Showing papers in "Journal of Nutrition in 1977"

Rat Liver Glutathione: Possible Role as a Reservoir of Cysteine

Abstract: Rat liver contains a high concentration (7-8mM) of reduced glutathione and its level changes rapidly when starving or feeding rats. We concluded that one of the functions of liver glutathione was to act as a reservoir of cysteine. When starved rats were fed a protein-free diet, the increase in liver glutathione was dependent on the amount of cysteine added to the diet. A cysteine-dependent increase of glutathione was also observed in rats fed a diet containing gelatin with cysteine, but the increase was relatively lowered compared with rats fed a protein-free diet containing the same amount of cysteine. This suppression of the increase in glutathione was observed much more clearly when the gelatin diet was fortified with tryptophan in addition to cysteine. In the presence of tryptophan, L-[35S]-cysteine in the diet appeared to be incorporated primarily into liver and serum proteins, and degradation of liver glutathione must also have been enhanced. Addition of excess cysteine to the diet masked the effects of gelatin and tryptophan, stimulated glutathione synthesis in the liver as well as incorporation of dietary cysteine into protein fractions. Prolonged starvation of rats or injection of dibutyryl-3',5'-cyclic AMP lowered the glutathione level,but the level did not decrease below 2 to 3 mM. These findings suggest that there may be at least two pools of glutathione. A labile fraction, constituting one-third to one-half the total liver glutathione, probably serves as a reservoir of cysteine which can be released by gamma-glutamyl-transferase when necessary.

Milk Production, Nitrogen Utilization and Glucose Synthesis in Lactating Cows Infused Postruminally with Sodium Caseinate and Glucose

Abstract: Four lactating Holstein cows were used in a 4 X 4 Latin Square design to determine the effects of postruminally administering sodium caseinate and/or glucose on milk production, milk composition, nitrogen utilization, amino acid utilization by the lactating mammary gland and glucose turnover rate. An 8.5% increase in milk yield and a 13.3% increase in milk protein production were obtained during infusion of sodium caseinate. No significant production responses were attributed to abomasal infusion of glucose. Arterial concentrations of most essential amino acids were increased during infusion of sodium caseinate. Uptake of phenylalanine, methionine and lysine by the mammary gland most closely paralleled their output in milk. The relative concentrations of methionine, lysine and phenylalanine in arterial plasma were considerably less than their concentrations in milk which resulted in a large percentage extraction of these amino acids by the mammary gland. If the availability of essential amino acids to the mammary gland, per se, was limiting the synthesis of milk protein, methionine, lysine and phenylalanine may have been the three amino acids most limiting. Measurements of glucose entry rate showed a trend toward increased glucose flux when either glucose, sodium caseinate or glucose plus sodium caseinate were infused abomasally. The similarity in glucose entry rates obtained during infusion of glucose and sodium caseinate suggest that the increase in milk production was not due totally to increased glucose flux resulting from sodium caseinate infusion.

Physiological responses of human adults to foods containing phosphate additives.

Abstract: An experiment was conducted to assess the physiological effects of a diet rich in foods cotaining phosphate additives. During a 4-week control period, eight adults were fed a balanced diet free of phosphate additives providing approximately 95 g protein 0.7 g Ca and 1.0 g P per day. During a subsequent 4-week period, food items containing phosphate additives were substituted for counterpart items devoid of added phosphates. This diet contained 0.7 g Ca and 2.1 g P per day. The introduction of foods containing phosphate additives was associated with intestinal distress, soft stools or mild diarrhea. These symptoms subsided in six subjects but occurred intermittently throughout the experimental period in the other two subjects. The high-phosphorus diet induced increases in serum phosphorus and urinary phosphorus and decreases in serum calcium and urinary calcium. Hydroxyproline excretion in the urine was increased and cyclic AMP excretion was elevated in six of the eight subjects. These changes are analogous to those seen in experimental animals fed high-phosphorus diets which were shown to be due to enhanced parathyroid activity (secondary hyperparathyroidism). The use of phosphate food additives is discussed with respect to their possible stimulating effect on adult bone resorption.

Lipid peroxidation in vivo during vitamin E and selenium deficiency in the rat as monitored by ethane evolution.

Abstract: Ethane evolution was monitored from vitamin E and selenium (Se)-deficient rats to determine if lipid peroxidation occurs in vivo when these rats develop fatal organ lesions. Weanling rats were fed a vitamin E and Se-deficient, or supplemented, diet for 40 to 90 days. Each was then prefasted for 4 hours and fasting was continued for 24 to 40 hours while ethane was collected. Approximately 50% of the doubly-deficient rats died as a result of fasting. Pathological signs included hematuria, lung hemorrhage, and liver necrosis. Ethane evolution increased exponentially 10 to 20 hours before death and then declined 2 hours before death. Rats that survived (at least 5 days after ethane collection) evolved 7.4+/-1.3 nmoles ethane/100 g body weight/24 hours compared to 100+/-6 for rats that died. Supplementation of the basal diet with vitamin E (200 IU/kg), Se (0.2 ppm, as Na2SeO3), or both, completely prevented mortality and reduced ethane evolution values to 0.4+/-0.2, 3.1+/-0.4, or 0.2+/-0.2, respectively. These experiments indicate that lipid peroxidation occurs in vivo as a result of vitamin E and Se deficiency, and the peroxidation process greatly accelerates during the terminal phase of the fatal disease.

Response of chick parathyroid glands to the vitamin D metabolites, 1,25-dihydroxycholecalciferol and 24,25-dihydroxycholecalciferol.

Abstract: Under conditions of chronic hypocalcemia, e.g. in vitamin D depletion, the parathyroid glands undergo marked hypertrophy and hyperplasia. Seven days of treatment ( 100 lU/day; 6.5 nmoles ) with cholecalciferol (CC) decreased parathyroid gland weight significantly from vitamin D depleted controls while increasing serum Ca from 6.3 to 8.6 mg/100 ml. 1,25-Dihydroxycholecalciferol (1.3 nmoles/day) also increased serum Ca to 8.6, but had no effect on gland weight. Both CC and 1,25dihydroxycholecalciferol stimulated the production of intestinal calcium binding protein. This same dose of 1,25-dihydroxycholecalciferol in com bination with small amounts of 24R,25-dihydroxycholecalciferol was as effective as CC in reducing parathyroid gland weight, but 24R,25-dihydroxycholecalciferol alone had no effect on gland weight or on calcium binding protein synthesis. When chicks received a twoto four-fold larger dose of 1,25-dihydroxycholecalciferol, parathyroid gland weight was sig nificantly reduced relative to vitamin D depleted controls. A time course of the action of CC indicated that 4 days treatment was sufficient for sig nificant parathyroid gland size reduction. Decreases in gland wet weight caused by CC were paralleled by decreases in dry weight, and loss of DNA and protein. It is concluded that parathyroid gland regression, involving loss of cells, occurs within a few days of treatment with vitamin D metab olites and that gland regression does not obligatorily follow an increase in serum Ca. At low doses, 1,25-dihydroxycholecalciferol requires the presence of 24R,25-dihydroxycholecalciferoI to cause gland regression (but not in testinal calcium binding protein production), whereas it is effective alone at higher doses. These results suggest that the dihy droxy lated vitamin D metabolites may play a role in modulating parathyroid gland as well as intestinal function. J. Nutr. 107: 1918-1926, 1977. INDEXING

Tannic acid and oxidized tannic acid on the functional state of rat intestinal epithelium.

Abstract: Diets containing tannic acid at the level of 3% of dry matter were fed to rats in order to ascertain the origin of fecal nitrogen and the effect of tannic acid on the intestinal mucosa. At the same time in order to explain the effect of oxidation of tannins, we administered diets containing oxidized tannic acid or tannic acid associated with an antioxidizer (sodium sulfite) at the level of 1% of dry matter. The increased excretion of sialic acid and glucosamine during ingestion of tannic acid indicated that the excess of fecal nitrogen mainly corresponds to the mucus hypersecretion observed by histology. Fecal analysis revealed perturbations in movements of water and ions. The study of the metabolic activity of isolated enterocytes and the activity of some enzymes in a homogenate of these cells showed an inhibition of oxygen consumption and succinic dehydrogenase activity. Addition of reducing agent (sodium sulfite) to the diet had little effect on the action of tannic acid; but previous oxidation of the tannin reduced the effects observed, particularly in the case of fecal nitrogen loss.

A comparison of hypocholesterolemic activity of β-sitosterol and β-sitostanol in rats

Abstract: The hypocholesterolemic activity of beta-sitosterol and its hydrogenated product, beta-sitostanol (dihydrositosterol or stigmastanol) has been compared in young male rats. When cholesterol was included in the diet, sitostanol consistently exhibited significantly greater hypocholesterolemic activity than sitosterol. There were no apparent differences in the effects of the sterol and the stanol on the concentration of liver cholesterol and triglyceride. Increases in plasma triglyceride due to feeding sitosterol were not observed with sitostanol. Incorporation of dietary sitostanol into plasma, liver and other tissues was always negligible, and thus this stanol was almost completely recovered in feces, while there was considerable deposition of sitosterol (mean fecal recovery being 85% to 92%). The increase in fecal output of dietary cholesterol was significantly greater with the stanol than with sterol. There was no demonstrable negative effect on growth and weight of major visceral tissues in rats fed the sterol as well as the stanol. These observations together with those reported previously indicate that hydorgenation of phytosterols is a novel approach to enhance their hypocholesterolemic activities without influencing the relative safety of the initial sterols.

Protection against carbon tetrachloride-induced lipid peroxidation in the rat by dietary vitamin E, selenium, and methionine as measured by ethane evolution.

Abstract: Dietary vitamin E, selenium (Se), and methionine were tested for their ability to inhibit carbon tetrachloride (CCL4)-induced lipid peroxidation. Peroxidation, in vivo, was monitored by the evolution of ethane, an autoxidation product of omega-3-unsaturated fatty acids. Weanling rats were fed a basal diet low in vitamin E, Se, and sulfur-containing amino acids, or diets individually supplemented with these factors. After 3 to 7 weeks, the rats were injected with CCL4 (ip) and ethane was collected for 9 hours. Cumulative ethane evolution was increased by CCl4 in all groups. Vitamin E, Se, and methionine reduced ethane evolution from CCl4-treated rats by 82%, 74%, and 60%, respectively. The toxicity of CCl4 was decreased in correlation with ethane evolution. Thus, methionine and Se, probably by maintaining intracellular glutathione and glutathione peroxidase, protected against CCl4-induced lipid peroxidation, as did vitamin E. Substitution of cod liver oil, which is rich in omega-3-unsaturated fat, for lard in the basal diet increased CCl4-induced ethane evolution six-fold. Relative inhibition by the dietary supplements was not changed. Thus, the feeding of cod liver oil greatly increased ethane production which facilitated the detection and measurement of lipid peroxidation in vivo.

Effect of dietary pH on amino acid utilization and the lysine requirement of fingerling channel catfish.

Abstract: The pH of amino acid test diets has been shown to be of major importance in dietary amino acid studies in the channel catfish (Ictalurus punctatus). Maximum growth rate and feed conversion was observed when the test diet was adjusted to pH 7. Growth studies, utilizing a 24% crude protein diet containing an amino acid pattern similar to whole egg protein, indicate that the lysine requirement for fingerling channel catfish is about 1.23% of the diet (dry weight basis) or 5.1% of the dietary protein. The dietary requirement was confirmed by serum free lysine analysis. A marked increase in serum free lysine occurred at a dietary lysine level of approximately 1.2% of the diet.

Sulfur amino acid requirement of channel catfish: L-methionine and L-cystine.

Abstract: Growth studies, utilizing a 24% crude protein diet containing an amino acid pattern similar to whole egg protein, indicate that the methionine requirement in the absence of cystine for fingerling channel catfish (Ictalurus punctalus) is about 0.56% of the diet (dry weight basis) or 2.34% of the dietary protein. The dietary requirement was confirmed by serum free methionine analysis. A marked increase in serum free methionine occurred at a dietary methionine level between 0.50% and 0.75% of the diet. The cystine replacement value for methionine on a mmole sulfur basis was found to be about 60%.

Malonaldehyde Content of Food

Abstract: Several types of commercially available food both cooked and uncooked were tested for the presence of the carcinogenic initiator and mutagen, malonaldehyde, which is a breakdown product of unsaturated fatty acids. The thiobarbituric acid derivative of malonaldehyde from meat extract was identified either by thin layer chromatography or by gas chromatography after silylation. Malonaldehyde was also identified directly by gas chromatography. Among the meats purchased from supermarkets, beef had the greatest amounts of malonaldehyde. Turkey and cooked chicken had high levels. Most cheeses had only small amounts of malonaldehyde. In contrast, many vegetables and fruits had either minute amounts or no malonaldehyde.

Differential Effects of Dietary Methyl Esters of Long-Chain Saturated and Polyunsaturated Fatty Acids on Rat Liver and Adipose Tissue Lipogenesis

Abstract: Four experiments were conducted to investigate what influence methyl esters of Ci«:o,Ci8:o, Ci8:i, C18:2, and Cis-.a fatty acids exert on rat liver and adipose tissue fatty acid synthesis and related enzymes when supplemented to a fat-free diet (FF). A randomized complete block design, in which rats were matched for body weight and food intake, was utilized. Rats previously adapted to a meal-eating regimen (access to food from 0900 to 1200 hours ) were fed a FF-diet for 7 days prior to the addition of the respective dietary fatty acids. In experiments 1 to 3, all esters were supplemented at a level of 3% of the daily FF-diet allotment. The apparent absorbabilities of C18:0 and Ci8:u were determined to be 40% and 35%, while values for Ci8:i, GI«^,and Ci8:3 were 88%, 87%, and 89%, respec tively. In comparison to the FF dietary treatment, polyunsaturated fatty acids (Ci8:2 and C^s) were able in three of four experiments to reduce the rate of hepatic fatty acid synthesis and the activities of hepatic fatty acid synthetase (FAS) and malic enzyme (ME). In all four experiments, glucose-6-phosphate dehydrogenase (G6PD) activity was significantly de pressed by Ci8:2 and CiR:3. Ci8:i produced an intermediate rate of in vitro liver fatty acid synthesis, but exerted no significant effect on hepatic lipo- genic enzyme activities. Adding Ci6:0 or Ci8:0 to the FF-diet had no de pressive effect on hepatic fatty acid synthesis, but Ci8;0 supplementation was associated with a significant increase in hepatic FAS, G6PD and ME activities. Neither unsaturated nor saturated fatty acids affected adipose tissue FAS, G6PD or ME activities or rates of fatty acid synthesis. The lack of influence of Ci6:u and Ci8:0 may have been partially due to their poor absorbability. Therefore, in experiment 4 a level of 7% Cieio supple mentation was compared to 3% C\g-.2or Ci8:3. This resulted in comparable amounts of fatty acid absorbed. Both Ci8:a and Cis-.a addition to the FF- diet were equally effective in significantly depressing in vivo hepatic fatty acid synthesis, and FAS, G6PD and ME activities by more than 50%. Cie:o had no suppressive action on liver fatty acid synthesis or related enzyme activities. Again adipose tissue lipogenesis remained unchanged by dietary fat treatment. These data clearly demonstrate that Ci8:2 and Ci8:3 specifically inhibit rat liver fatty acid synthesis, independent of carbohydrate intake. Under these conditions adipose tissue lipogenesis was unaffected by low levels of dietary fat regardless of the degree of unsaturation. J. Nutr. 107: 1170-1181,1977.

Influence of dietary lipid on lipogenic enzyme activities in coho salmon, Oncorhynchus kisutch (Walbaum).

Abstract: HUANGSHENG LIN, DALE R. ROMSOS,PETER I. TACK ANDGILBERT A. LE VEILLEDepartments of Fisheries and Wildlife and Food Scienceand Human Nutrition, Michigan State University,East Lansing, Michigan 48824ABSTRACT Coho salmon (Oncorhynchus kisutch), 8 to 18 months ofage, were maintained in culture tanks and were fed three semipurifieddiets. The diets contained 40% of energy from protein and 11.5%, 23%, or46% of energy from lipid. The body weight gain and food conversionfactors were similar among groups of fish fed the diets in each of thethree experiments. Wet weight of mesenteric adipose tissue increased withincreased amount of lipid in the diet; however, epaxial muscle lipid content was not influenced by the lipid content of the diet. Several hepaticand adipose tissue lipogenic enzymes (fatty acid synthetase, citrate cleavageenzyme, malic enzyme, glucose-6-phosphate dehydrogenase, 6-phospho-gluconate dehydrogenase, and NADP-isocitrate dehydrogenase) were assayed. These lipogenic enzymes exhibited high activities in liver and relatively low concentration in adipose tissue of the fish. The activities of allthe hepatic lipogenic enzymes assayed, except for NADP-isocitrate dehydrogenase, were depressed as the level of lipid in the diet was increased;however, the activities of these enzymes in mesenteric adipose tissue werenot influenced by the diets fed. The results of this study indicate thatdietary lipid depresses hepatic lipogenic enzyme activities and that theliver may be a more important site for fatty acid synthesis than is adiposetissue in coho salmon. J. Nutr. 107: 846-854, 1977.INDEXING KEY WORDS lipogenic enzymes •dietary fat •liver•adipose tissue •coho salmonFish diets are generally high in fat and process. To this end, the activities of se-low in carbohydrate (1). There is a paucity lected lipogenic enzymes were measured irof data on the ability of fish to metabolize liver and mesenteric adipose tissue of cohcreadily digestible sources of carbohydrate, salmon fed high-carbohydrate and high-For example, while the sites of conver- fat diets for several weeks.sion of dietary carbohydrate to fatty acidshave been investigated in numerous other MATERIALSAND METHODSspecies (2-11), the relative importance ofliver and adipose tissue as sites for con- Fish culture system and diets. Fresiversion of carbohydrate to fatty acids in water coho salmon (Oncorhynchus kisutcifish has not been elucidated. (Walbaum)) eggs were obtained from aiThe purpose of this report was to obtaininformation on the site of fatty acid syn- Jf! l h Em AM«MTDRR

Effects of Cellulose Added to Diets of Low and High Fiber Content upon the Metabolism of Calcium, Magnesium, Zinc and Phosphorus by Man

Abstract: Addition of 10 g of cellulose dispersed in 150 g of apple compote to the daily diet with a low fiber content for a 20-day period caused the fecal excretion of calcium and zinc of three men to increase significantly Balances of both metals became negative and their concentrations in plasma decreased Magnesium balances became negative in two subjects while phosphorus balance changed to negative in one In a similar experiment in which the cellulose was added to a fiber-rich diet, fecal excretions of calcium and zinc increased significantly in each of two men and excretion of magnesium in one Previously negative balances became more negative, and calcium and zinc concentrations decreased in plasma The dependence of fecal dry weight upon fecal fiber content measured by the acid-detergent method was confirmed However, increments of dry matter per g of fiber were less fecal fiber concentrations were high Fecal calcium content correlated significantly with fecal fiber in two subjects, and fecal fiber and zinc in one No correlations were demonstrated in the subject who apparently digested fiber most effectively Our findings indicate that high intakes of fiber can explain to a considerable extent the impaired utilization of zinc, calcium, and magnesium among villagers in rural Iran

Effects of a prolonged vitamin E deficiency in the rat.

Abstract: Rats fed a vitamin E-deficient diet containing 10% "stripped" corn oil had reduced growth rate and elevated platelet count by 12 weeks of age, and a normocytic anemia with elevated reticulocytes by 16 weeks of age. After 5 months, rats became emaciated and developed kyphoscoliosis. Some rats developed skin ulcers and tremors, and mortality was high. Neuromuscular lesions included a chronic necrotizing myopathy and localized axonal dystrophy. There was also a selective activation of lysosomes in the central nervous system microcirculation. Liver ascorbic acid of deficient rats was the same as in those receiving vitamin E. Urinary excretion of p-hydroxyphenylpyruvate after a tyrosine load was also the same in deficient and control rats. It was concluded that neither vitamin C synthesis or utilization was affected the E-deficient rats.

Potassium Requirement of the Growing Rat

Abstract: On the basis of maximum weight gain in weanling male rats fed a semipurified diet for 21 days, the requirement for potassium was found to be 0.23% of the diet. This compares with the NRC requirement of 0.18%. The higher requirement is believed to be due to the greater rate of growth, 6.6 to 7.0 g/day, compared with that obtained in older studies on which the NRC estimate was based. The higher potassium level also improved efficiency of food utilization.

Effects of the scheduling of meal-feeding at different phases of the circadian system in rats.

Abstract: This study was designed to determine whether or not a number of diverse rhythmic variables in the rat could be synchronized to meal timing. This was tested by restricting the availability of food; once during each 24-hour period an unrestricted quantity of food was made available for a 4-hour period to four different groups at different phases of the light-dark cycle, and the rhythms of the variables studied in the different groups were compared. Liver glycogen and serum glucose did synchronize to or were strongly influenced by feeding schedules; corti costerone and the several enzymes measured seemed to reflect an inter action of both the restricted feeding schedule and the light-dark cycle. The mitotic index in the corneal epithelium in all groups remained re markably synchronized to the light-dark cycle and was altered only minimally by restricted meal timing. All groups on restricted feeding schedules gained less weight than the group fed ad libitum and main tained on a light-dark cycle. These studies caution against assuming that all body functions react in the same manner to different synchronizers; and they emphasize that one must not generalize about the synchronizing effect of meal-timing or even the light-dark cycle. J. Nutr. 107: 176- 193,1977.

Role of dietary calcium and calcium binding protein in cadmium toxicity in rats.

Abstract: Growing male rats were fed a purified diet containing 0.6% Ca (two groups) or 0.1% Ca (two groups) for 8 weeks. One 0.6% Ca group and one 0.1% Ca group received 25 ppm Cd (as CdC12) in the drinking water. Diets were fed on an equalized basis with the 0.1% Ca + Cd group determining the amount of diet fed to the other groups. Water was provided ad libitum. Terminal body weights were not different among the four groups. Packed cell volumes were depressed in the Cd-exposed groups, especially the 0.1% Ca + Cd group. The highest concentrations of Cd were found in the lungs, liver, and kidneys of the 0.1% Ca + Cd group. More Cd was bound to low molecular weight proteins of the intestinal mucosa from the 0.1% Ca + Cd group than the 0.6% Ca + Cd group. Rats fed the 0.1% Ca diet appeared to have a greater capacity to absorb either Ca or Cd than rats fed the 0.6% Ca diet, as shown by an enhanced binding of 45Ca and 115mCd to intestinal calcium-binding protein (CaBP) in the rats fed the low calcium diet. A portion of the mucosal Cd was accounted for as Cd bound to metallothionein. It was concluded, based upon these experiments, that cadmium retention and signs of toxicity are enhanced by feeding low Ca diet and that the increased CaBP activity due to Ca restrictions is responsible for the increased Cd uptake observed.

Biological activity of vitamin E compounds and natural materials by the resorption-gestation test, and chemical determination of the vitamin E activity in foods and feeds.

Abstract: The biological activity of the tocopherols and tocotrienols has been re-examined by the rat resorption-gestation test. The following values have been obtained (with d,l-alpha-tocopheryl acetate = 100%): d-alpha-tocopherol 80%; d,l-alpha-tocopherol 59%; d-alpha-tocopheryl acetate 136%; d-alpha-tocotrienol 13%; d-beta-tocopherol 45%; d-beta-tocotrienol 4%; d-gamma-tocopherol 13%; d-delta-tocopherol less than 0.4%. The possibility of alpha- and gamma-tocopherol being synergists has been tested, but no significant effect was found. The antioxidants BHT and ethoxyquin were without effect on the utilization of alpha-tocopherol by the rat. After chemical determination of the tocopherols and tocotrienols in foods and mixed feeds, these biological activities were used to calculate the vitamin E activity. For two samples of margarine and two samples of mixed feed, the calculated value of the vitamin E activity after chemical determination of the tocopherols and tocotrienols was compared with the value found by direct bioassay, and reasonably good agreement was found. The authors suggest that determination of vitamin E in foods and feeds as a rule should be carried out as a chemical determination of the individual tocopherols and tocotrienols followed by a calculation of the vitamin E activity from the biological activity of the tocopherols and tocotrienols.

Adaptation of rat pancreatic amylase and chymotrypsinogen to changes in diet.

Abstract: This study represents an attempt to determine the effect of dietary protein quality and hypophysectomy on the enzymic adaptability of the pancreas in the rat. The specific enzymes studied were amylase, which was purified by immunologic techniques and chymotrypsinogen (activated), which was isolated by affinity column chromatography. Content and synthesis of each enzyme were accurately determined in relation to total pancreatic protein. When rats were fed a 64% sucrose diet (19% casein), there was a two- to three-fold increase in synthesis of amylase. However, if a poor-quality protein (gelatin, gluten, or zein) was substituted for casein, there was no increase in the synthesis of amylase in response to increased carbohydrate. When rats were fed a 19% sucrose diet (64% casein), there was a significant increase in chymotrypsinogen synthesis. Of the poor-quality proteins, gluten was the only one effective in stimulating synthesis of chymotrypsinogen. Peptides, either free or as part of a protein, were necessary for the stimulation of chymotrypsinogen synthesis. Amylase synthesis in hypophysectomized rats was considerably depressed and unresponsibe to increased carbohydrate. This effect could be partially relieved with hydrocortisone, corticosterone, or thyroxin, but not with growth hormone. Hypophysectomy had little effect on synthesis or content of chymotropsinogen.

Insulin Sensitivity and Adipose Tissue Weight of Rats Fed Starch or Sucrose Diets Ad Libitum or in Meals

Abstract: The deposition of edidymal and perirenal fat, serum insulin levels, and insulin sensitivity of epididymal fat, expressed as the insulin-stimulated production of CO2 from glucose, were determined in Wistar rats fed diets containing either 54% starch or sucrose ad libitum or pair-fed in meals Regardless of the pattern of feeding, sucrose-fed rats deposited more adipose tissue per 100 g body weight and exhibited less insulin sensitivity than did starch-fed rats Significant differences in adipose tissue weights were not always accompanied by significant differences in body weights Meal-fed rats deposited less adipose tissue and showed a greater insulin sensitivity than did ad libitum rats fed the same carbohydrate However, when changes in feeding pattern negated the difference in adipose weights there was no difference in the insulin sensitivity of the meal-fed and ad libitum-fed rats Rats consuming the sucrose diet generally exhibited significantly higher fasting serum insulin levels than did rats consuming the starch diet The serum insulin values tended to be higher in the ad libitum-fpididymal tissue from the meal-fed and starch-fed rats tended to be greater than that of the sucrose-fed or ad libitum-fed rats, respectively, suggesting differences in adipocyte composition Since obesity, insulin insensitivity, and hyperinsulinism are associated with an impairment of glucose tolerance, the observed metabolic effects of dietary sucrose are considered to be undesirable

Effect of zinc deficiency on the ultrastructure of the pancreatic acinar cell and intestinal epithelium in the rat.

Abstract: Ultrastructural changes in the pancreatic acinar cell and intestinal epithelium were studied in rats fed a zinc-deficient diet as com pared with those of pair-fed and ad libitum fed zinc-supplemented controls. The pancreatic acinar cells of zinc-deficient rats showed marked cellular alterations: a reduction in zymogen granules, rupture of zymogen granules, basal accumulation of lipid droplets, prominent lysosome-like bodies, focal degradation of the cytoplasm, and intracisternal granules within the dilated cisternae of the endoplasmic reticulum. The Golgi complex appeared in active, and nuclear pyknosis was noted. Defects in the endoplasmic reticu lum and ribosomes were shown by their presence in the foci of cytoplasmic degradation, which were subsequently subject to lysosomal digestion and degeneration. The microvilli of the intestinal epithelium in the zinc deficient rats were well organized and normal in size, demonstrating a typical geometric array when cross-sectioned. The intercellular boundaries, the junctional complexes, and the terminal web were well developed and appeared intact. However, the cell cytoplasm showed prominent cellular changes: an abundance of lysosome-like bodies, membrane-bound auto graphic vacuoles, sparse endoplasmic reticulum, a quiescent-appearing Golgi complex with tightly packed lamellae containing few vacuoles, pyknotic nuclei, and a dilated nuclear periphery. J. Nutr. A07:896-908, 1977.

Zinc excretion in young women on low zinc intakes and oral contraceptive agents.

Abstract: Zinc requirements of young women were assessed by the factorial method and whether use of oral contraceptive agents (OCAs) alters zinc endogenous losses was determined. Subjects were 10 18-26 year old women in a 35-day study. Half of the women had used a combination OCA for at least 6 months (positive OCA); the other 5 had not used an OCA for at least 6 months (negative OCA). Dietary treatment provided acceptable intakes of all nutrients except zinc iron and copper. Zinc intake averaged only .17 mg/day. By Day 36 of the test serum zinc had declined in all subjects. The mean decline was significantly greater in the positive OCA group (p less than or equal to .005) dropping nearly 40 mcg/dl or 47% of the initial value. In the negative OCA group values dropped only 21% of the initial value. Fecal zinc losses declined about 40% between Days 8-34. Urinary zinc declined about 83% in the positive OCA group and about 62% in the negative OCA group. The amount of zinc lost in sweat was greater than that excreted in the urine and feces. A 16-fold difference in dermal zinc loss was noted between the luteal and menstrual phases in the negative OCA group. These changes were due to the composition of the sweat. To replace total losses 5-8 mg of zinc/day should be adequate. The 1974 RDA allowance of 15 mg provides a wide margin of safety. Women who use OCAs do not have a different dietary requirement of zinc even though utilization of the element may be altered. Data from this study indicate that accessible zinc stores in humans are relatively small since the serum zinc levels dropped markedly after only 35 days of dietary inadequacy.

Effect of dietary amino acids, casein, and soybean trypsin inhibitor on pancreatic protein secretion in rats.

Abstract: Pancreatic enzyme output in response to various purified diets was studied in rats surgically prepared so that pancreatic secretion could be continuously collected, assayed and returned to the intestine. Intraduodenal infusion of phenylalanine and tryptophan alone did not stimulate secretion. Diets containing phenylalanine, tryptophan, a mixture of amino acids, or hydroxyzed casein, fed intragastrically, evoked a small pancreatic response that was similar to the response to a protein-free diet. intragastric infusion of a diet containing 18% casein stimulated a large initial secretion of enzyme that remained elevated throughout the 5.5 hour experiment. Addition of soybean trypsin inhibitor (SBTI) to the diet increased the pancreatic response over that due to dietary casein alone. When pancreatic juice was diverted from the intestine, the large pancreatic responses to casein or to casein + SBTI were greatly reduced and the response was similar to that of the protein-free diet.

Effect of aspartame and aspartate loading upon plasma and erythrocyte free amino acid levels in normal adult volunteers.

Abstract: Aspartame is a dipeptide (L-aspartyl-L-phenylalanyl-methyl ester) with a sweeting potential 180 to 200 times that of sucrose. Questions have been raised about potential toxic effects of its constituent amino acids, aspartate and phenylalanine when the compound is ingested in large amounts. Plasma and erythrocyte amino acid levels were measured in 12 normal subjects after administration of either Aspartame (34 mg/kg) or equimolar quantities of aspartate (13 mg/kg) in a crossover design. No changes in either plasma or erythrocyte aspartate levels were noted at any time after either Aspartame or aspartate ingestion. Plasma phenylalanine levels decrease slightly after aspartate loading, and increased from fasting levels (4.9 +/- 1 mumoles/100 ml) to 10.7 +/- 1.9 mumoles/100 ml about 45 to 60 minutes after Aspartame loading. Phenylalanine levels returned to baseline by 4 hours. Erythrocyte phenylalanine levels showed similar changes.

Analogous Effects of Zinc Deficiency and Aspirin Toxicity in the Pregnant Rat

Abstract: At or near term, zinc deficient pregnant rats are depressed and exhibit difficult and extended parturition with excessive bleeding. This investigation was designed to develop objective measures of this pathology and to apply these parameters to the assessment of possible interrelationships of zinc with aldosterone and the prostaglandins. Female rats were fed during gestation a low zinc diet based on soybean protein (less than 1 ppm Zn) or the same diet supplemented with zinc (100ppm). Some of the rats were treated with aldosterone or aspirin, a prostaglandin inhibitor. Following parturition, both body temperature and blood pressure were depressed in the zinc deficient dams. Bleeding time and blood loss were also increased. Plasma potassium value were slightly elevated, adrenal weights increased and thymus weights decreased. Aldosterone had no effect on the incidence of the postpartum illness: temperature and blood pressure were unchanged. Toxic doses of aspirin produced pathologic signs analogous to those of zinc deficiency, including extended gestation period, difficult and prolonged parturition, excess bleeding, and low blood pressure and rectal temperature. The results suggest a role for zinc in prostaglandin metabolism.