance. Furthermore, our results suggest that sucrose treatment may modulate dexamethasone action in skeletal muscle.     

Clinical and biochemical effects of aflatoxin in feed ration of chicks

Aflatoxin carcinogenesis appears to relate to multiple factors. This includes bulky adduct formation at DNA guanine N-7. The process also requires more extensive physiological degradation, possibly by the toxin alone as the active principle, but in instances also involving other assaults (e.g., hepatitis B virus). Since aflatoxin carcinogenesis involves complex effects, we have undertaken to define the range of influence of this common food contaminant upon a susceptible model, the broiler-type chick. Aflatoxicosis in two treated groups was indicated by jaundice, coagulopathy, dehydration of combs and shanks, retardation of body weight, and decrease in bursa weight. Blood clotting time, hemoglobin content, erythrocyte and packed-cell volume were affected. Hepatocytes were swollen and had undergone fatty degeneration. Bile duct hyperplasia was evident. Total serum protein, alkaline phosphatase, creatine, lactate dehydrogenase, serum glutamic oxalacetic transaminase and glutamyl transpeptidase were similarly abnormal in birds receiving the contaminated (0.5 and 2.5 micrograms/g aflatoxin B1) feed rations. The aflatoxin B1 and its metabolites were isolated by HPLC from chick serum, liver and muscle.     

Changes in metabolite concentration in the plasma, liver and muscle of feed restricted Japanese quail exposed to cold.

Quail fed ad libitum and 50% ad libitum were cold exposed for several weeks, during time control quail remained at 21 degrees C. The concentration of plasma glucose, FFA, and uric acid, tissue glycogen and carcass fat content was measured at the end of the cold exposure period. Quail fed ad libitum showed no significant change in the levels of plasma and tissue metabolites, or the carcass fat content, following cold exposure. The feed consumption by the cold exposed quail increased, and the mean body weight showed little variation from that of the controls. Feed restricted quail which were cold exposed lost significantly more weight, and had a lower ranked fat content than their controls. Whereas feed restriction caused a lowering of the liver glycogen concentration in both treatment groups, muscle glycogen levels were higher than in quail fed ad libitum. However, cold exposure was not accompanied by a change in muscle and liver glycogen levels in feed restricted quail. Feed restricted quail at 21 degrees C were hypoglycaemic and hyperlipaemic compared to quail fed ad libitum, but cold exposed feed restricted quail had a much higher plasma glucose concentration than the controls. The ranked carcass fat content was inversely related to plasma FFA level in both control and cold exposed feed restricted quail. It is suggested that both a glycolytic and lipid mobilizing response to cold is obtained in quail whose body reserves are not spared from catabolism by adequate dietary nutrient absorption, and the possibility of gluconeogenesis from precursors produced by proteolysis is indicated.     

A study of inadvertent domestication selection during start‐feeding of brown trout families

A study was undertaken to compare first‐feeding mortality among 10 brown trout families fed high (100%) and low (25%) rations in replicate mixed family tanks. Microsatellite DNA profiling was used to assign individual brown trout to family of origin. At the end of the 35 day experimental period, highly significant differences in overall mortality were observed between the two treatments, and within the treatments there were highly significant differences in family mortality. Both replicates displayed similar patterns of family mortality. Notably, the distribution of mortality among families differed significantly between the two ration treatments, although this was more distinct for some families than others. No correlation between mean family egg diameter and family mortality were observed within either feeding treatment, although a significant positive correlation between mean family egg diameter and timing of family mortality was observed. It is suggested that these data indicate the existence of a genotype x environment interaction relating to feeding level during the critical start‐feeding period.     

Cytotoxic effects of the dietary flavones chrysin and apigenin in a normal trout liver cell line

Many flavonoids have been shown to possess prooxidant properties, capable of causing oxidative stress, especially at larger doses. Here, we examined the potential cell toxicity caused by exposure to the hydroxylated flavones chrysin, apigenin, luteolin and quercetin in comparison to the methylated flavones 5,7-dimethoxyflavone and 3',4'-dimethoxyflavone in normal Rainbow trout hepatocytes. The hydroxylated flavones, especially chrysin, demonstrated cell toxicity and inhibition of DNA synthesis at very low (2 microM) concentrations. The cytotoxicity of chrysin may partially be due to its metabolism by myeloperoxidase, which was shown to be present in these normal trout liver cells (164pmol/(min mg protein)). In contrast, methylated flavones showed no significant metabolism by myeloperoxidase and no signs of toxicity, even at much higher concentrations. These results may be useful for further investigations of cytotoxicity of dietary flavonoids.     

Exercise and glycogen depletion: effects on ability to activate muscle phosphorylase

Phosphorylase activation reverses during prolonged contractile activity. Our first experiment was designed to determine whether this loss of ability to activate phosphorylase by stimulation of muscle contraction persists following exercise. Phosphorylase activation by stimulation of muscle contraction was markedly inhibited in rats 25 min after exhausting exercise. To evaluate the role of glycogen depletion, we accelerated glycogen utilization by nicotinic acid administration. A large difference in muscle glycogen depletion during exercise of the same duration did not influence the blunting of phosphorylase activation. Phosphorylase activation by stimulation of contraction was more severely inhibited following prolonged exercise than after a shorter bout of exercise under conditions that resulted in the same degree of glycogen depletion. A large difference in muscle glycogen repletion during 90 min of recovery was not associated with a significant difference in the ability of muscle stimulation to activate phosphorylase, which was still significantly blunted. Phosphorylase activation by epinephrine was also markedly inhibited in muscle 25 min after strenuous exercise but had recovered completely in glycogen-repleted muscle 90 min after exercise. These results provide evidence that an effect of exercise other than glycogen depletion is involved in causing the inhibition of phosphorylase activation; however, they do not rule out the possibility that glycogen depletion also plays a role in this process.     

The effects of dietary methionine and glycine on lead toxicity in choline-deficient chicks

A 2×2×2 factorial experiment was conducted to study the effects of dietary methionine, glycine, and lead (Pb) in cholinedeficient chicks. The variables were: adequate or deficient methionine; adequate or excess glycine; and 0 or 1000 ppm lead (as Pb acetate 3H₂O). Methionine stimulated growth when added to the methionine-deficient diets, but the response was greater when supplemental glycine was present. Addition of glycine to the glycine-adequate diets stimulated growth in the presence of adequate but not deficient methionine. The patterns of response to methionine were the same at both 0 and 1000 ppm dietary Pb. Added Pb depressed growth with all diets, but the depression was greater in methionine-deficient than in methionine-adequate diets. Hepatic nonprotein sulfhydryl (NPSH) and glutathione (GSH) concentrations were increased by both supplemental methionine and lead, and the effects were additive. Glycine levels did not significantly alter NPSH and GSH concentrations. Both methionine and glycine lowered Pb concentrations in kidney, and the effects were additive. The results are consistent with previous observations that added methionine ameliorates Pb-induced growth depression with choline-adequate diets, however, this effect is not as pronounced with choline-deficient diets. The results suggest (1) that glycine is limiting for growth in choline-deficient, methionine-adequate diets, and (2) that methionine and glycine may enhance Pb detoxification by different mechanisms.

Paper No. 10213 of the Journal Series of the NC Agricultural Research Service, Raleigh, NC 27695-7601. The use of trade names implies neither endorsement of the product named nor criticism of similar products not mentioned by the NCARS.     

The effect of pre-fasting diet and water temperature on liver glycogen and liver weight in rainbow trout, Salmo gairdneri Richardson, during fasting

The effect of feeding an isocaloric and isonitrogenous trout diet that contained different levels of digestible carbohydrate (cerelose) to rainbow trout at either 10 or 15° C on liver glycogen and liver weight was determined in two fasting studies of 12 and 41 days duration. Trout fed diets with increased levels of digestible carbohydrate (HC) had significantly higher liver-body weight ratios (LW) and liver glycogen (LG) than trout reared on low digestible carbohydrate diets (HF). Both LW and LG declined in fasting trout previously fed HC diets but declined little in fasting trout previously fed HF diets. Trout reared at 10° C had higher LW and LG than trout reared at 15° C on either the HC or HF diets. During fasting, the trout reared on HC diets at 10° C required a longer period of time for the LG and LW to decline to the levels of trout reared on the low carbohydrate diets, than did trout reared on the HC diets at 15° C. The results indicate that both pre-fasting diet and water temperature can affect liver glycogen utilization and liver weight in fasting trout. Prolonged elevation of LW and LG in fasting trout could jeopardize the survival rate of stocked trout, particularly at low water temperatures.     

Creatine feeding does not enhance intramyocellular glycogen concentration during carbohydrate loading: an in vivo study by31P-and13C-MRS

The main aim of this study was to examine the hypothesis that creatine (Cr) feeding enhances myocellular glycogen storage in humans undergoing carbohydrate loading. Twenty trained male subjects were randomly assigned to have their diets supplemented daily with 252 g of glucose polymer (GP) and either 21 g of Cr (CRGP, n=10) or placebo (PL-GP, n=10) for 5 days. Changes in resting myocellular glycogen and phosphocreatine (PCr) were determined with Magnetic Resonance Spectroscopy (¹³C- and³¹P-MRS, respectively). After CR-GP, the levels of intramyocellular glycogen increased from 147±13 (standard error) mmol·(kg wet weight)^?1) to 182±17 mmol·(kg wet weight)^?1, while it increased from 134±17 mmol·(kg wet weight)^? to 182±17 mmol·(kg wet weight)^?1 after PL-GP; the increments in intramyocellular glycogen concentrations were not statistically different. The increment in the PCr/ATP ratio after CR-GP (+0.20±0.12) was significantly different compared to PL-GP (?0.34±0.16) (p<0.05). The present results do not support the hypothesis that Cr loading increases muscle glycogen storage.