Immune function and serum vitamin D in shelter dogs: A case-control study.

This study sought to establish a baseline understanding of immune function and its association with serum vitamin D in shelter dogs. Ten apparently healthy shelter dogs housed in the Arizona Humane Society for ≥7 days and 10 apparently healthy, age, breed, and sex-matched control dogs were included. Serum 25-hydroxyvitamin D (25[OH]D), the major circulating vitamin D metabolite, was measured using high performance liquid chromatography. Whole blood samples were stimulated with lipopolysaccharide (LPS), lipoteichoic acid, or phosphate buffer solution, and tumor necrosis factor (TNF)-ɑ, interleukin (IL)-6, and IL-10 were measured using a canine-specific multiplex bead-based assay. Phagocytosis of opsonized-Escherichia coli and E. coli-induced oxidative burst were evaluated with flow cytometry. Shelter dogs had decreased percentages of granulocytes and monocytes (GM) that had phagocytized opsonized-E coli (P = 0.019) and performed E. coli-induced oxidative burst (P = 0.011). There were no significant differences in TNF-α, IL-6, IL-10, or 25(OH)D concentrations between shelter and control dogs. Serum 25(OH)D concentrations had a weak positive association with the intensity of GM E. coli-induced oxidative burst (r2 = 0.23, P = 0.03). There was a moderate inverse association between serum 25(OH)D concentration and LPS-stimulated TNF-ɑ production in shelter dogs (r2 = 0.40, P = 0.04). These results demonstrate immune dysregulation in vitro in shelter dogs housed for ≥7 days when compared to age, breed, and sex-matched control dogs. While serum 25(OH)D concentrations did not differ between shelter and control dogs, significant associations between 25(OH)D concentration and immune function parameters in vitro were identified.

Effect of increasing taurine and methionine supplementation on urinary taurine excretion in a model insectivore, the giant anteater (Myrmecophaga tridactyla).

The giant anteater (Mymercophaga tridactyla) is a highly specialized insectivore for which nutrient requirements are not clearly established, making diet formulation challenging for this species. Multiple clinical reports suggest anteaters have an obligate dietary taurine (TAU) requirement. Sulphur amino acid (SAA) metabolism in adult anteaters was evaluated using noninvasive methods to measure TAU synthesis potential from dietary methionine (MET) and a basal diet containing on a dry matter (DM) basis 1.7 mg TAU/kg DM and 6.9 g MET/kg DM. Urinary equilibrium times for TAU excretion were determined by feeding the basal diet with or without 1.5 g/kg DM supplemental TAU (crossover design; n = 4). Effects of supplemental dietary TAU (1.7, 2.0, 2.4, 2.7, 3.0, 3.3 g/kg DM) or MET (6.9, 9.0, 11.2 g/kg DM) on urinary TAU were evaluated (randomized block trials; n = 5 or 4 respectively). All urinary values (TAU, MET, unbound inorganic sulphate) were normalized to creatinine (CRT). Results indicate urinary TAU equilibrium in anteaters requires at least 2 weeks of feeding. Urinary ratio of TAU to CRT (TAU:CRT) increased as dietary TAU content increased from 1.7 to 3.0 g/kg DM, consistent with renal homoeostatic modulation of TAU excretion. Our data indicate that TAU needs were met by TAU in the basal diet or by de novo synthesis. Supplemental MET resulted in ~five- to eightfold increases in urinary TAU:CRT excretion, further supporting existence of mechanisms for TAU synthesis from dietary SAA in anteaters. Adult anteaters appear able to synthesize TAU when diets contain adequate SAA, but dietary TAU may be critical if protein intakes are low or of poor quality. This study may provide guidance on choice of domestic canids vs. felids as suitable physiologic models for improved nutrition in giant anteaters, and also outlines a noninvasive method for assessing TAU status/metabolism that may be useful across species.

Hemodynamic and biochemical alterations in dogs with lymphoma after induction of chemotherapy.

BACKGROUND: Doxorubicin is a common antineoplastic agent with dose-dependent cardiotoxic adverse effects, and pre-existing myocardial dysfunction is a contraindication to its use. OBJECTIVES: To systematically define the hemodynamic and biochemical alterations in dogs undergoing chemotherapy for newly diagnosed lymphoma and assess the reversibility of these alterations with fluid administration. ANIMALS: Twenty-one client-owned dogs with newly diagnosed lymphoma were evaluated 1 week after induction of chemotherapy. Underlying degenerative valve disease was exclusionary. Eighteen healthy age- and weight-matched dogs were used as controls. METHODS: Physical examination, blood pressure by Doppler, echocardiography, and biochemical evaluation (routine serum biochemistry, plasma renin activity and aldosterone concentrations, plasma and urine osmolalities, and urine electrolyte concentrations) were measured in dogs with lymphoma and compared to controls. Dogs with lymphoma received crystalloids IV at 6 mL/kg/h for 24 hours. All variables were reassessed at 4 and 24 hours. Deuterium oxide dilution and bromide dilution were used to determine total body water and extracellular water space, respectively. RESULTS: Baseline echocardiograms showed significantly smaller chamber dimensions in dogs with lymphoma compared to controls. These changes were reversed by fluid administration. Systolic blood pressure and urine sodium concentration were significantly increased, and bromide dilution space, PCV, urine specific gravity, and urine potassium concentration were significantly decreased compared to controls. CONCLUSION AND CLINICAL IMPORTANCE: Echocardiographic and biochemical abnormalities in dogs with lymphoma appear consistent with volume depletion, and may be the result of systemic hypertension and subsequent pressure natriuresis.

Age and body weight effects on glucose and insulin tolerance in colony cats maintained since weaning on high dietary carbohydrate.

High dietary carbohydrate is suggested to promote development of diabetes mellitus in cats. Glucose tolerance, insulin sensitivity, and insulin secretion were assessed in young [0.8-2.3 (median = 1.1) years, n = 13] and mature [4.0-7.0 (median 5.8) years, n = 12] sexually intact females of a large (n ≅ 700) feline colony in which only dry-type diets (35% metabolizable energy as carbohydrate) were fed from weaning. Insulin sensitivity was assessed from the 'late-phase' (60-120 min) plasma insulin response of intravenous glucose tolerance tests (IVGTTs) and from fractional change in glycaemia from baseline 15 min after an insulin bolus (0.1 U/kg, i.v.). Insulin secretion was assessed from the 'early-phase' (0-15 min) plasma insulin response of IVGTTs. Compared to the young cats, the mature cats had greater body weights [2.3-3.8 (median = 2.9) vs. 3.0-6.3 (median = 4.0) kg, p < 0.01], greater late-phase insulin responses (p < 0.05), lower insulin-induced glycaemic changes (p = 0.06), lower early-phase insulin responses (p < 0.05), and non-significantly different rates of glucose disposal. The late-phase insulin response was correlated with body weight and age (p < 0.05). When group assignments were balanced for body weight, the age-group differences and correlations became non-significant. The findings indicate that body weight gain is more likely than dry-type diets to induce the pre-diabetic conditions of insulin resistance and secretion dysfunction.

Oestradiol, but not genistein, inhibits the rise in food intake following gonadectomy in cats, but genistein is associated with an increase in lean body mass.

The prevalence of obesity in domestic cats is increasing worldwide, and is strongly associated with gonadectomy. We have previously demonstrated the effectiveness of oestradiol in reducing food intake in both male and female neutered cats. This experiment was designed to test the hypothesis that oestradiol or genistein would prevent the increase in food intake following gonadectomy of male and female cats, and would prevent an increase in body fat mass. Three groups of eight cats each were surgically neutered then treated daily with either 0.5 mug oestradiol subcutaneously, 100 mg/kg genistein orally, or vehicle only. Effect of treatment on food intake, vaginal cytology and body weight were recorded, and body composition was assayed using the D(2)O isotopic dilution method. Neutering was followed by an increase in food intake, bodyweight and body fat mass in the control group, which were almost completely prevented by treatment with oestradiol (p < 0.001). Treatment with genistein had no effect on food intake or bodyweight increase, but was associated with a significant increase in lean body mass (p = 0.018), and significantly less body fat accumulation than the control group (p = 0.01). There were no significant differences in responses to treatment between sexes. These findings demonstrate the importance of gonadal oestrogen for the control of food intake in male and female cats, and suggest the provision of an oestrogenic compound could help prevent obesity following neutering. In addition, the findings of this study are consistent with observations in rodents of the efficacy of genistein in inhibiting adipogenesis and promoting lean body tissue development.

The bioavailability and disposition kinetics of genistein in cats.

The absorption and disposition kinetics of the soy isoflavone genistein were determined in cats (n = 6). An oral dose of 100 mg/kg was administered, which has previously been demonstrated to be the minimum oral estrogenic dose, and was administered intravenously at a dose of 20 mg/kg, being the largest practical dose that could be safely administered. Plasma free, and total (conjugated + free) genistein concentrations were determined by HPLC following organic extraction. Noncompartmental analysis revealed a half-life of 21.67 +/- 7.9 h (free) and 9.95 +/- 2.7 h (conjugated), volume of distribution 31.94 +/- 10.38 L/kg (free) and 11.82 +/- 3.96 L/kg (conjugated) following intravenous administration. Following oral administration the half-lives were determined to be 17 +/- 4.8 h (free) and 8.56 +/- 4.65 h (conjugated), with tmax = 4.4 +/- 0.6 h (free) and 4.42 +/- 0.99 h (conjugated), and Cmax = 0.276 +/- 0.1 microg/mL (free) and 6.24 +/- 6.58 microg/mL (conjugated). Oral bioavailabilities were 1.379 +/- 0.9% (free) and 29.85 +/- 22.61% (conjugated). The ratio of total:free genistein ranged from 25.9 to 5.5. Poor oral absorption and efficient conjugation explain the low bioavailability of free genistein. Accumulation of genistein in peripheral lipophilic compartments may occur.

Oestradiol and genistein reduce food intake in male and female overweight cats after gonadectomy.

AIM: To determine if exogenous oestradiol or the phyto-oestrogen genistein could reduce food intake in male and female cats fed ad libitum that had been allowed to accrue excessive bodyfat following neutering. METHODS: Sixteen adult (eight female, eight male) cats were neutered and allowed to increase their bodyweight (BW) through feeding ad libitum of a complete and balanced dry diet. Oestradiol was injected subcutaneously for 5-day periods in incremental doses (0.25-4 microg per cat), then food intake was recorded, and vaginal cytological changes were observed in females. Similarly, genistein was administered orally for 5-day periods in incremental doses (5-100 mg/kg). RESULTS: In males and females, both oestradiol (p<0.001) and genistein (p=0.037) significantly reduced food intake during treatment, and the minimum daily doses that produced a significant effect were 0.5 mug and 100 mg/kg, respectively. The minimum daily dose of oestradiol that produced a significant effect on food intake was not associated with changes in vaginal cytology over the 5-day treatment period. CONCLUSIONS AND CLINICAL RELEVANCE: Gonadal oestradiol appeared to be a key modulator of food intake in both male and female cats, and replacement of oestrogen to neutered cats via oestradiol or an oestrogen surrogate such as genistein has potential for reducing the prevalence of obesity in neutered cats.

Elevation of plasma cholecystokinin concentration following a meal is increased by gonadectomy in male cats.

An overweight or obese body condition commonly develops after gonadectomy (GX) in domestic cats. The cause appears to be a rapid, quantal (approximately 12%), increase in food intake that is sustained and probably mediated by withdrawal of gonadal hormone. Recently, an interaction of gonadal hormone and cholecystokinin (CCK) effectiveness has been suggested. A reduction in the satiating potency of intestinal CCK was presently hypothesized to contribute to the disturbance of food intake control caused by GX in domestic cats. Pre- and post-prandial intestinal CCK secretion as indicated by plasma CCK concentrations were determined in 16 adult male cats (5.1 +/- 0.1 kg) 8 weeks before and 57 weeks after eight of the cats were gonadectomized. During ad libitum intake of a commercial dry, expanded diet, body weight increased from 22% to 28% in gonadectomized cats and was unchanged in intact cats. Baseline CCK concentrations were not different between gonadectomized and intact cats. Amounts of diet ingested during CCK determinations were 15-19% of daily metabolizable energy requirement and were not different between gonadectomized and intact cats. The post-prandial area under the curve (AUC; 0-400 min) CCK concentration increased linearly with meal size (p < 0.01) and was not correlated with body weight. Area under the curve CCK concentration, when normalized for meal size, was 34% greater (p < 0.01) in gonadectomized cats than that in intact cats. The findings indicate GX increases meal-induced intestinal CCK secretion and therefore, do not support the study hypothesis. The findings indicate GX may slow digestion and absorption and attenuate inhibition of food intake by CCK.

Determination of the selenium requirement in kittens.

The purpose of this study was to determine the selenium (Se) requirement in kittens. Thirty-six specific-pathogen-free kittens (9.8 weeks old) were utilized in a randomized complete block design to determine the Se requirement in cats with gender and weight used as blocking criteria. Kittens were fed a low Se (0.02 mg/kg Se) torula yeast-based diet for 5 weeks (pre-test) after which an amino acid-based diet (0.027 mg Se/kg diet) was fed for 8 weeks (experimental period). Six levels of Se (0, 0.05, 0.075, 0.10, 0.20 and 0.30 mg Se/kg diet) as Na2SeO3 were added to the diet and were used to construct a response curve. Response variables included Se concentrations and Se-dependent glutathione peroxidase activities (GSHpx) in plasma and red blood cells (RBC) as well as plasma total T3 (TT3) and total T4 (TT4). No significant changes in food intake, weight gain or clinical signs of Se deficiency were noted. Estimates of the kitten's Se requirement (i.e. breakpoints) were determined for RBC and plasma GSHpx (0.12 and 0.15 mg Se/kg diet, respectively), but no definitive breakpoint was determined for plasma Se. Plasma TT3 increased linearly, whereas plasma TT4 and the ratio of TT4 : TT3 decreased in a quadratic fashion to dietary Se concentration. The requirement estimate determined in this study (0.15 mg Se/kg) for kittens is in close agreement with other species. As pet foods for cats contain a high proportion of animal protein with a Se bioavailability of 30%, it is recommended that commercial diets for cats contain 0.5 mg Se/kg DM.

Taurine status in normal dogs fed a commercial diet associated with taurine deficiency and dilated cardiomyopathy.

Taurine (Tau) deficiencies have been associated with the feeding of commercial lamb-meal and rice diets to dogs. We hypothesized that the poor digestibility of some lamb-meals may limit sulphur amino acids availability for Tau synthesis and/or increase of Tau degradation in the gut. Growing dogs were fed either a lamb-meal-based (Diet A) or poultry by-product-based (Diet B) commercial diet. Plasma, whole blood and urinary Tau were measured for 22 weeks. Plasma and whole blood Tau concentrations were similar between the groups throughout the study. Urinary excretion of Tau in dogs fed diet A was 3.2 times greater than that from dogs fed Diet B, suggesting greater renal reabsorption and the need for conservation of Tau in the Diet A group. Food restriction affected Tau status as indicted by a positive correlation of food intake and urinary Tau. Dogs fed Diet A were given antibiotics to inhibit bacterial activity in the gut. Increases in breath hydrogen, indicative of increased bacterial activity, correlated negatively with urinary Tau. Urinary Tau increased by 54% when methionine (Met) was supplemented to Diet A, supporting the suggestion of a low bioavailability of sulphur amino acids and/or an increased fecal loss of Tau in dogs consuming Diet A.

Dietary crude protein concentration does not affect the leucine requirement of growing dogs.

The objective of the present study was to examine the interaction between graded levels of leucine and dietary crude protein. Dose-response curves were generated using four 3 x 3 Latin squares (two dogs/square). Each square represented one of two concentrations of crude protein (140 or 280 g/kg diet) and one of two combinations of three concentrations of leucine (5.0, 7.0 and 9.0 g/kg diet or 9.0, 11 and 13 g/kg diet). An additional experiment was performed by feeding crude protein at 210 g/kg diet with either 7.0 or 11 g leucine/kg diet. Weight gain, food intake, nitrogen retention, plasma albumin and plasma amino acids were measured. The requirement was determined to be the minimum leucine concentration required to maximize weight gain and nitrogen retention. For 8-14-week-old male Beagle dogs, 140 g crude protein/kg diet in a diet containing 18 kJ metabolizable energy/g does not appear to support maximal growth. The leucine requirement was not affected by doubling the dietary crude protein level from 140 to 280 g/kg diet. From these results, the leucine requirement of 8-14-week-old Beagle dogs appears to be 11 g leucine/kg diet independent of the level of dietary crude protein, whereas dogs over 14 weeks require only 7 g leucine/kg diet for maximal nitrogen retention.

Maternal expression of functional lipoprotein lipase and effects on body fat mass and body condition scores of mature cats with lipoprotein lipase deficiency.

OBJECTIVE: To assess effects of deficiency of lipoprotein lipase (LPL) on body condition scores and lean and fat body masses of adult cats. ANIMALS: 12 cats without LPL mutations and 23 cats that were heterozygous or homozygous carriers of the Gly412Arg LPL mutation. PROCEDURE: Lean and fat body masses were estimated by use of body condition scores and change in enrichment of serum after IV administration of deuterium oxide. Mass spectroscopy and infrared absorbance methods were used to determine deuterium enrichment. RESULTS: Fat body mass (mean +/- SD; 0.2 +/- 0.1 kg) and percentage body fat (6.2 +/- 1.4%) of homozygotes were significantly less than those of clinically normal cats and heterozygotes (0.7 +/- 0.1 kg, 18.2 +/- 1.6% and 0.5 +/- 0.1 kg, 15.6 +/- 1.7%, respectively). Homozygous offspring of homozygous dams had significantly less fat body mass (0.1 +/- 0.1 kg) and percentage body fat (2.1 +/- 1.0%) than homozygous offspring of heterozygous dams (0.3 +/- 0.1 kg and 9.2 +/- 1.7%, respectively). Lean body mass did not differ significantly among groups. For all groups, percentage body fat was significantly correlated with body condition score (r= 0.65), and body condition scores supported findings for fat body mass. CONCLUSIONS AND CLINICAL RELEVANCE: Deficiency of LPL activity in cats diminishes stores of body fat. This is consistent with a low rate of de novo synthesis of fat. The effect of dam on body masses in mature LPL-deficient cats indicates nutrient programming of adipose formation during gestation or lactation.

Relationship between serum leptin immunoreactivity and body fat mass as estimated by use of a novel gas-phase Fourier transform infrared spectroscopy deuterium dilution method in cats.

OBJECTIVE: To validate a recently developed commercially available leptin radioimmunoassay (RIA) for use with feline serum and evaluate the relationship between serum leptin concentrations and body fat mass in domestic cats. ANIMALS: 19 sexually intact male specific-pathogen-free domestic cats that weighed 3.8 to 7.1 kg and were 1.1 to 3.5 years old. PROCEDURE: Specificity for feline leptin was evaluated by use of gel filtration chromatography and reverse-phase high-performance liquid chromatography fractionation of serum. Body fat mass was determined by use of the deuterium oxide (D2O) dilution method. Serum water D2O enrichment was measured by use of gas-phase Fourier transform infrared spectroscopy. RESULTS: Body fat mass and percentage body fat ranged from 0.3 to 2.3 kg and 7.5 to 34.9%, respectively. Serum leptin concentrations were lower in the unfed versus the fed state and ranged between 1.6 and 4.9 ng/ml human equivalent (HE); mean +/- SD value was 2.9 +/- 0.2 ng/ml HE. Leptin concentrations increased with increasing body fat mass and percentage of body fat. CONCLUSIONS: Leptin is in the serum of domestic cats in free (> 78%) and apparently bound forms. The relationship between body fat and serum leptin concentration was similar to that observed in humans and rodents and indicative of a lipostatic role for leptin in cats. Cats that have an overabundance of body fat appear to be less sensitive to the weight-normalizing action of leptin than cats of ideal body condition.

Lean (Fa/Fa) but not obese (fa/fa) Zucker rats release cholecystokinin at PVN after a gavaged meal.

Neuropeptides play an important role in the integration of dietary signals. Cholecystokinin (CCK) has been implicated in regulating ingestive behavior, particularly satiety. The primary objective of this study was to examine whether the hyperphagia characteristic of obese (fa/fa) rats involves impaired neural CCK secretion. Dynamic release of CCK at the hypothalamic paraventricular nucleus (PVN) of age-matched lean (Fa/Fa) and obese Zucker rats was determined using push-pull perfusion. The gavage of a 10.3-kcal (6 ml) liquid diet during lights off was followed by increased CCK release in lean rats (from 13.6 +/- 1.1 to 22.1 +/- 1.4 fmol in the 1st postprandial period and 18.4 +/- 2.5 fmol in the 2nd postprandial period). An identical meal load resulted in no postprandial increase in CCK release in obese rats, despite the fact that high-K+ artificial cerebrospinal fluid evoked CCK outflow in all animals. Intubation of 6 ml of nonnutritive 1% carboxymethylcellulose had no effect. These results are consistent with the suggestion that hypothalamic CCK plays a physiological role in satiety, and they demonstrate that obese Zucker rats have blunted hypothalamic CCK release in response to dietary cues.

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.

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.

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.

Microbial degradation of taurine in fecal cultures from cats given commercial and purified diets.

Freshly passed feces were collected from cats (n = 5-7) given cooked and uncooked commercial canned-type diets, casein and soy protein containing purified diets and a commercial extruded diet. The feces were anaerobically cultured in medium containing either taurine, taurocholic acid or [2-3H]taurine for 24 h at 37 degrees C. Taurine degradation in cultures was greatest for cultures from cats receiving diets reputed to cause taurine depletion. Diaminopimelic acid in feces indicated that differences in taurine degradation rate among groups was associated with differences in bacterial numbers in feces. After 6 h of incubation, < 10% of taurocholate and > 60% of taurine remained. Nearly all the tritium on the labeled taurine was recovered as water. These results indicate that deconjugation and deamination are the initial steps in microbial catabolism of taurocholic acid and that enteric microbial growth may be a major determinant of dietary taurine requirement of cats.