Effects of dietary oyster extract on lipid metabolism, blood pressure, and blood glucose in SD rats, hypertensive rats, and diabetic rats

Oyster extract was prepared by hydrolysis of oyster protein with proteases, Aloase (a protease from Bacillus subtilis), and Pancitase (a protease from Aspergillus oryzae). Rats were fed a diet containing 20% casein (the control diet) or 15% casein and 5% oyster extract (the oyster extract diet) as the protein source. The oyster extract diet exerted a significant reduction in serum cholesterol and liver triglyceride concentrations as compared with the control diet in Sprague-Dawley (SD) rats fed cholesterol-supplemented diets for 4 weeks. The activities of cytosolic fatty acid synthase and glucose-6-phosphate dehydrogenase were significantly lower in the oyster extract group than in the control group in the liver of SD rats. Hepatic cholesterol and triglyceride concentrations were significantly lower in spontaneously hypertensive (SH) rats and Otsuka Long-Evans Tokushima Fatty (OLETF) rats, type 2 diabetic rats, fed the oyster extract diet, for 4 weeks and 4 months respectively, than in those fed the control diet in the cholesterol-free diet. Blood pressure was significantly lower in the oyster extract group than in the control group at the 2nd and 4th weeks after the beginning of feeding experimental diets in SH rats. These results suggest that oyster extract prepared by hydrolysis of oyster induces triglyceride-lowering activity in the liver through a decrease in hepatic lipogenesis in SD rats, and that it exerts the antihypertensive effect in SH rats.     

Satiety, fasting, and refeeding study of absorption in rats

In the rat, small intestine preparation was studied with the aid of our modification of Na(+)-dependent nutrient absorption short-circuit current method. In experiments on rats, it was shown that reaction of the gut to animal state changes (fasting, satiety and refeeding) depended on its medial or distal localization. Active Na+ absorption in medial part of small intestine after refeeding rose 3-6-fold depending on period of previous fasting (2 or 5 days). Two states of satiety were elucidated: when the rats were in cage with meal and after refeeding following a 5-day fasting; at least in distal small intestine, absorption of nutrients in the latter state was much higher. Fast nutrient adaptation (approximately 30 min) of absorption was revealed, second responses of short-circuit current to glyala were 3.4-fold higher than the first one: 33.4 +/- 9.7 (n = 6) and 9.9 +/- 2.9 microA/cm2 (n = 6) (P < 0.05). It is possible that increased nutrients (glucose and aminoacids) entering in mucose after the 5th day refeeding play role as a primary signal for change of animal behavior.     

Interactions among nickel,copper, and iron in rats

In two fully-crossed, three-way, two-by-three-by-three, factorially arranged experiments, female weanling rats were fed a basal diet supplemented with iron at 15 and 45 μg/g, nickel at 0, 5, and 50 μg/g, and copper at either 0, 0.5, and 5 μ/g (Expt. 1) or 0, 0.25, and 12 μg/g (Expt. 2) A gram of basal diet contained in Expt. 1 approximately 16 ng of nickel, 2.3 μg of iron, and 0.47 μg of copper; and in Expt. 2, 20 ng of nickel, 1.3 μg of iron, and 0.39 μg of copper. Expt. 1 was terminated at 11 weeks, and Expt. 2 at 8 weeks because, at those times, some rats fed no supplemental copper and the high level of nickel began to lose weight, or die from heart rupture. The findings demonstrated that relationships are complex among nickel, copper, and iron. Nickel interacted with copper and this interaction was influenced by dietary iron. Signs of copper deficiency were more severe when nickel was supplemented to the diet provided that copper deprivation was neither very severe nor mild. Iron deprivation apparently enhanced the antagonism by exacerbating copper deficiency. Signs of copper deficiency that were made more severe by nickel supplementation were depressed weight gain (Expt. 2), hematocrit (Expt. 1), hemoglobin, and plasma alkaline phosphatase activity; and elevated ratios of heart wt/body wt, kidney wt/body wt, and liver wt/body wt. Because nickel and copper have similar physical and chemical properties, the interactions between those two elements were probably the result, of isomorphous replacement of copper by nickel at various functional sites that interfered with some biological processes.     

Delayed postnatal behavioral development in spontaneously epileptic rats and tremor rats, and poor operant performance in spontaneously epileptic rats

Postnatal behavioral development and learning ability of operant performance were examined in spontaneously epileptic rats (SER: zi/zi, tm/tm), and the original tremorous mutant strains of rats, tremor rats (tm/tm) and zitter rats (zi/zi) and their controls. Before the eyes opened, the increase in body weight and the age of achieving the righting reflex on a surface were no significantly different between the SER and their littermates without epileptic seizures (SER-N: zi/zi, tm/+ or zi/zi, +/+), and between tremor rats and the original strain Kyo: Wistar rats. After the eyes opened, the increase in body weight, age of achieving the righting reflex in air and traction performance, and the development of rotarod performance, were delayed in SER and tremor rats in comparison with other groups of rats. The zitter rats were apparently inferior in their development of rotarod performance in comparison with the same zitter homozygous SER-N. Operant performance was more inferior in SER than in SER-N and in tremor rats than in Kyo: Wistar rats. The differences were much more marked between SER and SER-N than between tremor and Kyo: Wistar rats. Thus, homologous tm genes and the coexistence of homologous tm and zi genes have an inhibitory effect on postnatal behavioral development and learning ability.     

Interactions among nickel,copper, and iron in rats

In two fully crossed, three-way, two by three by three, factorially arranged experiments, female weanling rats were fed a basal diet supplemented with iron at 15 and 45 μg/g, nickel at 0, 5, and 50 μg/g and copper at 0, 0.5, and 5 μg/g (Expt. 1) or 0, 0.25, and 12 μg/g (Expt. 2). Expt. 1 was terminated at 11 weeks, and Expt. 2 at 8 weeks because, at those times, some rats fed no supplemental copper and the high level of nickel began to lose weight, or die from heart rupture. The experiments showed that nickel interacted with copper and this interaction was influenced by dietary iron. If copper deficiency was neither very severe or mild, copper deficiency signs of elevated levels of total lipids and lipid phosphorus in liver and plasma, and cholesterol in plasma, were made more severe by supplemental dietary nickel. Rats in which nickel supplementation exacerbated copper deficiency did not exhibit a depressed level of copper in liver and plasma. Also, although iron deprivation enhanced the interaction between nickel and copper, iron deprivation did not significantly depress the level of copper in liver and plasma. The findings confirmed that, in rats, a complex relationship exists between nickel, copper, and iron, thus indicating that both the iron and copper status of experimental animals must be controlled before data about nickel nutriture and metabolism can be compared among studies.     

Cholecystokinin octapeptide, proglumide, and passive avoidance in rats

Rats were conditioned to avoid a darkened chamber using electric footshock (0.25 mA for 2 sec). Cholecystokinin octapeptide (CCK-8), a CCK-8 antagonist proglumide, or 0.9% NaCl solution was injected immediately following the footshock to study the effect upon passive avoidance behavior. The passive avoidance behavior was observed one day following the conditioning footshock and treatment. CCK-8 produced a reduction of the passive avoidance latency of rats at doses ranging from 30 micrograms/kg to 500 micrograms/kg. Proglumide (5 mg/kg) was able to block the CCK-8 effect on rat passive avoidance conditioning. Proglumide by itself at a dose of 2 mg/kg decreased the latency to enter the darkened chamber. Endogenous CCK-8 activity may be involved in passive avoidance conditioning in rats.     

Metabolism of adenosine, AMP and ATP in rats

Metabolism of [14C]adenosine in a dose of 100 mg per 1 kg of mass and [14C]ATP in the equimolar quantity was studied in rats after intraperitoneal administration. Adenosine is shown to enter tissues of the liver, spleen, thymus, heart and erythrocytes where it phosphorylates into adenine nucleotides (mainly ATP) and deaminates into inosine. The content of adenosine increases for a short period in the above tissues, except for erythrocytes and plasma. The latter accumulates a considerable amount of inosine and hypoxanthine, but only traces of uric acid, xanthine and adenine nucleotides. ATP administered to rats catabolizes through the adenosine formation. The exogenic adenosine and ATP replace in tissues and erythrocytes only a slight part (1-12%) of their total adenine nucleotide pool. The content of these metabolites and ADP in the blood plasma does not change essentially under the effect of adenosine, ATP and AMP. It is shown on rats whose adenine nucleotide pool of cells is marked by the previous administration of [14C]adenine that injections of adenosine, ATP and inosine do not accelerate catabolism of adenine nucleotides in tissues and erythrocytes as well as do not increase the level of catabolism products in the blood plasma. Adenosine enhances and ATP lowers the content of cAMP in spleen and myocardium, respectively.     

Excretion of catecholamines in rats,mice and chicken

Stress assessment favours methods, which do not interfere with an animal's endocrine status. To develop such non-invasive methods, detailed knowledge about the excretion of hormone metabolites in the faeces and urine is necessary. Our study was therefore designed to generate basic information about catecholamine excretion in rats, mice and chickens. After administration of (3)H-epinephrine or (3)H-norepinephrine to male and female rats, mice and chickens, all voided excreta were collected for 4 weeks, 3 weeks or for 10 days, respectively. Peak concentrations of radioactivity appeared in one of the first urinary samples of mice and rats and in the first droppings in chickens 0.2-7.2 h after injection. In rats, between 77.3 and 95.6% of the recovered catecholamine metabolites were found in the urine, while in mice, a mean of 76.3% were excreted in the urine. Peak concentrations in the faeces were found 7.4 h post injection in mice, and after about 16.4 h in rats (means). Our study provides valuable data about the route and the profile of catecholamine excretion in three frequently used species of laboratory animals. This represents the first step in the development of a reliable, non-invasive quantification of epinephrine and norepinephrine to monitor sympatho-adrenomedullary activity, although promising results for the development of a non-invasive method were found only for the chicken.