Biomedical subjects

Q R Rogers

Publications and source records attributed to Q R Rogers.

At least 55 records · Page 3Linked to original sources

PubMed1998

Taurine status in cats is not maintained by dietary cysteinesulfinic acid.

Endogenous synthesis of taurine by cats is limited. Putative precursors of taurine, cysteinesulfinic acid and cysteic acid, were fed to cats to determine whether they were utilized. Groups of five cats were depleted of taurine by a resin (Colestipol(R)) diet, then given 6 dietary treatments containing (g/kg diet): 0.0, 0.4, or 0.8 taurine; or 0.98 or 1.96 cysteinesulfinic acid, or 0.4 taurine + 1.0 cysteic acid for 12 wk. Plasma and whole blood taurine concentrations and body weights were measured weekly. Concentration of taurine in semitendinosus muscle was measured initially, after 2 wk of taurine depletion (after resin-diet), and monthly thereafter. The resin diet decreased concentrations of taurine in plasma, whole blood, and muscle to 0.20, 0.49, and 0.37 of initial values, respectively. Cysteinesulfinic acid diets resulted in no significant (P > 0.05) increase in the concentration of taurine in plasma, whole blood, or muscle, and no increased excretion of cysteinesulfinate or taurine in urine or feces. Cats fed the diets containing 1.0 g cysteic acid + 0.4 g taurine, or 0.8 g taurine/kg diet had similar concentrations of taurine in plasma, whole blood, and muscle. Aminotransferase activity for cysteinesulfinic acid in the liver and intestinal mucosa of cats and rats was higher than that for aspartic or cysteic acids. Transamination of dietary cysteinesulfinic acid to beta-sulfinylpyruvate (which spontaneously decomposes), rather than decarboxylation is postulated as the basis for no detectable conversion to taurine. In contrast, cysteic acid is reversibly transaminated to beta-sulfopyruvate which is stable and thereby is a precursor for taurine in cats.

Animals↗

PubMed1998

Neurochemical changes after imbalanced diets suggest a brain circuit mediating anorectic responses to amino acid deficiency in rats.

Amino acid-imbalanced (IMB) diets induce an acute amino acid deficiency and hypophagic responses in most animals. The neural circuits underlying these responses are unknown. To ascertain potential neural circuits involved in the recognition of IMB, we measured the concentrations of norepinephrine, dopamine, serotonin, their metabolites and 20 amino acids in 14 rat brain areas in three studies. Rats were prefed a basal diet with L-amino acids as the protein source for at least 1 wk. For the experiments, either threonine or isoleucine IMB diet was offered for 2.5 or 3.5 h. Brains were taken before (using a mildly IMB diet) or after (using moderately or severely IMB diet) food intake was significantly (P < 0.05) depressed. Brain areas were dissected and analyzed for monoamines, metabolites and amino acids. Only in the anterior piriform cortex (APC), a brain area that may contain the amino acid chemosensor, was the limiting amino acid lower in IMB groups than in controls across all of the experiments. Before the onset of the anorectic response to the IMB diets, monoaminergic activity was affected in areas that have recognized monosynaptic connections with the APC. We propose a circuit for the neural responses in the initial recognition of acute amino acid deprivation that begins with activation of the APC and includes areas in the hindbrain and hypothalamus. After a significant hypophagic response, serotonergic indicators were altered in areas of the taste pathway and the limbic system. These results suggest that different circuits mediate the initial recognition and secondary conditioned responses to IMB diets.

Amino Acids↗

PubMed1997

The potency of dietary amino acids in elevating plasma cholecystokinin immunoreactivity in cats is related to amino acid hydrophobicity.

Incomplete agreement exists on the relative potency of amino acids in stimulating endocrine secretion of cholecystokinin (CCK). Species and methodological variations have been suggested to account for the apparent inconsistencies. In the present research, the CCK-releasing potency of dietary amino acids was evaluated in cats using plasma CCK-like immunoreactivity (CCK-LI) as an indicator of CCK secretion rather than pancreatic protein and enzyme secretion, as has been used in past research. Oral-gastric administrations of a casein-simulating amino acid mixture increased (P < 0.05) plasma CCK-LI but not to the extent of that observed for casein or sodium oleate. The response in plasma CCK-LI to administrations of 50 mM solutions of amino acids was significant (P < 0.05) for tryptophan, phenylalanine, leucine, and isoleucine and the response increased linearly (P < 0.01) with increasing amino side-chain hydrophobicity. Control administrations of water and saline also evoked elevation in plasma CCK-LI, but the responses were so transient that amino acid effects were not obscured. This was substantiated by the finding of a significant linear (P < 0.001) dose response to phenylalanine administration. Cholecystokinin-8, 33 and 58 were among the CCK molecular forms identified by HPLC in plasma after administrations of phenylalanine and water. The present findings indicate that lipophilic amino acids released during digestion account for at least part of the endocrine CCK response in cats to ingested protein. The greater CCK-releasing potency observed for intact protein relative to free amino acids may have been the result of a slow digestive release of amino acids, elaboration of peptide secretogogues or protection of protease-sensitive releasing factors.

Amino Acids↗

PubMed1997

Absence of a salt (NaCl) preference or appetite in sodium-replete or depleted kittens.

Many omnivores and herbivores exhibit an appetite for sodium or salt (NaCl) solutions, but a similar sodium appetite has not been demonstrated in carnivores. The choice for or against sodium-adequate diets of sodium-replete and depleted kittens (confirmed by an elevated plasma aldosterone concentration) was examined using a two-bowl choice test. Both bowls contained purified diets, one bowl with one of various levels of sodium (as NaCl) and the other bowl a sodium-deficient diet (0.1 g Na/Kg). Neither sodium-replete nor depleted kittens showed a choice of the diet containing 2 g Na/kg over the deficient diet. Both groups of kittens showed significant aversion to a diet containing 10 g Na/kg diet, with no change in total food intake. Kittens previously exposed to a diet containing 10 g Na/kg diet appeared to have a learned aversion to sodium in subsequent choice tests. We conclude that kittens do not possess an innate sodium appetite and that a sodium appetite is not induced in sodium-depleted kittens.

Animals↗

PubMed1997

Small changes in essential amino acid concentrations alter diet selection in amino acid-deficient rats.

The rat's sensitivity to changes in the dietary limiting amino acid concentration (LAA) was examined on the basis of dietary selection. Rats were adapted to purified low protein basal (Basal) diets in which threonine (Thr) was the LAA (0.188-0.212% wt/wt of diet). In Experiment 1, rats made a clear selection for their adaptation diet over a diet containing 0.012% less threonine after 2-3 d of choice. Rats made no clear dietary selection when given a choice between their adaptation diet and a diet containing 0.012% more threonine. Experiment 2 was conducted to examine the rat's sensitivity to small decreases in the LAA concentration. Rats adapted to a 0.200% Thr-Basal diet clearly responded to decreases as small as 0.009% in the concentration of threonine and selected against the more deficient diet when given a choice between it and the 0.200% Thr-Basal adaptation diet. Because plasma and brain amino acid concentrations are important for detection of other amino acid deficiencies, these variables were measured to determine whether they were affected by such small changes in dietary amino acid concentration. In Experiments 3 and 4, rats were adapted to the 0.200% Thr-Basal diet and then fed 0.188, 0.200 or 0.212% Thr-Basal diets for 6 h, or 0.188 and 0.212% Thr-Basal for 54 h. Amino acid concentrations in plasma, prepiriform cortex and anterior cingulate cortex were not significantly different among treatments. Norepinephrine concentration in the prepiriform cortex was not affected by dietary treatment. We conclude that small decreases in LAA concentration can cause selection against the more deficient diet, but that detection of such deficiencies does not require significant changes in plasma and brain amino acid concentrations.

Amino Acids↗

PubMed1997

Dietary modulation of methotrexate-induced enteritis in cats.

OBJECTIVE: To determine effects of purified and dry expanded (complex) diets on intestinal structure and function in healthy cats and in a feline model of methotrexate-induced enteritis. ANIMALS: 19 adult specific-pathogen-free cats. PROCEDURE: Cats were randomized in groups to receive a purified diet intragastrically or a complex diet orally to meet their daily metabolizable energy requirements. After 21 days, cats received either methotrexate (MTX; 10 mg/kg of body weight, i.v., n = 12) or saline solution i.v. (n = 7), and were anesthetized 72 hours later. Celiotomy was performed for aseptic removal of mesenteric lymph nodes, full-thickness biopsy of the gastrointestinal tract, and collection of aortic and portal venous blood samples for determination of arteriovenous amino acid concentrations across the intestine. RESULTS: MTX was associated with severe enterotoxicosis in cats receiving the purified diet, as manifested by diarrhea (4 of 6 cats) and vomiting (2 of 6 cats). One cat receiving the complex diet developed mild diarrhea, and none of these cats vomited. The purified diet was associated with marked villus blunting in the proximal and distal portions of the duodenum and increased bacterial translocation (3 of 6 cats), whereas none of the cats in the complex diet group developed bacterial translocation after MTX administration. For the cats given saline solution, bacterial translocation occurred in 1 of 4 cats receiving the complex diet versus 2 of 3 cats receiving the purified diet. CONCLUSIONS: Feeding of a complex diet containing intact protein as the nitrogen source abrogated the proximal small intestinal atrophy and bacterial translocation associated with feeding an amino acid-based purified diet. CLINICAL RELEVANCE: Use of purified diets containing free amino acids as the only nitrogen source cannot be endorsed in human and animal cancer patients receiving systemic chemotherapy.

Animal Feed↗

PubMed1997

Diet-induced atherosclerosis in the domestic cat.

The domestic cat has not been used in studies of atherosclerosis, with the exception of a single study published in 1970. We have further evaluated the susceptibility of the domestic cat to diet-induced atherosclerosis, the ultimate intent being to discern the atherogenic risk due to lipoprotein lipase deficiency in an affected feline kindred with a phenotype very similar to that of the human form of this condition. We subjected a group of normal domestic cats to a moderately high-fat, cholesterol-enriched diet (30% fat and 3% cholesterol) for a period of 2 to 8 months. Plasma lipid levels were monitored monthly. At the time of killing, all organs and the entire vascular tree were removed, sectioned, processed, and stained with hematoxylin and eosin. The entire vascular tree was also stained with Movat's pentachrome and oil red O (ORO) and assessed semiquantitatively (0 to 5+/5+) and quantitatively (mean intimal area and ORO positivity, mm2). Both blood lipid measurements (total cholesterol, high-density lipoprotein-cholesterol, triglycerides, and low-density lipoprotein-cholesterol) and vessel wall lesion assessment (intimal area, mm2) were statistically elevated (p < 0.05) in the cholesterol-fed cats as compared to those on a normal diet. The highest correlations obtained between blood lipid components and vessel wall measures were the percent increase in triglyceride from base line versus the ORO measurement or foam cell grade (r = 0.86), and percent increase in triglycerides versus the intimal area in the lower abdominal aorta (r = 0.91). Similar relationships were found when the intimal area in the brachiocephalic/subclavian vessels was correlated with the absolute triglyceride values (r = 0.85) or with the percent increase in triglycerides (r = 0.83). Thus, we produced atherosclerotic lesions in the cat within 2 to 4 months on a cholesterol-enriched diet; blood lipid levels were highly correlated with lesional measurements in the vessel wall. This study will provide the basis for evaluation of the susceptibility of New Zealand lipoprotein lipase-deficient cats to diet-induced atherosclerosis.

Animal Feed↗

PubMed1996

Acid-base balance affects dietary choice in cats.

The effect of acid-base status on self-selection of dietary protein was examined in three groups of adult male cats fed 20% soybean-protein and lactalbumin diets formulated to produce acidic, neutral or alkaline status. In two experiments, cats were offered a choice between the 20% protein diets or (1) the same diet with additional protein as casein (49% total crude protein) or (2) the same diet with added soybean-protein and lactalbumin (43% crude protein). Casein contained 0.63 mmol H+/g and caused all three groups to avoid the high casein diets by day 4. The high soybean-protein-lactalbumin diets did not contain added acid but would produce some extra acid upon catabolism of the sulfur-containing amino acids. Again, all three groups avoided the high protein diets by day 4. In a third choice trial, cats adapted to three low protein diets containing appropriate electrolytes to cause neutrality, acidemia or alkalemia, were offered a choice between: neutral vs. acidic; acidic vs. neutral or basic vs. acidic. The cats chose the neutral, neutral and basic diet respectively, restoring or maintaining acid-base homeostasis for each situation. The diets producing acidosis lowered serum sodium and potassium concentrations. We conclude that cats select appropriate diets in an attempt to maintain acid-base homeostasis.

Acid-Base Equilibrium↗

PubMed1996

Maillard reaction products in purified diets induce taurine depletion in cats which is reversed by antibiotics.

The effects of heat processing (Maillard reaction) and addition of antibiotics to diets on the metabolism of taurine in adult cats were studied. Groups of four cats were given daily 22 g/kg body weight one of four purified diets based on casein and starch. All diets contained the same major ingredients as the control (diet 1), except for starch substitutions. Diet 2 was autoclaved; in diet 3, 50 g glucose replaced 50 g starch before autoclaving; in diet 4, only the casein component was autoclaved with 50 g glucose before addition to the diet. Diets were fed for 5 wk, then a mixture of antibiotics was added to all diets and they were fed for a further 5 wk. In the first (no antibiotics) period, cats given the Maillard reaction products (diets 3 and 4) had a significant depletion of plasma and whole blood taurine and had twice the fecal, but less than half the urinary total taurine excretion of control cats. The addition of antibiotics to the diets restored plasma and whole blood concentration in cats given diets 3 and 4, reduced fecal and increased urinary taurine excretion, and decreased fecal cholyltaurine hydrolase activity. These results suggest that Maillard reaction products promote an enteric flora that favors degradation of taurine and decreases recycling of taurine by the enterohepatic route.

Amidohydrolases↗

PubMed1996

Dietary antibiotics decrease taurine loss in cats fed a canned heat-processed diet.

In a crossover design, cats were fed a canned heat-processed diet (18 g dry matter/kg initial body wt) either with (+) or without (-) antibiotics [a mixture of penicillin G, procaine (25 mg/18 g diet) and tetracycline (50 mg/18 g diet)]. The (-/+) group received no antibiotics during the first 5-wk period and received antibiotics during the second 5-wk period; the (+/-) group received the reverse. Plasma, whole blood, urinary and fecal concentrations of taurine, fecal bile acid excretion and cholyltaurine hydrolase activities were measured. Consumption of antibiotics for 5 wk resulted in a lower rate of depletion of plasma taurine. Taurine concentrations decreased more over the first 5 wk in cats in the (-/+) group than in cats in the (+/-) group [from 116 +/- 26 to 26 +/- 6 mumol/L (-/+) and from 109 +/- 6 to 77 +/- 7 mumol/L (+/-) for plasma, and from 546 +/- 8 to 292 +/- 29 mumol/L (-/+) and from 560 +/- 11 to 431 +/- 20 mumol/L (+/-) for whole blood]. Urinary total taurine excretions during the 5th week were 54 mumol/d for the (-/+) group and 135 mumol/d for the (+/-) group (pooled SEM, +/- 13). Fecal total taurine excretions during the 5th week were 184 and 53 mumol/d for the (-/+) and (+/-) groups, respectively, (pooled SEM +/- 9). Most of the fecal taurine was unconjugated (free). Fecal bile acid excretions during the 5th week were 235 +/- 18 and 106 +/- 11 mumol/d for the (-/+) and (+/-) groups, respectively. Dietary antibiotics suppressed fecal cholyltaurine hydrolase activity of cats. Fecal cholyltaurine hydrolase activities during the 5th week were 279 +/- 54 and 42 +/- 10 nmol cholic acid released.min-1.g dry feces-1 in the (-/+) and (+/-) groups, respectively. After the crossover, mean values for the groups were reversed, showing that the observed changes were due to the antibiotic treatment. These results support the hypothesis that the dietary taurine requirement of cats is largely determined by the extent of microbial degradation of taurine in the gastrointestinal tract.

Amidohydrolases↗

PubMed1996

Dietary crude protein increases slightly the requirement for threonine in kittens.

Previous work indicates that the essential amino acid requirements for kittens are not positively correlated with the concentration of dietary nitrogen as they are in other species. In the studies presented here, the interaction between graded levels of threonine and dietary crude protein was investigated. Dose-response curves were generated using six 4 x 4 Latin squares. Each square represented one concentration of threonine (4.0, 5.0, 6.0, 7.0, 9.0 or 12.0 g/kg diet) and four concentrations of crude protein (150, 200, 300 and 500 g/kg diet). Food intake, weight gain, nitrogen retention and plasma amino acids were measured. There was no strong positive relationship between the threonine requirement of kittens and dietary crude protein. Increasing crude protein when threonine was limiting in the diet increased growth and food intake under some conditions, whereas under other conditions food intake and growth were decreased in a manner consistent with an amino acid imbalance response. An additional experiment was done to verify some of these findings. The requirement for threonine was found to increase from 5.0 g/kg diet at 150 and 200 g crude protein/kg diet to 6.0 g/kg diet when crude protein was 300 or 500 g/kg diet. The requirement for crude protein in the kitten appears to be between 200 and 300 g/kg diet.

Amino Acids↗

PubMed1996

Threonine is catabolized by L-threonine 3-dehydrogenase and threonine dehydratase in hepatocytes from domestic cats (Felis domestica).

Isolated hepatocytes were used to study threonine catabolism in kittens, and dietary threonine and crude protein were varied to study enzyme adaptation. Cells were isolated from 21-wk-old kittens which had been fed diets containing threonine at 4 or 8 g/kg of diet with either 200 or 500 g crude protein/kg of diet (2 x 2 factorial, n = 4/group). Production of CO2, glucose and various metabolites from [U-14C]threonine were measured. Inclusion of 10 mmol/L glycine, or glycine in combination with 10 mmol/L acetaldehyde +ethanol, in the incubation medium decreased formation of 14CO2 and [14C]glucose. At the same time, large amounts of [14C]glycine but no [14C]ethanol was formed. Inclusion of 10 mmol/L 2-ketobutyrate + 2-hydroxybutyrate decreased 14CO2 but not [14C]glucose production and resulted in the formation of [14C]2-hydroxybutyrate. Under all incubation conditions, 14CO2 and [14C]glucose production changed in response to alterations in dietary protein but not dietary threonine. It appears that threonine dehydratase and L-threonine 3-dehydrogenase, but not threonine aldolase, are active pathways for threonine metabolism in cats, and both enzymes are sensitive to levels of dietary protein.

Acetaldehyde↗

PubMed1996

Optimizing the pattern of essential amino acids as the sole source of dietary nitrogen supports near-maximal growth in kittens.

Most experiments conducted to determine the optimal essential amino acid (EAA) nitrogen to total nitrogen (E:T) ratio in rats, chicks and other species have shown that weight gain and nitrogen retention are optimal when the ratio is between 0.5 and 0.65. Two experiments were conducted to determine if weight gains of kittens fed EAA as a sole source of dietary nitrogen were equivalent to those of kittens fed a control diet that contained equal amounts of EAA and dispensable amino acids (DAA). In the first experiment, kittens fed diets that contained only EAA lost weight. Amino acid analysis of plasma showed that the concentration of methionine was 9.1 times that of controls, supporting the premise that the weight loss that occurred was the result of an adverse effect of excess methionine. Also, plasma threonine and arginine were elevated whereas proline and asparagine were very low. In the second experiment, feeding lower concentrations of methionine and arginine in a diet containing only EAA resulted in weight gains and nitrogen retention that were not significantly different from results for kittens fed the control diet (E:T ratio = 0.5). The addition of proline and asparagine to this EAA diet or their removal from the control diet did not improve or reduce weight gain or nitrogen retention. It is concluded that the decreased weight gain found in kittens (and probably other species) fed only EAA is the result of an adverse effect of excesses of methionine and possibly other EAA, and not the inability to synthesize DAA. If excesses of certain EAA are avoided, near-maximal weight gain can be achieved without any DAA in the diet.

Amino Acids, Essential↗

PubMed1996

Vitamin K deficiency in cats fed commercial fish-based diets.

Clinical signs of vitamin K deficiency have been observed in cats offered two commercial canned diets high in salmon or tuna. Some of the queens and kittens offered these diets had died while survivors had increased coagulation times. Necropsies revealed hepatic and, or, gastrointestinal haemorrhages. Coagulation times of survivors returned to normal after vitamin K therapy. The purpose of this study was to induce a vitamin K deficiency in kittens and determine the dietary requirement. Kittens were offered vitamin K-deficient purified diets containing antibiotics and, or, substances inherent in canned fish diets that may have contributed to the deficiency. Clinical signs of vitamin K deficiency were not observed, even though one purified diet contained only 4 micrograms K1/kg diet compared with 60 micrograms in the commercial tuna diet. Therefore, a minimum vitamin K requirement could not be determined using purified diets; nevertheless, canned commercial diets formulated primarily with fish should contain more than 60 micrograms K1/kg diet.

Animals↗

PubMed1995

Elevation of plasma cholecystokinin (CCK) immunoreactivity by fat, protein, and amino acids in the cat, a carnivore.

The cat requires a diet high in protein and certain nutrients that are found only in animal tissue. It is possible that secretogogues of intestinal CCK in the cat may be different from those observed in non-carnivorous species. Plasma CCK concentrations were determined in cats (n = 6) given by oral-gastric tube either casein, whey protein, corn oil, or corn starch suspended in water. CCK was measured by RIA with a tyrosine sulfate-specific, C-terminal antibody, DINO. HPLC of plasma revealed that most CCK-immunoreactivity (CCK-LI) was associated with CCK-33 and a late eluting peak, presumably CCK-58. Casein, whey protein, and corn oil increased (P < 0.05) post-administration plasma CCK-LI, and at least for casein, the effect was dose related. An amino acid mixture approximating the residue composition of casein increased plasma CCK-LI (P < 0.05), however, the increase tended to be less than that caused by casein. Evaluation of post-administration levels of plasma amino acids indicated that intact protein and amino acids in the intestinal lumen affect CCK release by different mechanisms. Collectively, the results indicated that although cats are carnivores cats and humans secrete CCK in response to the same nutrients.

Amino Acids↗

PubMed1995

Diets causing taurine depletion in cats substantially elevate postprandial plasma cholecystokinin concentration.

Excessive secretion of the intestinal hormone cholecystokinin (CCK) was postulated to cause diet-related taurine depletion in cats. To test this hypothesis, plasma CCK-like immunoreactivity (CCK-LI) was measured in cats given four diets, two purified and two canned, that contained similar concentrations of protein, fat, moisture and taurine but produced variable rates of taurine depletion. Plasma CCK-LI was measured by RIA with a tyrosine-sulfate specific, C-terminal anti-serum, validated for use in cat plasma. As indicated by measurements of taurine in whole blood and urine, a purified diet containing casein maintained body taurine, whereas the same diet containing soybean protein and a commercial canned diet preserved either by freezing or cooking depleted body taurine. Preprandial and peak postprandial plasma CCK-LI in cats given the casein-containing diet were 10.6 +/- 1.4 and 27.6 +/- 4.8 pmol/L, respectively, approximately two- to tenfold greater than those reported in humans. Integrated postprandial plasma CCK-LI was less for cats given the casein diet than cats given both forms of the canned diet; it tended to be lower in cats given the casein diet than in cats given the soy protein diet. A negative linear correlation was observed between apparent nitrogen digestibilities of the diets and integrated plasma CCK-LI. The results indicated that diets that cause taurine depletion have lower protein digestibilities and cause greater endocrine secretion of CCK than diets that maintain body taurine status.

Animals↗

PubMed1995

Dietary soybean protein decreases plasma taurine in cats.

Commercial dry and canned diets fed to cats cause approximately two- and fourfold increase in the taurine requirement, respectively, as compared with that observed for purified diets. In two experiments, the effect of source and level of protein and fiber in the diet on the concentration of taurine in plasma and whole blood of cats was studied. All diets contained 1 g taurine/kg dry matter. When a casein-based diet containing either 25% or 50% protein was given to cats for 6 wk, no difference in plasma taurine concentration was observed; however, substituting soybean protein for casein resulted in a significant (P < 0.01) decrease in plasma taurine concentration of cats in the 50% soybean protein group, but not in the 25% soybean protein group. In Experiment 2, the food intake of cats was limited [26 g dry matter/(kg body weight.d)], and the protein was 30 or 60% of the diet. Cats fed 60% soybean protein or casein diets had significantly lower plasma taurine concentrations than cats fed a 30% casein diet, with the 60% soybean protein diet causing the greater decrease. There was no effect of either 2 or 4% soybean fiber on plasma taurine concentration as compared with the same diet without the added fiber. The taurine concentration in plasma was higher (P < 0.05) in male cats than in female cats. Protein source, amount in the diet and gender did not affect the whole blood taurine concentration. Cats given diets containing 60% casein or soybean protein diets excreted a greater amount of fecal total bile acid and total taurine than cats given a 30% casein diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Nutritional Physiological Phenomena↗

PubMed1995

Serotonin3 antagonists block aversion to saccharin in an amino acid-imbalanced diet.

Conditioned taste aversion presumably plays a role in the anorectic responses to amino acid-imbalanced diets that induce acute amino acid deficiency. The serotonin3 (5-HT3) receptor antagonists, tropisetron (Trop), MDL-72222 (MDL), and ondansetron, increase intake of imbalanced amino acid diets. Therefore, we tested whether 5-HT3 receptor antagonists would block an aversion to powdered saccharin after it was included in an amino acid-imbalanced diet. Rats were given an intraperitoneal injection of Trop, MDL, or vehicle (Veh), just before introducing one of four diets: imbalanced amino acid diet +/- saccharin (Imb or ImbSac) or a balanced (corrected) diet +/- saccharin (Cor or CorSac). Subsequent aversion to saccharin was shown in preference tests using Cor and CorSac. Saccharin preference was significantly decreased (8.3% on test day 1) in the Veh/ImbSac group, but the Trop/ImbSac group's saccharin preference (57.8%) was similar to controls (49.6-70.3%); MDL also blocked the aversion to saccharin after ImbSac. This confirms previous reports of conditioned taste aversions with amino acid limitation and suggests a role for the 5-HT3 receptor in the development of these aversions.

Amino Acids↗