Subnormal concentrations of serum cobalamin (vitamin B12) in cats with gastrointestinal disease.

The present study sought to determine the spectrum of diseases associated with subnormal concentrations of serum cobalamin in cats undergoing investigation of suspected gastrointestinal problems. The solid-phase boil radioassay (RA) for cobalamin employed in the present study was immunologically specific, precise, and accurate, with a sensitivity of 15 pg/mL. The RA yielded results that strongly correlated with those obtained by bioassay (Spearmann rho = .805; P < .0001), although the absolute values were lower for the RA. Forty-nine of 80 serum samples submitted during the period of January 1996-January 1998 had cobalamin concentrations below the reference range for healthy cats (range 900-2,800 pg/mL; mean +/- SD, 1,775 +/- 535 pg/mL; n = 33). Cats with subnormal cobalamin concentrations (mean +/- SD; 384 +/- 272 pg/mL, range 3-883 pg/mL) were middle-aged or older and were presented for weight loss. diarrhea, vomiting, anorexia, and thickened intestines. Definitive diagnoses in 22 cats included inflammatory bowel disease (IBD), intestinal lymphoma, cholangiohepatitis or cholangits, and pancreatic inflammation. Serum concentrations of cobalamin were particularly low in cats with intestinal lymphoma, three-fifths of whom also had subnormal serum concentrations of folate (< 9 ng/mL). The simultaneous presence of disease in the intestines, pancreas, or hepatobiliary system in many cats made it difficult to determine the cause of subnormal cobalamin concentrations. The circulating half-life of parenteral cyanocobalamin was shorter in 2 cats with IBD (5 days) than in 4 healthy cats (12.75 days). The presence of subnormal serum concentrations of cobalamin in 49 of 80 cats evaluated suggests that the measurement of serum cobalamin may be a useful indirect indicator of enteric or pancreatic disease in cats. The rapid depletion of circulating cobalamin in cats suggests that cats may be highly susceptible to cobalamin deficiency. However, the relationship of subnormal serum cobalamin concentrations to cobalamin deficiency and the effect of cobalamin deficiency on cats remain to be determined.

Adrenocortical function in neonatal and weanling beagle pups.

Adrenocortical function was assessed in 27 Beagle pups at 2, 4, 6, 8, 10, and 12 weeks of age by determination of plasma sodium, potassium, and chloride concentrations; serum aldosterone and cortisol concentrations; and plasma ACTH concentrations. Serum cortisol concentration was measured before and 1 and 2 hours after IM administration of 2.2 IU of ACTH/kg of body weight. Serum progesterone concentration also was determined for all pups at 2, 4, and 6 weeks of age. Mean baseline cortisol concentration was lower for pups 8 weeks old or younger than for mature dogs. Nevertheless, mean serum ACTH-stimulated cortisol concentration in dogs of all age groups increased into the adult reference range after administration of ACTH. For pups 4 weeks old or younger, increase in cortisol concentration was maximal at 2 hours after ACTH administration. However, in pups between 6 and 12 weeks of age, the increase in cortisol concentration was maximal 1 hour after ACTH administration in about a third of the pups, whereas the remaining pups had peak values at 2 hours. Mean plasma sodium, potassium, and chloride concentrations for each age group were within the reference ranges established for mature dogs, with the exception of lower mean plasma sodium and chloride concentrations in pups 4 weeks old or younger. Mean serum aldosterone concentration in pups of each age group was substantially higher than the range of aldosterone concentrations for clinically normal mature dogs. Median progesterone concentration was uniformly less than 0.2 ng/ml for all pups 6 weeks old or younger.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of urinary cortisol:creatinine ratios for the diagnosis of hyperadrenocorticism associated with adrenal gland tumors in ferrets.

Assays were validated for the measurement of urinary concentrations of cortisol and creatinine in domestic ferrets (Mustela putorius furo). Urinary concentrations of cortisol and creatinine and the calculated urinary cortisol:creatinine ratio (UCCR) values were determined for 29 clinically normal female ferrets, 22 clinically normal male ferrets, and 12 ferrets with adrenal gland tumors. The UCCR values for the 51 clinically normal ferrets ranged from 0.04 x 10(-6) to 1.66 x 10(-6), with a median value of 0.22 x 10(-6). The UCCR values were significantly (P < or = 0.01) higher in the 12 ferrets with adrenal tumors, with a range of 0.5 x 10(-6) to 60.13 x 10(-6) and a median of 5.98 x 10(-6). We concluded that determination of UCCR values was useful in the diagnosis of hyperadrenocorticism associated with adrenal neoplasia in domestic ferrets.

Estrogen production by bovine binucleate and mononucleate trophoblastic cells in vitro.

The bovine placenta has long been known as a source of steroid hormones. We performed three experiments to compare production of estrogens by bovine mononucleate and binucleate trophoblastic cells and examined effects of cortisol, progesterone, pregnenolone, testosterone, and androstenedione. In the first experiment, binucleate trophoblastic cells were purified by unit gravity sedimentation from six enzymatically dispersed placentas between 150 and 180 days of gestation. Cells (8 x 10(5)/ml) were incubated first at 37 degrees C for 6 h with Medium 199 alone (M199/6h) or with 10(-7) M cortisol (cortisol/6h). Medium then was replaced with 10(-7) M progesterone, 10(-7) M pregnenolone, 10(-7) M testosterone, or M199, and a second incubation was conducted for 4 h. Estradiol production did not differ between cells incubated for the first 6 h in M199 vs. cortisol and was not affected by progesterone or pregnenolone. Testosterone increased (p < 0.05) estradiol production. Estrone production did not differ between cells incubated for the first 6 h in M199 vs. cortisol; estrone production was not affected by either progesterone, pregnenolone, or testosterone. Mononucleate as well as binucleate cells were purified from placentas between 165 and 180 days of gestation and used in two other experiments. In the first of these, enriched populations of binucleate and mononucleate cells were incubated first for 6 h with Medium 199 (M199) or 10(-7) M cortisol. Medium then was replaced with 10(-7) M testosterone, 10(-7) M androstenedione, or M199 and incubation continued for 4 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Histopathologic features, environmental factors, and serum estrogen, progesterone, and prolactin values associated with ovarian phase and inflammatory uterine disease in cats.

Forty-four female American Shorthair cats with inflammatory uterine disease or infertility were evaluated. Data collected included age, month of diagnosis, housing, reproductive history, results of bacteriologic culture of uterine specimens, serum concentrations of estrogen, progesterone, and prolactin and histopathologic features of the ovaries and uterus. Histologically, the ovaries of 19 cats were dominated by active or cystic follicles, whereas 25 cats had luteal-phase ovaries. Of the 25 cats with active corpora lutea, 20 had either recently weaned litters (n = 11) without subsequent exposure to a male cat, or had been housed individually for lengthy periods (n = 9). The finding of active corpora lutea under these circumstances indicates that in queens, ovulation may occur by mechanisms not involving coitus. Prominent, active corpora lutea on the ovaries were associated with adenomatotic proliferative changes in the superficial and glandular epithelium of the uterus and with myometrial hyperplasia, compared with the uterus of cats with follicular ovaries (P less than 0.01). Serum progesterone concentration greater than or equal to 1.87 ng/ml was consistently associated with luteal-phase ovaries. Serum progesterone values less than or equal to 0.15 ng/ml were consistently associated with follicular-phase ovaries. Escherichia coli was the organism most commonly isolated from uterine contents.

Effects of hyperlipemia on radioimmunoassays for progesterone, testosterone, thyroxine, and cortisol in serum and plasma samples from dogs.

Hyperlipemic serum and plasma samples often are received by clinical laboratories for endocrinologic analysis by radioimmunoassay. We designed a study to determine what effect, if any, hyperlipemia has on estimation of lipid-soluble hormone concentrations determined by solid-phase radioimmunoassays. Progesterone, testosterone, thyroxine, and cortisol concentrations were determined in canine plasma and serum with various degrees of lipemia. Samples of serum, heparinized plasma, and EDTA-treated plasma were obtained from blood collected from 4 female and 4 male Beagles by use of evacuated tubes. To induce hyperlipemia in vitro, IV fat emulsion was diluted in deionized water to produce 0 (water only), 33, 67, or 100% mixtures. Twenty microliters of each mixture then was added to the subsamples of serum and plasma from each dog. Hormone concentrations were determined, using validated radioimmunoassays. Triglyceride concentrations were determined by enzymatic assay. Addition of IV fat emulsion in vitro was an accurate and reproducible means of altering triglyceride concentrations in the samples. Triglyceride concentrations as high as 700 mg/dl had no effect on radioimmunoassays for progesterone, testosterone, and thyroxine in serum, heparinized plasma, or EDTA-treated plasma. Addition of 100% (but not 33 or 67%) fat emulsion reduced the mean cortisol concentration in heparinized plasma by 12% (P less than 0.05). This severe hyperlipemia did not affect quantification of cortisol in serum or EDTA-treated plasma.

Effects of hemolysis and storage on quantification of hormones in blood samples from dogs, cattle, and horses.

Veterinary diagnostic endocrinology laboratories frequently receive hemolyzed plasma, serum, or blood samples for hormone analyses. However, except for the previously reported harm done by hemolysis to canine insulin, effects of hemolysis on quantification of other clinically important hormones are unknown. Therefore, these studies were designed to evaluate effects of hemolysis on radioimmunoassay of thyroxine, 3,5,3'-triiodothyronine, progesterone, testosterone, estradiol, cortisol, and insulin in equine, bovine, and canine plasma. In the first experiment, hormones were measured in plasma obtained from hemolyzed blood that had been stored for 18 hours. Blood samples were drawn from pregnant cows, male and diestrous female dogs, and male and pregnant female horses. Each sample was divided into 2 equal portions. One portion was ejected 4 times with a syringe through a 20-gauge (dogs, horses) or 22-gauge (cows) hypodermic needle to induce variable degrees of hemolysis. Two subsamples of the blood were taken before the first and after the first, second, and fourth ejections. One subsample of each pair was stored at 2 to 4 C and the other was stored at 20 to 22 C for 18 to 22 hours before plasma was recovered and stored at -20 C. The second portion of blood from each animal was centrifuged after collection; plasma was recovered and treated similarly as was blood. Concentrations of thyroxine in equine plasma, of 3,5,3'-triiodothyronine, estradiol, and testosterone in equine and canine plasma, and of cortisol in equine plasma were not affected by hemolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of maternal cocaine administration on maternal and fetal glucose, lactate, and insulin in sheep.

Although cocaine use during pregnancy is an important cause of perinatal morbidity and mortality, there are no reports of its effect on maternal and fetal carbohydrate metabolism. Six pregnant ewes and their fetuses were instrumented under halothane general anesthesia at 113-119 days' gestation. Between 124-135 days' gestation, the ewes received a single infusion of vehicle or cocaine (1.0 or 2.0 mg/kg) into the jugular vein. At least 24 hours was allowed between successive injections. Maternal and fetal blood samples were drawn at 30 and 20 minutes before and at 5, 15, 30, and 60 minutes after the injection. Both maternal and fetal glucose and lactate concentrations increased (P less than .05) after injection of cocaine at 2.0 mg/kg. There were no significant changes in maternal or fetal plasma insulin concentrations after vehicle or cocaine administration. Induction of hyperglycemia and lactacidemia could be mechanisms whereby cocaine exerts its adverse effects during pregnancy.

Radioimmunoassay of parathyroid hormone in cats.

A radioimmunoassay for measurement of midmolecule parathyroid hormone (PTH) concentration in serum from dogs was validated for use on serum from cats. The assay detected an increase in serum concentration of PTH after IV infusion of Na2 EDTA in healthy cats. Infusion of calcium chloride caused a decrease in measured PTH. Accuracy of the assay was demonstrated by quantitative recovery of a feline parathyroid gland extract added to pooled feline sera. Mean interassay and intra-assay coefficients of variation were 0.13 and 0.07, respectively. Sensitivity of the assay was 0.1 ng of PTH/ml. The median PTH concentration measured in 40 adult cats was 3.5 ng/ml, with a range of 1.16 to 11.0 ng/ml.

Pseudohyperparathyroidism in a mare associated with squamous cell carcinoma of the vulva.

An 18-year-old Appaloosa mare was examined because of squamous cell carcinoma of the vulva, anorexia with pronounced weight loss, and hypercalcemia. The tumor had developed rapidly over a period of 3 months and externally extended ventrally involving the perineum and the dorsal aspect of the udder. Necropsy examination demonstrated a large primary squamous cell carcinoma of the vulva, perineum, and mammary gland with metastases to the supramammary, sublumbar, deep inguinal, and mediastinal lymph nodes. No gross renal lesions were observed and, histologically, there was only mild vacuolation of renal tubular epithelium. Based on the normal concentration of serum parathyroid hormone, the absence of evidence of hypervitaminosis D, and normal renal function, a diagnosis was made of hypercalcemia of malignancy or pseudohyperparathyroidism. The mechanism responsible for hypercalcemia was not determined, but the histologic type of the neoplasm and the clinical course suggested possible production of a humoral hypercalcemic factor by the neoplasm, similar to that demonstrated in certain types of human squamous cell carcinoma.

Effects of age, sex, and body size on serum concentrations of thyroid and adrenocortical hormones in dogs.

Thyroxine (T4), 3,5,3'-triiodothyronine (T3), and cortisol frequently are quantified in canine serum or plasma samples to aid in the diagnosis of hypothyroidism, hypoadrenocorticism, and hyperadrenocorticism. Many laboratories have established reliable references values for concentrations of these hormones in blood of clinically normal animals. However, nonpathologic factors that affect thyroidal and adrenocortical secretion may lead to misinterpretation of test results when values for individual animals are compared with reference values. The objective of the study reported here was to identify effects of age, sex, and body size (ie, breed) on serum concentrations of T3, T4, and cortisol in dogs. Blood samples were collected from 1,074 healthy dogs, and serum concentrations of the iodothyronines and cortisol were evaluated for effects of breed/size, sex, and age. Mean (+/- SEM) serum concentration of T4 was greater in small (2.45 +/- 0.06 micrograms/dl)- than in medium (1.94 +/- 0.04 micrograms/dl)- or large (2.03 +/- 0.03 micrograms/dl)-breed dogs, the same in females (2.11 +/- 0.04 micrograms/dl) and males (2.08 +/- 0.04 micrograms/dl), and greater in nursing pups (3.04 +/- 0.05 micrograms/dl) than in weanling pups (1.94 +/- 0.05 micrograms/dl), rapidly growing dogs (1.95 +/- 0.04 micrograms/dl), and young adult (1.90 +/- 0.06 micrograms/dl), middle-aged adult (1.72 +/- 0.05 micrograms/dl), or old adult (1.50 +/- 0.05 micrograms/dl) dogs. Dogs greater than 6 years old had lower mean serum T4 concentration than did dogs of all other ages, except middle-aged adults. Mean serum T3 concentration in medium-sized dogs (1.00 +/- 0.01 ng/ml) was greater than that in small (0.90 +/- 0.01 ng/ml)- and large (0.88 +/- 0.01 ng/ml)-breed dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Continuous central vasopressin infusion increases peripheral fetal corticotropin and cortisol in the fetal sheep.

In previous studies on regulation of fetal adrenocorticotropin (ACTH) secretion, corticotropin releasing factor (CRF) and arginine vasopressin (AVP) have been administered by peripheral intravascular infusion. In order to look at an alternate route of administration, we investigated the effect of continuous intracerebroventricular administration of AVP to the fetus on fetal plasma ACTH and fetal and maternal plasma cortisol concentrations. Sheep fetuses (n = 9) were instrumental with carotid artery and lateral cerebral ventricular catheters. Fetuses were given intracerebroventricular infusion from 125-134 days gestational age of artificial cerebrospinal fluid vehicle (n = 4), or AVP 250 mu U.min-1 continuously in artificial cerebrospinal fluid vehicle (n =5). Fetal blood was obtained daily between 09.00 and 12.00h and 20.00 and 23.00h. Over the infusion period, fetal plasma ACTH and cortisol concentrations in AVP infused fetuses increased (P less than 0.05) compared with the vehicle infused group. Gestation length for the fetuses in the AVP and vehicle infused groups were 139 +/- 4.9 (n =4) and 145 +/- 4.6 (n = 3) days respectively (n.s.). Fetal plasma AVP concentrations in the AVP infused group were not different from the vehicle infused group.

Endocrine changes during 48 hours of food withdrawal in the pregnant rhesus monkey in the last third of gestation.

We studied the hormonal responses in four pregnant rhesus monkeys between 112 and 149 days gestation. After 2 days, during which the monkeys were fed ad libitum, their food was withdrawn at 1500 h for 48 h while allowing free access to water. The food then was returned, and the animals were studied for a further 2 days. The mean maternal whole blood glucose concentration significantly decreased, and plasma cortisol and dehydroepiandrosterone sulfate (DHEAS) concentrations significantly increased within 30 h of food withdrawal (P less than 0.05). The maternal plasma estradiol concentration increased significantly at 1000 h on the second day of food withdrawal (P less than 0.05), whereas the plasma progesterone concentration did not change. The maternal blood glucose and plasma cortisol, DHEAS and estradiol concentrations returned to baseline by the second day of food replacement. We conclude that the stress of hypoglycemia and/or the attendant inability to eat, together or separately, stimulate maternal adrenal glucocorticoid and androgen secretion during the period of food withdrawal. The increased maternal DHEAS and perhaps other adrenal androgen concentrations result in increased maternal estrogen production.

Progesterone production by binucleate trophoblastic cells of cows.

Incubation of 1 x 10(6) bovine binucleate trophoblastic cells (BTC) for 6 h with 0.20 and 0.30 microM-Ca2+ ionophore A23187 increased (P less than 0.01) net progesterone production 49% and 111%, respectively, compared to BTC without A23187. Addition of 3 mM-8-bromo-cAMP with A23187 had no effect on the response. Trifluoperazine (40 microM), an inhibitor of calmodulin, and ethylene glycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (1.0 mM), a Ca2+ chelator, decreased (P less than 0.01) progesterone production. Progesterone production by BTC incubated for 6 h with fetal bovine serum or lipoprotein-deficient serum (LPDS) did not differ. Addition of bovine serum low-density lipoprotein or high-density lipoprotein to LPDS did not affect progesterone production. Aminoglutethimide (100 microM) decreased (P less than 0.01) progesterone production by BTC. These results indicate that progesterone production by bovine BTC is Ca2+-dependent, cyclic nucleotide-independent, and not stimulated by bovine serum lipoproteins.

Effects of obesity and ovarian steroids on insulin secretion and removal in sheep.

The interactive effects of sex steroids and obesity on glucose metabolism and pancreatic secretion and organ removal of insulin were determined in multicatheterized lean and obese sheep by multiplying venoarterial concentration differences by plasma flows. Ovariectomized lean and dietary obese ewes received implants of progesterone and estradiol-17 beta that produced plasma concentrations of each equivalent to those during either anestrus (low progesterone), diestrus or pregnancy (high progesterone), or estrus (high estradiol). Sheep were exposed to each of the three steroid treatments for 2 days and fasted overnight before blood samples were collected for 5 h before (basal) and 90 min after injecting glucose (200 mg/kg) to simulate an intravenous glucose tolerance test (IVGTT). Regardless of steroid treatment, pancreatic secretory (18 vs. 5 mU/min) and hepatic (10 vs. 2 mU/min) and hindquarters (1.8 vs. 0.5 mU/min) removal rates of insulin in the basal state were greater (P less than 0.005) in obese than lean sheep. Obese sheep had greater (P less than 0.025) basal hepatic glucose output (66 vs. 47 mg/min) and similar hindquarters glucose removal (37 vs. 32 mg/min) as lean sheep even though arterial concentrations of insulin were fourfold higher (25 vs. 6 microU/ml; P less than 0.01) in the obese sheep. High progesterone increased (P less than 0.05) basal hepatic insulin removal in obese sheep. High progesterone and high estradiol increased insulin but decreased (P less than 0.05) glucose removal in hindquarters of obese sheep in the basal state. High progesterone potentiated significantly glucose-induced hyperinsulinemia in obese sheep, whereas high estradiol suppressed hepatic insulin removal but increased the removal of insulin by hindquarters during glucose stimulation in the obese sheep. We concluded that excessive insulin secretion, not decreased insulin removal, maintains the basal hyperinsulinemia in moderately obese sheep and that the progesterone-to-estradiol ratio has marked and divergent effects on insulin and glucose metabolism in individual tissues of sheep both in the basal state and during an IVGTT.

Calcium-dependent translocation of calbindin-D28k from intestine to blood.

Calbindin-D (vitamin D-induced calcium-binding protein; CaBP) is known to be present in blood at concentrations which vary directly with levels in the intestinal mucosa. Employing a sensitive radioimmunoassay and sampling mesentery venous blood, the present experiments demonstrated a direct relationship between intestinal calcium absorption and serum CaBP. Solutions containing 150 mM NaCl and 45Ca-labeled calcium chloride (5 or 20 mM) were placed in the lumen of ligated duodenal preparations in situ and mesentery venous blood sampled with time. The concentration of absorbed 45Ca in serum was maximal at 5 min, followed by a significant increase in mesentery CaBP maximizing at 15-20 min. Elevation of serum CaBP was not observed when calcium in the dosing solution was omitted or replaced by either glucose or glycine. The possible transfer of absorbed calcium from the enterocyte to the circulation as a CaBP complex was ruled out by calculations revealing that considerably more calcium was transferred than could be accounted for by the low and high affinity binding sites on the protein. It is proposed that vitamin D-dependent enhanced transcellular calcium transport constitutes a stimulus for the increased release of intestinal CaBP into the circulation.

Calbindin-D in peripheral nerve cells is vitamin D and calcium dependent.

The vitamin D-induced calcium-binding protein calbindin-D (CaBP) was localized immunohistochemically in some but not all of the cell bodies and axons within the intestinalis nerve of the chicken. Unlike other nerve tissue thus far examined, the CaBP content of the intestinalis nerve was decreased in vitamin D deficiency and increased in chicken adapted to a calcium-deficient diet. These changes are qualitatively similar to the pattern of response of enterocytes. The inclusion of calcium-containing solutions within the duodenal lumen caused, directly or indirectly, a decrease in the amount of CaBP in this nerve in a dose-dependent manner. The exact role of CaBP in intestinalis nerve cells is unknown but may be in the regulation of intracellular ionic Ca2+ concentrations during excitation, although other functions of CaBP cannot be excluded.

Glucose-dose dependent characteristics of insulin secretion in obese and lean sheep.

We previously reported that obesity in sheep and cattle was associated with basal hyperinsulinemia, insulin resistance, and an exaggerated insulin response to a single dose (350 mg/kg) of glucose. In this study, the glucose-dose dependency of insulin secretion in obese and lean sheep was determined by 1) using jugular venous concentrations of insulin (Exp 1) and 2) arteriovenous differences in insulin concentrations across the pancreas together with plasma flow rates in the portal vein (Exp 2). Sheep were injected with glucose doses of 0 (water), 10, 30, 100, and 350 mg glucose/kg body weight in Exp 1 (six sheep per group) and with a low (20 mg/kg) and high (200 mg/kg) dose of glucose in exp 2 (four sheep per group). In Exp 1, mean (+/- SE) pretreatment plasma concentrations of insulin (22.0 +/- 1.7 vs. 9.4 +/- 0.4 microU/ml) and glucose (56.1 +/- 0.5 vs. 52.4 +/- 0.8 mg/dl) were greater (P less than 0.01) in obese than lean sheep fasted for 12 h. The glucose-induced rises in insulin concentrations above pretreatment levels were always greater (P less than 0.05) in obese than lean sheep regardless of glucose dose. Eadie-Scatchard plot analysis of the hyperbolic relationship between the acute insulin and acute glucose response areas (0 to +10 min) indicated that the maximum (Vmax) early phase insulin response was greater (P less than 0.025) in obese than lean sheep (568 +/- 148 vs. 156 +/- 33 microU ml-1 X min). In Exp 2, pretreatment concentrations of insulin (25.1 +/- 3.4 vs. 5.6 +/- 1.2 microU/ml) and glucose (58.3 +/- 1.8 vs. 45.5 +/- 1.1 mg/dl) in arterial plasma were greater (P less than 0.01) in obese than in lean sheep fasted 18 to 22 h. Similarly, pretreatment pancreatic secretion rates of insulin were greater (P less than 0.01) in obese (17.8 +/- 5.8 mU/min) than in lean (4.9 +/- 1.3 mU/min) sheep. Glucose-induced acute (0 to +10 min) increments in pancreatic secretory rates of insulin also were greater (P less than 0.05) in obese than in lean sheep after the low (215 +/- 73 vs. 11 +/- 15 mU) and high (881 +/- 281 vs. 232 +/- 66 mU) doses of glucose. It was concluded that insulin secretion in response to a range of stimulatory concentrations of glucose was greater in obese than in lean sheep because the obese sheep had greater maximum (i.e. Vmax) acute phases of glucose-induced insulin secretion.

Effect of fasting on thyroxine, 3,5,3'-triiodothyronine, and cortisol concentrations in serum of dogs.

The present study was designed to compare basal and stimulated concentrations of 3,5,3'-triiodothyronine (T3), thyroxine (T4), and cortisol in serum of dogs fasted 12 or 18 hours (to represent overnight fasting) or 24 or 36 hours (to represent prolonged inappetence) with those of dogs that were not fasted. Twenty-five adult Beagle bitches were allotted to 5 experimental fasting groups (0, 12, 18, 24, and 36 hours). Blood samples for hormonal analyses were obtained 4, 3, 2, and 1 hour before food was removed; at the time of food removal; 1 hour after food was removed; and every 2 hours during experimental fasting until 0800 hours on the day fasting ended. Dogs were injected with 5 IU of thyrotropin, IV, and 2.2 IU of adrenocorticotropin/kg, IM, to evaluate thyroidal and adrenocortical endocrine reserves. Additional blood samples were collected 0.5, 1, 2, 3, and 4 hours after injections were given. Serum concentrations of T3, T4, and cortisol were determined by validated radioimmunoassays. Body weights and ages of the dogs and food consumption during a 2-hour preliminary feeding period before dogs were fasted did not differ among fasting groups. Length of fasting did not affect serum concentrations of T3 or T4 in dogs at 12, 18, 24, or 36 hours after food was removed. Mean serum concentrations of cortisol in dogs fasted 12 or 24 hours were lower than those in dogs that were not fasted. Serum concentrations of the hormones after thyrotropin and adrenocorticotropin were injected were not affected by fasting.(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin and glucose responses to glucose injection in fed and fasted obese and lean sheep.

Effects of short-term fasting on the insulin and glucose responses to injected glucose were determined in obese (n = 6) and lean (n = 6) Dorset ewes that were fed a maintenance level of energy intake. Sheep were assigned by Latin-square design to be fasted for 0 (fed), 12 or 24 h before glucose (350 mg/kg) was injected via jugular cannula at 2000 h with at least 7 d between successive tests. Insulin and glucose were quantified in jugular plasma samples. Pretreatment concentrations of insulin were affected (P less than 0.005) only by body condition with higher mean values in obese (23.5 +/- 3.3 microU/ml) than in lean (9.4 +/- 1.0 microU/ml) sheep. Pretreatment concentrations of glucose (53.6 +/- 1.8 mg/dl) were unaffected by body condition and fasting. The insulin responses to glucose, whether determined as absolute levels or response areas above base-line levels, were greater (P less than 0.005) in obese than in lean sheep regardless of fasting period. Insulin and glucose concentrations after glucose injection in lean sheep were unaffected by fasting. In contrast, the insulin response to glucose was greater (P less than 0.005) in fed obese than 12- or 24-h fasted obese sheep while glucose levels in the fed sheep were similar to those in the fasted obese sheep. Thus, factors associated with feeding enhanced the insulin response to glucose in obese sheep. In addition, obesity in sheep was associated with insulin resistance because basal hyperinsulinemia coexisted with euglycemia and because fractional removal rates of injected glucose were similar in obese and lean sheep despite much greater concentrations of insulin in obese sheep.