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Geelong West, Australia

Shephard R.W.,Herd Health Pty Ltd | Shephard R.W.,Charles Sturt University | Morton J.M.,Jemora Pty Ltd. | Norman S.T.,Charles Sturt University
Animal Reproduction Science | Year: 2014

A controlled trial investigating the effect on conception of administration of 250. μg of gonadotropin-releasing hormone (GnRH) at artificial insemination (AI) in dairy cows in seasonal or split calving herds was conducted. Time of detection of estrus, body condition, extent of estrous expression, treatment, breed, age and milk production from the most recent herd test of the current lactation was recorded. Cows were tested for pregnancy with fetal aging between 35 and 135 days after AI. Sixteen herds provided 2344 spring-calved cows and 3007 inseminations. Logistic regression adjusting for clustering at herd level was used to examine the effect of treatment for first (2344) and second (579) inseminations separately. For first AI, treatment significantly improved conception rate in cows with milk protein concentrations of 3.75% or greater and for cows with milk protein concentrations between 3.00% and 3.50% and less than 40 days calved; increased conception rate from 41.2% to 53.4%. Treatment reduced conception rates in cows with milk protein concentrations of 2.75% or less. Treating only cows identified as responding positively to treatment (11% of all study cows) was estimated to increase first service conception rate in herds from 48.1% to 49.4%. There was no significant effect of treatment on conception to second AI, nor any significant interactions. These findings indicate that GnRH at AI should be limited to the sub-group cows most likely to respond. The positive effect of GnRH at AI may be mediated through improved oocyte maturation and/or improved luteal function, rather than by reducing AI-to-ovulation intervals. © 2013 Elsevier B.V. Source

Baral R.M.,Paddington Cat Hospital | Baral R.M.,University of Sydney | Dhand N.K.,University of Sydney | Morton J.M.,Jemora Pty Ltd. | And 2 more authors.
Journal of Feline Medicine and Surgery | Year: 2015

In-house analysers are commonplace in small animal practices but cannot be calibrated by the operator; therefore, any bias in the generated plasma analyte values cannot be corrected. Guidelines such as grading of renal disease and published reference intervals (RIs) in veterinary textbooks assume plasma biochemistry values generated by different analysers are equivalent. This study evaluated the degree of bias, as well as if bias was constant or proportional, for feline plasma biochemical analytes assessed by three in-house biochemistry analysers compared with a commercial laboratory analyser. Blood samples were collected on 101 occasions from 94 cats and, after centrifugation, plasma was divided into four aliquots. One aliquot was sent to the commercial laboratory and the remaining three were tested using the in-house biochemistry analysers. Results from each analyser were compared with the commercial laboratory results by difference plots and analyses, and by comparing percentages of results within provided RIs. Substantial bias was evident relative to the results of the commercial analyser for at least half of the analytes tested for each machine. In most cases, bias was proportional, meaning that the difference between the methods varied with the concentration of the analyte. The results demonstrate that values obtained from these analysers should not be directly compared and that RIs are not transferable between these analysers. Potential effects of bias on clinical decision-making may be overcome by use of appropriately generated RIs, or reference change values which, for most biochemistry analytes, are more appropriate than subject-based RIs. © ISFM and AAFP 2014. Source

Farrow H.,University of Queensland | Rand J.S.,University of Queensland | Morton J.M.,University of Queensland | Morton J.M.,Jemora Pty Ltd. | Sunvold G.,The Iams Company
Journal of Feline Medicine and Surgery | Year: 2012

The postprandial increase in glucose concentration is typically not considered in selecting diets to manage diabetic and pre-diabetic cats. This study describes increases in glucose and insulin concentrations in 24 clinically healthy, neutered adult cats following one meal (59 kcal/kg) of a moderate carbohydrate diet (25% of energy). Median time to return to baseline after feeding for glucose was 12.2 h (1.8-≥24 h) and for insulin was 12.3 h (1.5-≥24 h). Time to return to baseline for glucose was not different between male (10.2 h) and female (17.2 h) cats. There was evidence female cats had a longer return to baseline for insulin (18.9 h versus 9.8 h) and females had higher (0.9 mmol/l difference) peak glucose than males. This demonstrates that the duration of postprandial glycaemia in cats is markedly longer than in dogs and humans, and should be considered when managing diabetic and pre-diabetic cats. © ISFM and AAFP 2012. Source

Verkest K.R.,University of Queensland | Fleeman L.M.,University of Queensland | Rand J.S.,University of Queensland | Morton J.M.,University of Queensland | Morton J.M.,Jemora Pty Ltd.
American Journal of Veterinary Research | Year: 2011

Objective - To compare beta-cell sensitivity to glucose, first-phase insulin secretion, and glucose tolerance between dogs with naturally occurring obesity of > 2 years' duration and lean dogs. Animals - 17 client-owned obese or lean dogs. Procedures - Frequently sampled IV glucose tolerance tests were performed with minimal model analysis on 6 obese dogs and matched controls. Glucagon stimulation tests were performed on 5 obese dogs and matched controls. Results - Obese dogs were half as sensitive to the effects of insulin as lean dogs. Plasma glucose concentrations after food withholding did not differ significantly between groups; plasma insulin concentrations were 3 to 4 times as great in obese as in lean dogs. Obese dogs had plasma insulin concentrations twice those of lean dogs after administration of glucose and 4 times as great after administration of glucagon. First-phase insulin secretion was greater in obese dogs. Conclusions and Clinical Relevance - Obese dogs compensated for obesity-induced insulin resistance by secreting more insulin. First-phase insulin secretion and beta-cell glucose sensitivity were not lost despite years of obesity-induced insulin resistance and compensatory hyperinsulinemia. These findings help explain why dogs, unlike cats and humans, have not been documented to develop type 2 diabetes mellitus. Source

Verkest K.R.,University of Queensland | Rand J.S.,University of Queensland | Fleeman L.M.,University of Queensland | Morton J.M.,University of Queensland | Morton J.M.,Jemora Pty Ltd.
Domestic Animal Endocrinology | Year: 2012

Dogs do not appear to progress from obesity-induced insulin resistance to type 2 diabetes mellitus. Both postprandial hyperglycemia and postprandial hypertriglyceridemia have been proposed to cause or maintain beta cell failure and progression to type 2 diabetes mellitus in other species. Postprandial glucose, triglyceride, and insulin concentrations have not been compared in lean and obese dogs. We measured serum glucose, triglyceride, and insulin concentrations in nine naturally occurring obese and nine age- and gender-matched lean dogs. After a 24-h fast, dogs were fed half their calculated daily energy requirement of a standardized diet that provided 37% and 40% of metabolizable energy as carbohydrate and fat, respectively. Fasting and postprandial glucose and triglyceride concentrations were greater in the obese dogs (P < 0.001), although the mean insulin concentration for this group was five times greater than that of the lean group (P < 0.001). Most of the 0.6 mM (11 mg/dL) difference in mean postprandial glucose concentrations between lean and obese dogs was attributable to a subset of persistently hyperglycemic obese dogs with mean postprandial glucose concentrations 1.0 mM (18 mg/dL) greater than that in lean dogs. Persistently hyperglycemic obese dogs had lower triglyceride (P = 0.02 to 0.04) and insulin (P < 0.02) concentrations than other obese dogs. None of the dogs developed clinical signs of diabetes mellitus during follow-up for a median of 2.6 yr. We conclude that pancreatic beta cells in dogs are either not sensitive to toxicity because of mild hyperglycemia or lack another component of the pathophysiology of beta cell failure in type 2 diabetes mellitus. © 2012 Elsevier Inc. Source

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