This study was undertaken to examine whether some stressful conditions affected urinary output of catecholamine of 3 and 18month-old vitamin E-deficient rats and control rats. Basal levels of urinary norepinephrine (NE) and epinephrine (E) excretion of aged vitamin Edeficient rats was 2 to 3-fold higher than those of control rats. In both groups of young rats, cold exposure, administration of insulin, and immobilization stress provoked a marked increase in urinary output of NE, E, NE and E, respectively. However, the urinary catecholamine responses to these stresses were markedly diminished in aged rats. No significant changes were observed in excretion of catecholamine during these stresses in aged rats receiving vitamin E-deficient diet. Therefore, these results suggested that the responses of sympathetic nervous activity to these stresses were significantly lowered in the chronic vitamin Edeficient rats compared to control rats.

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Whether or not factors besides hyperphagia influence cellularity of adipose tissue in gold thioglucose (GTG)-treated mice was examined. The animals were treated with GTG (800mg/kg body weight) or saline as control. Control and one of the GTG-treated groups were given a diet ad libitum and another of the GTG-treated groups was pair-fed to control. In GTG-treated group fed ad libitum, hyperphagia and obesity were observed and an enlargement in the parametrial adipose tissue was mainly due to increases both in size and number of adipocytes. The GTG-treated group became obese compared to control even if food intake was comparable. The pair-feeding failed to inhibit completely the increase of both size and number of adipocytes in the fat pads. These results suggest that other factors besides hyperphagia might influence changes of cellularity of the parametrial adipose tissue in the GTG-induced obesity.

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To study the effect of Shiitake (Lentinus edodes) and Maitake (Grifola frondosa) on hypertension, spontaneously hypertensive rats (SHR) were fed a diet containing 5% mushroom powder and 0.5 NaCl solution as drinking water for 9 weeks. The dietary mushrooms decreased the blood pressure. The plasma free cholesterol level decreased in Shiitake-fed animals, whereas in Maitake-fed animals the total cholesterol level decreased. There was no difference in the plasma triglyceride and phospholipid levels among the experimental groups. Shiitake feeding resulted in a decrease in VLDL and HDL-cholesterol whereas Maitake feeding caused a decrease in VLDL-cholesterol only. Plasma LDLcholesterol was not affected by dietary mushrooms. The results suggest that dietary mushrooms prevent blood pressure increase in hypertension.

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Forty male STD-Wistar rats, weighing about 210g on the average, were divided into two dietary groups. These were, further subdivided into the following eight groups: 1) control rats fed the normal diet (N rats: group #1), N rats treated with 0.1mg Cd (group #2), 0.5mg Cd (group #3), and 1.0mg Cd (group 114); 2)mg-deficient rats (D rats: group #5), D rats treated with 0.1mg Cd (group #6), 0.5mg Cd (group #7), and 1.0mg Cd (group #8). Before Cd treatment the rats were given the normal diet or themg-deficient diet for 14 consecutive days (day -14). Subcutaneous injection of 0.1 ml of cadmium chloride (CdCl₂) in the backs of the animals given a normal diet or amg-deficient diet at the three doses of 0.1, 0.5, and 1.0mg/kg body was performed twice a day (12h intervals) (time-zero) for 7 consecutive days and then these animals were maintained without Cd treatment for an additional period of 20 days (+28 days). Body weight gain inmg-deficient rats (D rats) was significantly decreased. The effects of Cd treatment in the rats fed the normal diet (N rats) were also significant.mg deficiency enhanced the decreased body weight gain in D rats treated with Cd on day 24 though no enhancement of the decreased food consumption in those rats was observed.mg deficiency lowered the blood pressure in rats and this response was more pronounced in D rats treated with Cd. The increased urinary Na excretion and the decreased water retention were not observed in the D rats; this response was not pronounced in the D rats treated with Cd. These results suggest that an enhancement of the decreased blood pressure in Cd-treated rats by themg deficiency is not responsible for the decreased water retention. Ca concentration in the heart and aorta of D rats was within the same range as that of N rats.mg deficiency increased Ca concentration in the heart and aorta of the D rats treated with 0.5 and 1.0mg Cd though Cd itself did not affect the Ca and ATP concentrations, Ca andmg balance (Ca/Mg), and heart weight in the heart of N rats. These results suggest thatmg deficiency may increase the overload of Ca in the heart and aorta of D rats treated with Cd, which may in turn lead to enhancement of the Cd-induced cardiotoxic effects. The decrease in urinary total Ca and Cd excretion of D rats treated with Cd may result from the increased Ca and Cd concentrations in body burden, Enhancement of Cd-Induced cardiotoxic effectes bymg deficiency may be factors for the pronounced lower blood pressure in D rats treated with Cd.

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A proteinaceous inhibitor that inhibits mammalian α-amylases was prepared from cranberry bean and examined for its reactivity with α-amylases from various origins. The cranberry bean α-amylase inhibitor (CBAI) exhibited inhibitory effects on pancreatic α-amylases from the following mammals: pig, dog, cat, horse, sheep, cow, rabbit, guinea pig, rat, and mouse. CBAI showed a maximal inhibition at pH 5.5 against porcine pancreatic α-amylase (PPA). It was confirmed by gel filtration that a complex was formed in the 1:1 ratio between CBAI and PPA when they were incubated at 37°C for 30 min at pH 5.5. A similar inhibition pattern was also observed at pH 6.9 that is optimal for the amylase reaction, but much higher concentrations of CBAI were required to give 50% inhibition at pH 6:9 than at pH 5.5. Especially, both bovine and rat α-amylases were virtually unreactive to CBAI at pH 6.9.

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The effects of dietary choline chloride and phosphatidylcholine (PC) on plasma and liver lipid levels were investigated with rats fed a choline-deficient high cholesterol diet. The plasma cholesterol level significantly increased as the dietary level of choline chloride was increased. The addition of PC to the choline-free diet also resulted in an increase in the plasma cholesterol level, but the magnitude of the increase was significantly lower than that by choline chloride. There was no difference, on the other hand, in the effect of choline chloride and PC on the plasma triglyceride level. The contents of cholesterol and triglyceride in the liver markedly decreased in rats fed a diet containing PC at a high level. The fecal excretion of neutral sterol significantly increased by the addition of PC at a high level, but not at a low level. The results indicate that the plasma cholesterol level, but not triglyceride, is differentially influenced by dietary choline chloride and PC, and that PC has both hyper and antihypercholesterolemic effects when compared with a choline-free diet and a diet supplemented with choline chloride, respectively.

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The mechanism by which the consumption of high fat, low carbohydrate diets impair glucose tolerance and decrease insulin sensitivity is poorly understood. In an attempt to clarify this question, intravenous glucose tolerance and insulin action in the liver and skeletal muscle were examined in rats after two weeks feeding of either a high fat (HF; 66% energy as fat) or a low fat (LF; 12% energy as fat) diet. Both diets had a P/S ratio (ratio of polyunsaturated to saturated fat in the diet) of 1.3. The high fat diet resulted in mild impairment of intravenous glucose tolerance. Postprandial glucose levels were elevated in the presence of a sustained insulin response. In vitro insulin-stimulated glucose utilisation was decreased significantly in soleus muscle of HF rats, as indicated by decreased [¹⁴C] glucose incorporation into muscle glycogen. In contrast, muscle lipogenesis from glucose was not affected by dietary composition. There was no difference in insulin binding to soleus muscle of HF and LF rats, indicating a dissociation between insulin receptor binding and postreceptor metabolic events. Dietary composition did not influence the incorporation of increasing [¹⁴C] glucose loads into muscle glycogen or lipid in vivo. However, the HF diet was associated with reduced incorporation of [¹⁴C] glucose into lipids and glycogen in the liver and, to a smaller extent, reduced incorporation into adipose tissue lipids in vivo- These results suggest that the mechanism by which HF diets impaired glucose tolerance was mainly hepatic in origin. Decreased glucose uptake, secondary to reduced glucokinase activity, may result in a reduction in glucose utilisation in the liver.

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