Jun-ichi Okumura

Energy cost of whole-body protein synthesis measured in vivo in chicks

1. Energy cost of whole-body protein synthesis was measured in vivo in chicks by comparing the changes in protein synthesis and heat production after the administration of cycloheximide, an inhibitor of protein synthesis. 2. Incorporation of phenylalanine into whole-body protein fraction was promptly inhibited after the intravenous injection of cycloheximide, and the effect was sustained for at least 3 hr. 3. Both whole-body protein synthesis and total heat production were significantly reduced by the cycloheximide administration. 4. The energy cost of whole-body protein synthesis was calculated to be 5.35 kJ per g protein synthesis, and hence on a molar basis 7.52 ATPs are required per peptide bond synthesis.

Intracerebroventricular injection of mammalian and chicken glucagon-like peptide-1 inhibits food intake of the neonatal chick

Glucagon-like peptide-1 (GLP-1), structurally similar to glucagon, is synthesized from a larger precursor, preproglucagon, and has been postulated to be a novel incretin. Recently, it was reported that central administration of GLP-1 decreased food intake in rats. The amino acid sequences of GLP-1 are identical in all mammals, and chicken GLP-1 exhibits a high homology with mammalian GLP-1. The aim of this study was to elucidate whether central injection of mammalian or chicken GLP-1 inhibits food intake in the chick, and to compare their effects. Intracerebroventricular administration of mammalian and chicken GLP-1 strongly inhibited food intake of chicks. However, the suppressive effect of both GLP-1 on food intake was similar. These results show that GLP-1 with a variety of amino acid sequences may be the most potent inhibitor of food intake in the chicken.

Nitric oxide controls feeding behavior in the chicken.

To investigate the effect of nitric oxide (NO) on food intake in the chicken, L-NG-nitro-arginine methyl ester HCl (L-NNA), an inhibitor of NO synthase, was applied. When i.p. administered, L-NNA significantly inhibited the food intake of broiler chickens in a dose response manner. Food ingestion was also depressed by the i.c.v. injection of L-NNA in a dose response fashion. The effect of L-NNA was attenuated by i.c.v. administration of L-arginine. These results suggest that central NO may control feeding behavior in the chicken.

Control of postprandial hyperglycaemia by galactosyl maltobionolactone and its novel anti-amylase effect in mice.

The ability to control carbohydrate digestion is useful in the treatment of diabetes mellitus and obesity. In the present study, we examined whether recently developed 4(2)-O-beta-D-galactosyl maltobionolactone (LG2O) having anti-amylase activity is able to control postprandial blood glucose concentration in mice. In addition, we tried to determine how LG2O regulates carbohydrate delivery in the gut lumen by conducting in vivo and in vitro studies. Male non-diabetic ddY mice and KK-A(y) mice, a spontaneously diabetic strain, had free access to a carbohydrate rich diet supplemented with LG2O (3 or 10 g/kg) for 0.5 hr, and blood glucose concentration was measured. LG2O suppressed any steep increase in postprandial blood glucose concentration in both ddY and KK-A(y) mice. Corresponding to the blood glucose response, LG2O also markedly suppressed any increase in postprandial plasma insulin concentration. After ingestion of the diet, LG2O produced a 1.5-3.5 fold increase in the gut contents and reducible sugar content in the small intestine but not in the stomach. Although alpha-amylase activity in the stomach was much lower compared with the activity in the small intestine, LG2O still strongly inhibited alpha-amylase activity in the stomach. In contrast, LG2O had little or no influence on alpha-amylase activity in the proximal intestine. From the in vitro carbohydrate digestion stimulation, LG2O at 7.5 mM decreased glucose production by 75% for dextrin, 25% for alpha-starch and 60% for raw starch. In conclusion, administration of LG2O inhibits carbohydrate digestion in the gut, and produces significant improvements in both blood glucose and insulin response following ingestion as part of the diet, and this evidence provides support for its therapeutic potential in treating diabetes mellitus and obesity.

Cholinergic factors are not involved in the delayed diet passage from the crop of chicks given medium chain triacylglycerol.

The role of cholinergic mechanisms in the delayed food passage from the crop induced by medium chain triacylglycerol was investigated in the young chicken. Vagotomy altered the crop emptying of chicks given dietary long chain triacylglycerol, but did not alter it in chicks given dietary medium chain triacylglycerol. On the contrary, denervation in the cranial rete and lateral commissure of the gizzard further inhibited the food passage induced by medium chain triacylglycerol. Administration of cisapride, which induces acetylcholine release from the myenteric nerves, and atropine, a muscarinic cholinergic antagonist, both delayed crop emptying of chicks given medium chain triacylglycerol. These results demonstrate that cholinergic factors are not involved in the delayed forward movement of the food containing medium chain triacylglycerol from the crop of chicks.

Contribution of whole-body protein synthesis to basal metabolism in layer and broiler chickens.

The effect of starvation on whole-body protein synthesis and on the contribution of protein synthesis to basal metabolic rate was investigated in young chickens (Expt 1). Strain differences between layer and broiler chickens in whole-body protein synthesis and degradation rates were examined when the birds were starved (Expt 2). In Expt 1, 15-d-old White Leghorn male chickens were used, while in Expt 2 Hubbard (broiler) and White Leghorn (layer) male chickens at 14 d of age were used. They were starved for 4 d, and heat production was determined by carcass analysis after 2 and 4 d of starvation. Whole-body protein synthesis rates were measured on 0, 2 and 4 d of starvation (Expt 1), and on 0 and 4 d of starvation (Expt 2). The results showed that starving reduced whole-body protein synthesis in terms of fractional synthesis rate and the amount synthesized. Whole-body protein degradation was increased by starvation both in terms of fractional synthesis rate and the amount degraded on a per kg body-weight basis. Reduced fractional synthesis rate of protein in the whole body was accounted for by reductions in both protein synthesis per unit RNA and RNA:protein ratio. In the fed state, whole-body protein synthesis and degradation rates, whether expressed as fractional rates or amounts per unit body-weight, tended to be higher in layer than in broiler chickens. In the starved state, the difference in the rate of protein synthesis between the two strains virtually disappeared, while the degradation rates were higher in layer than in broiler birds.(ABSTRACT TRUNCATED AT 250 WORDS)

Feeding behavior in rats fed diets containing medium chain triglyceride

The effect of dietary medium chain triglyceride (MCT) on short-term food intake was compared with the effect of long chain triglyceride (LCT) in rats. Corn oil and glyceryl tricaprylate were used as LCT and MCT sources, respectively. Rats were given diets containing 200 g MCT/kg diet (MCT diet), 100 g MCT + 100 g LCT/kg diet (ML diet), or 200 g LCT/kg diet (LCT diet) in Experiment 1. Cumulative food intake was determined every h for the first 12 h, then at 2-h intervals thereafter during the subsequent 12 h. As early as 1 h after feeding, cumulative food intake significantly decreased in MCT-fed animals in a dose-dependent fashion. In Experiment 2, rats were given a choice between MCT and LCT diets for 1 h to confirm whether or not the palatability of diets was influenced by dietary fat sources. There was no difference in food intake between the two diets. In Experiment 3, the responsibility of endogenous cholecystokinin (CCK) for the difference in food intake between the two diets was investigated for 6 h by using a CCK-A receptor antagonist, Devazepide (DVZ, 1 mg/kg b. wt.). Food intake in the MCT diet and also in the LCT diet was improved by DVZ. It is concluded that the satiety, but not the palatability, is affected by carbon chain length in dietary triglyceride sources, although the responsibility of endogenous CCK is very small.

Dietary L-carnitine increases plasma insulin-like growth factor-I concentration in chicks fed a diet with adequate dietary protein level

1. The effect of L-carnitine supplemented into experimental diets with varying dietary protein concentrations (50, 200 and 400 g/kg) on body weight gain and plasma insulin-like growth factor-I (IGF-I) concentration in chicks was examined. 2. Dietary L-carnitine supplementation provided 0, 200, 500 and 1000 mg/kg. Chicks were given the diet ad libitum for 10 d. 3. When L-carnitine was provided as 500 or 1000 mg/kg, body weight gain was significantly improved in birds receiving the 200 and 400 g protein/kg diets. 4. There was an interaction between dietary L-carnitine and protein content on plasma IGF-I concentration. L-carnitine supplementation had little influence on plasma IGF-I concentrations in birds receiving the low protein (50 g/kg) diet. When dietary L-carnitine concentrations were increased from 0 to 1000 mg/kg in the adequate protein (200 g/kg) diet, plasma IGF-I concentrations were also increased. However, when dietary L-carnitine content was more than 500 mg/kg in the 400 g/kg protein group, plasma IGF-I concentration decreased with increasing dietary L-carnitine content. 5. Body weight change correlated significantly with the alteration in plasma IGF-I concentrations in chicks given diets with adequate dietary protein. 6. In conclusion, the improvement in body supplementation was achieved when chicks were given their dietary protein requirement, which may be partially explained by an increase in plasma IGF-I concentration. weight gain caused by dietary L-carnitine

Modification of energy metabolism by the presence of the gut microflora in the chicken

Whether the association with gut microflora modifies the energy metabolism of chickens was investigated by varying the metabolizable energy consumption level from zero to above the maintenance requirement in the germ-free and conventional states. Single comb White Leghorn chicks were either fasted for 3 d (Expt 1), or fed for 6 d at a fixed daily meal intake of 2, 5 or 8 g/d (Expt 2), or 5, 10 or 15 g/d (Expt 3). Changes in carcass energy deposition and heat production indicated that when no dietary energy was available the presence of the gut microflora could benefit the birds by reducing energy losses, whereas when dietary energy was supplied the efficiency of energy utilization was reduced by the presence of the gut microflora. It was concluded, therefore, that the heavy burden of the gut microflora modifies energy metabolism by exerting a buffering or a counter-productive action on the energy utilization of the chicken.

Effect of deficiencies of single essential amino acids on nitrogen and energy utilisation in chicks

1. Diets 50% deficient in single essential amino acids were fed to chicks from day 8 to day 18 after hatching to evaluate body-weight gain, food consumption, body composition, nitrogen (N) and energy utilisation. 2. Body-weight gain was reduced most severely by deficiency of isoleucine followed in decreasing order by threonine, arginine, valine, histidine, tryptophan, methionine plus cystine, phenylalanine plus tyrosine, leucine and lysine, and possible reasons for the differences are discussed. 3. Body-weight gain and food efficiency were highly correlated with food consumption but metabolisable energy value of diets was not affected by single essential amino acid deficiencies. 4. Generally N retention (N retained/N consumed) and energy retention (energy retained/energy consumed) reflected food consumption, except for a lower N retention by chicks fed on the methionine plus cystine-deficient diet and for a lower energy retention by chicks fed on the valine deficient diet. 5. The amino acid deficient in the diet was present at very low concentration in the blood plasma.