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You are here: Home / Publications / Bibliographies and Resource Guides / Canine Models in Biomedical Research, 1990-2009  / Endocrine System  Printer Friendly Page
Canine Models in Biomedical Research,  1990-2009
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Endocrine System

Bailhache, E., K. Ouguerram, C. Gayet, M. Krempf, B. Siliart, T. Magot, and P. Nguyen (2003). An insulin-resistant hypertriglyceridaemic normotensive obese dog model: assessment of insulin resistance by the euglycaemic hyperinsulinaemic clamp in combination with the stable isotope technique. Journal of Animal Physiology and Animal Nutrition 87(3-4): 86-95. ISSN: 0931-2439.
NAL Call Number: 389.78 Z3
Abstract: Many studies have shown that in humans insulin resistance (IR) is associated with obesity and hypertriglyceridaemia. The aim of our study was to develop slowly dietary-induced obesity in dogs through long-term overfeeding of a high-fat diet, and to characterize this IR, hypertriglyceridaemic and normotensive model. Insulin resistance was assessed by the euglycaemic hyperinsulinaemic clamp technique. The contribution of hepatic glucose production during the clamp was evaluated using a constant stable-isotope-labelled glucose infusion. Overfeeding a high-fat diet for 7 months was associated with a 43+-5% body weight increase. Insulin resistance was characterized by hyperinsulinaemia in the unfed state (10+-1 vs. 24+-1 muU/ml, in healthy and obese dogs, respectively, p<0.02) and by a reduction of the insulin-mediated glucose uptake (28+-3 vs. 16+-1 mg/kg/min, p<0.02). Hepatic glucose production suppression under insulin infusion allowed to conclude that this reduced glucose uptake resulted from a decrease of insulin sensitivity in obese dogs. Furthermore, animals remained normotensive and exhibited a marked hypertriglyceridaemia (0.26+-0.04 vs. 0.76+-0.15 mmol/l, in healthy and obese dogs, respectively, p<0.02). Because hypertriglyceridaemia is the most common lipid abnormality in insulin-resistant humans, this dog with slowly induced obesity may constitute a good model to study the consequences of IR in lipid metabolism independently of vascular changes.
Descriptors: endocrine system, metabolism, nutrition, hypertriglyceridemia, insulin resistance, obesity, nutritional disease, euglycemic hyperinsulinemic clamp technique, laboratory techniques, high fat diet, applied and field techniques.

Costa, M.J., Y. Song, P. Macours, C. Massart, M.C. Many, S. Costagliola, J.E. Dumont, J. Van Sande, and V. Vanvooren (2004). Sphingolipid-cholesterol domains (lipid rafts) in normal human and dog thyroid follicular cells are not involved in thyrotropin receptor signaling. Endocrinology 145(3): 1464-1472. ISSN: 0013-7227.
NAL Call Number: 448.8 EN2
Abstract: Partition of signaling molecules in sphingolipid-cholesterol-enriched membrane domains, among which are the caveolae, may contribute to signal transduction efficiency. In normal thyroid, nothing is known about a putative TSH/cAMP cascade compartmentation in caveolae or other sphingolipid-cholesterol-enriched membrane domains. In this study we show for the first time that caveolae are present in the apical membrane of dog and human thyrocytes: caveolin-1 mRNA presence is demonstrated by Northern blotting in primary cultures and that of the caveolin-1 protein by immunohistochemistry performed on human thyroid tissue. The TSH receptor located in the basal membrane can therefore not be located in caveolae. We demonstrate for the first time by biochemical methods the existence of sphingolipid-cholesterol-enriched domains in human and dog thyroid follicular cells that contain caveolin, flotillin-2, and the insulin receptor. We assessed a possible sphingolipid-cholesterol-enriched domains compartmentation of the TSH receptor and the alpha-subunit of the heterotrimeric Gs and Gq proteins using two approaches: Western blotting on detergent-resistant membranes isolated from thyrocytes in primary cultures and the influence of 10 mM methyl-beta-cyclodextrin, a cholesterol chelator, on basal and stimulated cAMP accumulation in intact thyrocytes. The results from both types of experiments strongly suggest that the TSH/cAMP cascade in thyroid cells is not associated with sphingolipid-cholesterol-enriched membrane domains.
Descriptors: biochemistry and molecular biophysics, endocrine system, chemical coordination and homeostasis, northern blot, genetic techniques, laboratory techniques, signal transduction efficiency.

Critchley, L., B. Ding, B. Fok, D. Wang, B. Tomlinson, A. James, G.N. Thomas, and J. Critchley (2004). The effects of candesartan and ramipril on adrenal catecholamine release in anaesthetized dogs. European Journal of Pharmacology 489(1-2): 67-75. ISSN: 0014-2999.
NAL Call Number: QP901.E8
Descriptors: angiotensin II type 1 receptor antagonist, angiotensin II converting enzyme inhibitor ramipril, endocrine system, chemical coordination and homeostasis, pharmacology, blood pressure.

Fosgerau, K., S.D. Mittelman, A. Sunehag, M.K. Dea, K. Lundgren, and R.N. Bergman (2001). Lack of hepatic "interregulation" during inhibition of glycogenolysis in a canine model. American Journal of Physiology 281(2 Part 1): E375-E383. ISSN: 0002-9513.
NAL Call Number: 447.8 Am3
Abstract: It has been proposed that the glycogenolytic and gluconeogenic pathways contributing to endogenous glucose production are interrelated. Thus a change in one source of glucose 6-phosphate might be compensated for by an inverse change in the other pathway. We therefore investigated the effects of 1,4-dideoxy-1,4-imino-D-arabinitol (DAB), a potent glycogen phosphorylase inhibitor, on glucose production in fasted conscious dogs. When dogs were treated acutely with high glucagon, glucose production rose from 1.93+-0.14 to 3.07+-0.37 mgcntdotkg-1cntdotmin-1 (P<0.01). When dogs were treated acutely with DAB in addition to high glucagon infusion, the stimulation of the glycogenolytic rate was completely suppressed. Glucose production rose from 1.85+-0.20 to 2.41+-0.17 mgcntdotkg-1cntdotmin-1 (P<0.05), which was due to the increase in gluconeogenesis from 0.93+-0.09 to 1.54+-0.08 mgcntdotkg-1cntdotmin-1 (P<0.001). In conclusion, infusion of DAB inhibited glycogenolysis; however, the absolute contribution of gluconeogenesis to glucose production was not affected. These results suggest that inhibition of glycogenolysis could be an effective antidiabetic treatment.
Descriptors: endocrine system, type 2 diabetes, non insulin dependent, endocrine disease, pancreas, metabolic disease, treatment , gluconeogenesis, glycogenolysis, inhibition, hepatic interregulation.

Furukawa, N., M. Hatano, and E. Nakamura (2003). Antro-pancreatic reflexes: long- and short-route reflexes in exocrine and endocrine pancreatic secretion in dogs. Autonomic Neuroscience Basic and Clinical 106(2): 110-118. ISSN: 1566-0702.
Abstract: Pancreatic exocrine secretion is known to be facilitated by gastric antral distension via long- and short-route reflexes. In this study, we studied the effects of gastric distension on intra-pancreatic nerve discharges and blood insulin level as well as pancreatic exocrine secretion. Mongrel dogs were anesthetized with ketamine and thiopental, and immediately decerebrated. This study consisted of two series of experiments. In the first series, efferent discharges in an intra-pancreatic nerve branch were recorded, and its responses to antral distension were analyzed. In the second series, effects of antral distension on pancreatic exocrine secretion and blood insulin level were observed before and after vagotomy in splanchnicectomized dogs. Efferent discharges in a pancreatic nerve branch were increased by antral distension. Neither vagotomy nor splanchnicectomy produced obvious changes in the neural response. In splanchnicectomized dogs, antral distension elevated blood insulin level and increased pancreatic exocrine secretion. After subsequent vagotomy, these effects were reduced, but the increases were still greater than 50%. These results indicate that the antro-pancreatic short-route reflex plays a significant role in exocrine secretion, and also suggest that insulin release is increased by antral distension independent of blood glucose level.
Descriptors: endocrine system, chemical coordination and homeostasis, nervous system, neural coordination, splanchnicectomy, experimental surgical techniques, laboratory techniques, vagotomy, antro pancreatic reflexes, gastric distension.

Gayet, C., B. Siliart, H. Shibata, T. Honjoh, M. Saito, and P. Nguyen (2004). Adiponectin and leptin: early markers of insulin resistance (ir) in a canine model of obesity. International Journal of Obesity 28(Suppl. 1): S168. ISSN: 0307-0565.
NAL Call Number: RC628.A1O2
Descriptors: metabolism, endocrine system, obesity, nutritional disease, insulin resistance, endocrine disease, pancreas, metabolic disease, disease progression, body weight, insulin sensitivity, glucose infusion rate.
Notes: Meeting Information: 13th European Congress on Obesity, Prague, Czech Republic; May 26 -29, 2004.

Gustavson, S.M., M. Nishizawa, B. Farmer, D. Neal, M. Brissova, A.C. Powers, and A.D. Cherrington (2003). A fall in portal vein insulin does not cause the alpha-cell response to mild, non-insulin-induced hypoglycemia in conscious dogs. Metabolism Clinical and Experimental 52(11): 1418-1425. ISSN: 0026-0495.
NAL Call Number: 448.8 M56
Abstract: The aim of the present study was to determine whether a decrease in the portal vein insulin level during non-insulin-induced hypoglycemia is sensed and is responsible for the normal increase in glucagon release from the alpha cell. To address this aim, a glycogen phosphorylase inhibitor was used to create mild, non-insulin-induced hypoglycemia in 2 groups of 18-hour fasted conscious dogs. Arterial insulin was clamped at a basal level in both groups, but in one group (PE) the portal vein insulin level was permitted to fall by approximately 65% while in the other group (POR) it was clamped at a basal level. In both groups glucose was infused at a variable rate to clamp the plasma glucose level at approximately 70 mg/dL. Plasma glucagon (pg/mL) rose to indistinguishable maxima in both groups (56+-3 in PE and 67+-9 in POR). Likewise, glucagon secretion (pg/kg/min) increased similarly (189+-32 to 455+-203 in PE and 192+-50 to 686+-237 in POR). Thus, the increase in glucagon release was not inhibited when the portal vein insulin level was prevented from decreasing (POR group). Clearly, a fall in the portal vein insulin level is not required for a normal alpha-cell response to mild, non-insulin-induced hypoglycemia.
Descriptors: endocrine system, chemical coordination and homeostasis, metabolism, mild non insulin induced hypoglycemia, metabolic disease, alpha cell response.

Harris, G.D., S.J. Vore, K. Salleng, D. Aycock, and C. Yu (2004). Intracranial pressure (icp) during treatment of a diabetic hyperglycemic canine model: 0.45% Vs. 0.9% Saline. Diabetes 53(Suppl. 2): A421. ISSN: 0012-1797.
NAL Call Number: RC658.A1D5
Descriptors: endocrine system, diabetic ketoacidosis, endocrine disease, pancreas, metabolic disease, diabetic hyperglycemia, drug therapy, drug induced, anesthesia, clinical techniques, hematocrit, clinical techniques, diagnostic techniques, mechanical ventilation, laboratory techniques, pancreatectomy.

Kim, S.P., M. Ellmerer, E.L. Kirkman, and R.N.A.R.A. Bergman (2007). Beta-cell "rest" accompanies reduced first-pass hepatic insulin extraction in the insulin-resistant, fat-fed canine model. American Journal of Physiology: Endocrinology and Metabolism 292(6): E1581-E1589. ISSN: 0193-1849.
NAL Call Number: 447.8 Am3
Descriptors: biochemistry and molecular biophysics, nutrition, metabolism, endocrine system, hyperinsulinemia, obesity, magnetic resonance imaging, laboratory techniques, diagnostic techniques, clinical techniques, imaging and microscopy techniques, insulin sensitivity, insulin resistance, glucose homeostasis, isocaloric diet, fat, diet, physiological mechanism, first pass hepatic insulin extraction.

Lamouche, S. and N. Yamaguchi (2003). PACAP release from the canine adrenal gland in vivo: its functional role in severe hypotension. American Journal of Physiology 284(2 Part 2): R588-R597. ISSN: 0002-9513.
NAL Call Number: 447.8 Am3
Abstract: This study was to investigate if endogenous pituitary adenylate cyclase-activating polypeptide (PACAP) can be released during direct splanchnic nerve stimulation in vivo and to determine whether PACAP in the adrenal gland can modulate the medullary response to sympathoadrenal reflex. The output of adrenal catecholamine and PACAP-38-like immunoreactivity (PACAP-38-ir) increased in a frequency-dependent manner after direct splanchnic nerve stimulation (0.2-20 Hz). Both responses were highly reproducible, and PACAP-38-ir output closely correlated with catecholamine output. Sodium nitroprusside (SNP; 0.1 mg/kg iv bolus) caused a severe hypotension resulting in marked increases in catecholamine secretion. In the presence of local PACAP-27 (125 ng), the maximum catecholamine response to SNP was significantly potentiated in a synergistic manner compared with that obtained in the group receiving SNP or PACAP-27 alone. The study indicates that endogenous PACAP-38 can be released particularly when the sympathoadrenal system is highly activated and that the local exogenous PACAP-27 enhanced the reflex-induced catecholamine release, suggesting collectively a facilitating role of PACAP as neuromodulator in the sympathoadrenal function in vivo.
Descriptors: endocrine system, chemical coordination and homeostasis, nervous system, neural coordination, hypotension,vascular disease, sympathoadrenal reflex.

Lantinga Van Leeuwen, I.S., J.A. Mol, H.S. Kooistra, A. Rijnberk, M. Breen, C. Renier, and B.A. Van Oost (2000). Cloning of the canine gene encoding transcription factor pit-1 and its exclusion as candidate gene in a canine model of pituitary dwarfism. Mammalian Genome 11(1): 31-36. ISSN: 0938-8990.
NAL Call Number: QL738.5.M359
Abstract: Combined pituitary hormone deficiency (CPHD) is an autosomal recessive inherited disease of German shepherd dogs characterized primarily by dwarfism. In mice and humans a similar genetic disorder has been described that results from an alteration in the gene encoding the transcription factor Pit-1. In this study we characterized the canine Pit-1 gene, determined the chromosomal localization of the Pit-1 gene, and screened dwarf German shepherd dogs for the presence of mutations in this gene. The full-length canine Pit-1 cDNA contained an open reading frame encoding 291 amino acids, 92 bp of 5'-untranslated region, and 1959 bp of 3'-untranslated region. The deduced amino acid sequence was highly homologous with Pit-1 of other mammalian species. Using a Pit-1 BAC clone as probe, the Pit-1 gene was mapped by FISH to canine Chromosome (Chr) 31. In dwarf German shepherd dogs a C to A transversion was detected, causing a Phe (TTC) to Leu (TTA) substitution at codon 81. This alteration was present neither in other canine breeds analyzed nor in other mammalian species. However, healthy German shepherd dogs were also homozygous for the mutant allele, indicating that it is not the primary disease-causing mutation. In addition, linkage analysis of polymorphic DNA markers flanking the Pit-1 gene, 41K19 and 52L05, revealed no co-segregation between the Pit-1 locus and the CPHD phenotype. These findings suggest that a gene other than Pit-1 is responsible for the pituitary anomaly in dwarf German shepherd dogs.
Descriptors: molecular genetics, endocrine system, chemical coordination and homeostasis, pituitary dwarfism, bone disease, amino acid sequence, chromosome 31.

Lavine, S.J. and P. Prcevski (2007). Effect of glycemic control in a canine model of diabetes and left ventricular dysfunction on left ventricular performance: utility of the index of myocardial performance. Journal of the American College of Cardiology 49(9, Suppl. A): 62A. ISSN: 0735-1097.
NAL Call Number: RC681.A1
Descriptors: metabolism, endocrine system, diabetes, left ventricular dysfunction, heart disease, diabetic cardiomyopathy, glycemic control.
Notes: Meeting Information: 56th Annual Scientific Session of the American College of Cardiology, New Orleans, LA, USA; March 24 -27, 2007.

Lee, T.M., M.S. Lin, T.F. Chou, C.H. Tsai, and N.C. Chang (2004). Adjunctive 17beta-estradiol administration reduces infarct size by altered expression of canine myocardial connexin43 protein. Cardiovascular Research 63(1): 109-117. ISSN: 0008-6363.
NAL Call Number: QM178.A1C38
Descriptors: cardiovascular system, transport and circulation, endocrine system, chemical coordination and homeostasis, pharmacology, coronary occlusion, heart disease, ischemia, vascular disease, ischemia reperfusion injury, myocardial infarction, western blot, genetic techniques, confocal microscopy, imaging and microscopy techniques, lucigenin derived chemiluminescence, laboratory techniques, infarct size.

Liberty, I.F., V. Ionut, S.P. Kim, M. Ader, M. Lottati, and R.N. Bergman (2005). Hiv-protease inhibitor treatment, a new canine experimental model of insulin resistance. Journal of Investigative Medicine 53(1, Suppl. S): S106-S107. ISSN: 1081-5589.
NAL Call Number: R11.C5
Descriptors: endocrine system, chemical coordination and homeostasis, insulin resistance, metabolic disease, endocrine disease, insulin sensitivity.
Notes: Meeting Information: Western Student Medical Research Forum held in conjunction with the Western Section of the American Federation for Medical Research/Western Society for Clinical Investigation/Western Association of Physicians/Western Society for Pediatric Research, Carmel, CA, USA; February 3-5, 2005.

Mraovic, B.A., F.A. Kehl, P.S. Pagel, D.C. Warltier, and J.R. Kersten (2002). Hyperglycemia attenuates coronary collateral development in a canine model of repetitive coronary artery occlusion. Anesthesiology Abstracts of Scientific Papers Annual Meeting(2001): Abstract No. A-635.
Descriptors: anesthesiology, medical sciences, cardiovascular medicine, clinical endocrinology, human medicine, pharmacology, diabetes mellitus, endocrine disease, pancreas, metabolic disease, complications, hyperglycemia , repetitive coronary artery occlusion, heart disease, vascular disease, hemodynamics .
Notes: Meeting Information: 2001 Annual Meeting of the American Society of Anesthesiologists, New Orleans, LA, USA; October 13-17, 2001.

Oktaei, H., M.H. Shokouh Amiri, L. Gaber, O. Gaber, A. Salem, and A.E. Kitabchi (2005). The effect of chronic hyperinsulinemia on coronary arteries in nontransplant dog model. Journal of Investigative Medicine 53(1, Suppl. S): S322. ISSN: 1081-5589.
NAL Call Number: R11.C5
Descriptors: cardiovascular system, transport and circulation, endocrine system, chemical coordination and homeostasis, atherosclerosis, vascular disease, chronic hyperinsulinemia, endocrine disease, pancreas, endocrine disease, risk factor.
Notes: Meeting Information: Western Student Medical Research Forum held in conjunction with the Western Section of the American Federation for Medical Research/Western Society for Clinical Investigation/Western Association of Physicians/Western Society for Pediatric Research, Carmel, CA, USA; February 3-5, 2005.

Oktaei, H., S.A. Hosein, G. Osama, B.A. Michael, A. Salem, and A. Kitabch (2003). The effect of surgical menopause on lipid and carbohydrate metabolism, in six years model of hyperinsulinemia in dogs. Diabetes 52(Supplement 1): A293. ISSN: 0012-1797.
NAL Call Number: RC658.A1D5
Descriptors: endocrine system, chemical coordination and homeostasis, metabolism, hyperinsulinemia , endocrine disease, pancreas, metabolic disease, ovariectomy, experimental surgical techniques, laboratory techniques, menopause.
Notes: Meeting Information: 63rd Scientific Sessions of the American Diabetes Association, New Orleans, LA, USA; June 13-17, 2003.

Okuda, Y., J. Pena, J. Chou, and J.B. Field (2001). Acute effects of growth hormone on metabolism of pancreatic hormones, glucose and ketone bodies. Diabetes Research and Clinical Practice 53(1): 1-8. ISSN: 0168-8227.
Abstract: Controversy exists as to whether acute administration of growth hormone has insulin-like effects. In conscious dogs, acute effects on plasma flows, plasma glucose, hepatic glucose output, free fatty acids, ketone bodies, insulin, and glucagon were determined following intravenous injection of 1 mg of growth hormone extracted from the canine pituitary gland. The following results were obtained: (1) Plasma flows in the portal vein, hepatic artery and hepatic vein were significantly increased 20 min after growth hormone administration. (2) By 40 min after growth hormone, the glucose concentration in these three vessels was significantly increased. (3) Hepatic glucose output was significantly increased 60 min after growth hormone administration. (4) Free fatty acids levels were significantly but transiently increased at 20 min, while ketone body concentrations were elevated at 120-180 min. (5) The insulin levels in the three vessels demonstrated a biphasic response. In the portal vein, they were significantly higher 20 min after growth hormone and again at 150-180 min. Glucagon concentrations were increased in all three vessels by 20 min and remained elevated for the remainder of the experiment. These results do not support an acute insulin-like action of growth hormone in normal dogs.
Descriptors: animal model, growth hormone, insulin-like effects, plasma glucose, glucagon.

Ozaki, K.I., K. Yogo, H. Sudo, H. Muramatsu, K. Kamei, Y. Kawabe, Z. Itoh, S. Omura, and H. Takanashi (2007). Mitemcinal (gm-611), an orally active motilin receptor agonist, accelerates gastric emptying in a diabetic gastroparesis dog model. Gastroenterology 132(4, Suppl. 2): A685. ISSN: 0016-5085.
Descriptors: pharmacology, nervous system, neural coordination, digestive system, ingestion and assimilation, veterinary medicine, medical sciences, hyperglycemia ,metabolic disease, renal failure, urologic disease, liver failure, digestive system disease, gastroparesis, nervous system disease, digestive system disease, diabetes, endocrine disease, pancreas, toxicity, metabolic disease, drug induced, aap method, laboratory techniques, gastric emptying.
Notes: Meeting Information: Digestive Disease Week Meeting/108th Annual Meeting of the American Gastroenterological Association, Washington, DC, USA; May 19-24, 2007.

Rashid, S., Z.Q. Shi, M. Niwa, J.M.R. Mathoo, M. Vandelangeryt, D. Bilinski, G.F. Lewis, and M. Vranic (2000). Beta-blockade, but not normoglycemia or hyperinsulinemia, markedly diminishes stress-induced hyperglycemia in diabetic dogs. Diabetes 49(2): 253-262. ISSN: 0012-1797.
NAL Call Number: RC658.A1D5
Abstract: Stress-induced hyperglycemia can lead to significant deterioration in glycemic control in individuals with diabetes. Previously, we have shown in normal dogs that, after intracerebroventricular (ICV) administration of carbachol (a model of moderate stress), increases in both the metabolic clearance rate (MCR) of glucose and endogenous glucose production (GP) occur. However, in hyperglycemic diabetic dogs subjected to the same stress, the MCR of glucose does not increase and glycemia therefore markedly deteriorates because of stimulation of GP. Our aims were to determine the following: 1) whether insulin-induced acute normalization of glycemia, with or without beta-blockade, would correct glucose clearance and prevent the hyperglycemic effect of stress, and 2) whether hyperinsulinemia per se could correct these abnormalities. Stress was induced by ICV carbachol in 27 experiments in five alloxan-administered diabetic dogs subjected to the following protocols in random order: 1) basal insulin infusion (BI) to restore normoglycemia; 2) basal insulin infusion with beta-blockade (BI+block); 3) normoglycemic-hyperinsulinemic clamp with threefold elevation of insulin above basal (3X BI); and 4) normoglycemic-hyperinsulinemic clamp with fivefold elevation of insulin above basal (5X BI). The BI+block protocol fully prevented stress-induced hyperglycemia, both by increasing MCR (DELTAMCR at peak: 0.72+-0.25 mlcntdotkg-1cntdotmin-1 vs. no change in BI, P<0.05) and by diminishing the stress-induced increment in GP observed in BI (DELTAGP at peak: 3.72+-0.09 mumolcntdotkg-1cntdotmin-1 for BI+block vs. 14.10+-0.31 mumolcntdotkg-1cntdotmin-1 for BI, P<0.0001). In contrast, 3X BI and 5X BI treatments with normoglycemic-hyperinsulinemic clamps proportionately increased basal MCR at baseline, but paradoxically were not associated with an increase in MCR in response to stress, which induced a twofold increase in GP. Thus, in alloxan-administered diabetic dogs, stress increased GP but not MCR, despite normalization of glycemia with basal or high insulin. In contrast, beta-adrenergic blockade almost completely restored the metabolic response to stress to normal and prevented marked hyperglycemia, both by limiting the rise in GP and by increasing glucose MCR. We conclude that acute normalization of glycemia with basal insulin or hyperinsulinemia does not prevent hyperglycemic effects of stress unless accompanied by beta-blockade, and we speculate that short-term beta-blockade may be a useful treatment modality under some stress conditions in patients with diabetes.
Descriptors: behavior, endocrine system, chemical coordination and homeostasis, metabolism, diabetes, endocrine disease, pancreas, metabolic disease, hyperinsulinemia, pancreas, stress induced hyperglycemia, beta blockade therapy, clinical potential, pharmacological method, physiological method, short term, glycemic control, metabolic clearance rate, normoglycemia.

Shackleford, D.M., W.A.F. Faassen, N. Houwing, H. Lass, G.A. Edwards, C.J.H. Porter, and W.N. Charman (2003). Contribution of lymphatically transported testosterone undecanoate to the systemic exposure of testosterone after oral administration of two andriol formulations in conscious lymph duct-cannulated dogs. Journal of Pharmacology and Experimental Therapeutics 306(3): 925-933. ISSN: 0022-3565.
NAL Call Number: 396.8 J82
Abstract: Orally administered testosterone (T) is ineffective in the treatment of male androgen deficiency syndromes due to extensive presystemic first-pass metabolism. In contrast, the lipophilic long-chain ester testosterone undecanoate (TU) exhibits androgenic activity that has been attributed to formation of T via systemic hydrolysis of lymphatically transported TU. However, there are no definitive data regarding the oral bioavailability of TU or the extent to which lymphatically transported TU contributes to the systemic availability of T after oral TU administration. This report describes the application of stable isotope methodology in a thoracic lymph duct-cannulated dog model to study the oral bioavailability and lymphatic transport of TU after postprandial administration. When administered as either Andriol or Andriol Testocaps, the mean (+-S.E., n=4) absolute bioavailability of TU was 3.25+-0.48 and 2.88+-0.88%, respectively, and lymphatically transported TU accounted for between 91.5 and 99.7% of the systemically available ester. Model-independent pharmacokinetic analysis indicated that 83.6+-1.6 and 84.1+-8.2% of the systemically available T, resulting from Andriol or Andriol Testocaps, respectively, was due to systemic hydrolysis of lymphatically transported TU. These data demonstrate that intestinal lymphatic transport of TU produces increased systemic exposure of T by avoiding the extensive first-pass effect responsible for the inactivation of T after oral administration.
Descriptors: blood and lymphatics, transport and circulation, endocrine system, chemical coordination and homeostasis, pharmacology, androgen deficiency syndrome, reproductive system disease, pharmacokinetic analysis, laboratory techniques.

Sivakumar, A.V.N., V. Leela, S. Viswanathan, and M. Nayeem (2001). Effect of induced hyperthyroidism by thyroxine injection on cardiovascular function in canine model. Indian Veterinary Journal 78(5): 397-399. ISSN: 0019-6479.
NAL Call Number: 41.8 IN2
Abstract: Experimental hyperthyroidism was produced in dogs by L-thyroxine injection and it was observed that most of the segments of ECG were increased and both the B.P. and heart rate were found to be increased. Hence care must be taken to regulate the dosage of thyroxine in substitution therapy in clinical cases of hypothyroidism.
Descriptors: cardiovascular system, transport and circulation, endocrine system, chemical coordination and homeostasis, pharmacology, hyperthyroidism , endocrine disease, thyroid, electrocardiography, analytical method, blood pressure, cardiovascular function, heart rate.

Tashiro, H., H. Iwata, G.L. Warnock, Y. Ikada, and T. Tsuji (1997). Application of agarose microcapsule to allo-islet transplantation in canine model. Acta Diabetologica 34(2): 103. ISSN: 0940-5429.
NAL Call Number: RC660.A1
Descriptors: endocrine system, chemical coordination and homeostasis, metabolism, physiology, agarose microcapsule, animal model, bioartificial pancreas, diabetes, endocrine disease, pancreas, endocrine system, functional efficacy, independence, insulin, islet allotransplantation, metabolic disease, therapeutic method.
Notes: Meeting Information: 6th Congress of the International Pancreas and Islet Transplant Association (IPITA) 1997, Milan, Italy; September 24-27, 1997.

Tolan, I.A., D. Ragoobirsingh, and E.Y.S.A. Morrison (1997). In vivo studies of the effects of capsaicin on blood glucose levels and insulin binding using dog models. Diabetologia 40(SUPPL. 1): A243. ISSN: 0012-186X.
NAL Call Number: RC660.A1D52
Descriptors: blood and lymphatics, transport and circulation, endocrine system, chemical coordination and homeostasis, metabolism, pharmacognosy, antidiabetic drug binding, blood levels, capsaicin, diabetes, glucose, pharmacodynamics.
Notes: Meeting Information: 16th International Diabetes Federation Congress, Helsinki, Finland; July 20-25, 1997.

Wu Jian Hui , Sun Zu Yue , Zhong En Hong , Zhu Yan , Liu Gui Ming , He Gui Lin , and Cao Lin (2003). Pathology changes of vas deferens in benign prostatic hyperplasia model of beagle dogs. Zhongguo Yaolixue Yu Dulixue Zazhi 17(3): 221-226. ISSN: 1000-3002.
Abstract: AIM: The objective of this investigation was to research the proliferation mechanism of vas deferens in benign prostatic hyperplasia. METHODS: The vas deferens, from beagle dogs which have been administered testosterone propionate(TP) to build benign prostatic hyperplasia model in vivo, was analyzed by a series of methods. Dihydrotestosterone (DHT) in vas deferens was detected by radioimmunoassay, the slices (4 mum) of vas deferens were stained with HE, and the duct area as well as the height of epithelial cell were measured with videodensitometer. The apoptosis rate was determined by flow cytometry method. The expression of prostatic specific antigen (PSA), prostatic acid phosphatase (PAP), Bcl-2 and P53 were determined by immunohistochemical methods. The nucleosomal DNA fragmentation was monitored by agarose gel electrophoresis. RESULTS: DHT level of vas deferens was increased with increasing TP doses, but there was no significant difference between groups. After being administered TP, the duct area of vas deferens was enlarged (P<0.01), and the height of epithelial cell was increased (P<0.01). The cell apoptosis rate of control was higher than that of 0.8 and 7.5 mgcntdotkg-1 TP groups(P<0.01). While there were no differences in expression of PSA, PAP and Bcl-2 between control and other groups, the expression of P53 of control was higher than that of the other groups(P<0.05). In agarose gel electrophoresis, the 200 bp base pair DNA fragments and the multiples of them were observed in control, while similar phenomenon didn't find in other groups. CONCLUSION: DHT induces vas deferens to proliferate, and the proliferation of vas deferens is related to inhibition of apoptosis.
Descriptors: endocrine system, chemical coordination and homeostasis, reproductive system, reproduction, tumor biology, benign prostatic hyperplasia, reproductive system disease, male, urologic disease, pathology changes, proliferation mechanism.
Language of Text: Chinese.

Yamaguchi, N., T.R. Minassian, and S. Yamaguchi (2003). Effects of pacap1-27 on the canine endocrine pancreas in vivo: interaction with cholinergic mechanism. Canadian Journal of Physiology and Pharmacology 81(7): 720-729. ISSN: 0008-4212.
NAL Call Number: 470 C16E
Abstract: The aim of the present study was to characterize the effects of pituitary adenylate cyclase activating polypeptide (PACAP) on the endocrine pancreas in anesthetized dogs. PACAP1-27 and a PACAP receptor (PAC1) blocker, PACAP6-27, were locally administered to the pancreas. PACAP1-27 (0.005-5 mug) increased basal insulin and glucagon secretion in a dose-dependent manner. PACAP6-27 (200 mug) blocked the glucagon response to PACAP1-27 (0.5 mug) by about 80%, while the insulin response remained unchanged. With a higher dose of PACAP6-27 (500 mug), both responses to PACAP1-27 were inhibited by more than 80%. In the presence of atropine with an equivalent dose (128.2 mug) of PACAP6-27 (500 mug) on a molar basis, the insulin response to PACAP1-27 was diminished by about 20%, while the glucagon response was enhanced by about 80%. The PACAP1-27-induced increase in pancreatic venous blood flow was blocked by PACAP6-27 but not by atropine. The study suggests that the endocrine secretagogue effect of PACAP1-27 is primarily mediated by the PAC1 receptor, and that PACAP1-27 may interact with muscarinic receptor function in PACAP-induced insulin and glucagon secretion in the canine pancreas in vivo.
Descriptors: biochemistry and molecular biophysics, endocrine system, chemical coordination and homeostasis, cholinergic mechanism, pancreatic venous blood flow.

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