D. J. Appleton
University of Queensland
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Featured researches published by D. J. Appleton.
Journal of Feline Medicine and Surgery | 2001
D. J. Appleton; J. S. Rand; Gregory Dean Sunvold
This study quantifies the effects of marked weight gain on glucose and insulin metabolism in 16 cats which increased their weight by an average of 44.2% over 10 months. Significantly, the development of feline obesity was accompanied by a 52% decrease in tissue sensitivity to insulin and diminished glucose effectiveness. In addition, glucose intolerance and abnormal insulin response occurred in some cats. An important finding was that normal weight cats with low insulin sensitivity and glucose effectiveness were at increased risk of developing impaired glucose tolerance with obesity. High basal insulin concentrations or low acute insulin response to glucose also independently increased the risk for developing impaired glucose tolerance. Male cats gained more weight relative to females and this, combined with their tendency to lower insulin sensitivity and higher insulin concentrations, may explain why male cats are at greater risk for diabetes. Results suggest an underlying predisposition for glucose intolerance in some cats, which is exacerbated by obesity. These cats may be more at risk of progressing to overt type 2 diabetes mellitus.
Journal of Feline Medicine and Surgery | 2000
D. J. Appleton; J. S. Rand; Gregory Dean Sunvold
The aims of our study were to determine a reference range for plasma leptin in healthy, normal-weight cats and to measure the effect of weight gain on plasma leptin levels. To increase our understanding of the association between leptin and feline obesity, we investigated the relationship between plasma leptin and measures of adiposity in cats. Twenty-six normal-weight cats were used to determine the reference range for feline leptin using a multispecies radioimmunoassay. In the second part of the study, plasma leptin concentrations were determined in 16 cats before and after approximately 10 months of spontaneous weight gain. Dual energy X-ray absorptiometry scans (DEXA) were performed after weight gain. The tolerance interval for plasma leptin concentrations was 0.92–11.9 ng/ml Human Equivalent (HE) with a mean concentration of 6.41 ± 2.19 ng/ml HE. In part two of the study, 16 cats gained on average 44.2% bodyweight over 10 months. The percentage of body fat in obese cats ranged from 34.2 to 48.7%. Mean plasma leptin concentrations increased from 7.88 ± 4.02 ng/ml HE before weight gain to 24.5 ± 12.1 ng/ml HE after weight gain, (P < 0.001). Total body fat and body fat per cent were the strongest predictors of plasma leptin in obese cats (r = 0.8 and r = 0.78, P < 0.001, respectively). In conclusion, plasma leptin concentrations increased three-fold in cats as a result of weight gain and were strongly correlated with the amount of adipose tissue present. Despite elevated leptin levels, cats continued to eat and gain weight, suggesting decreased sensitivity to leptin. This investigation into the biology of leptin in cats may aid the overall understanding of the role of leptin and the development of future treatments to help prevent and manage feline obesity.
Journal of Feline Medicine and Surgery | 2005
D. J. Appleton; J. S. Rand; Gregory Dean Sunvold
The objective of this study was to compare simpler indices of insulin sensitivity with the minimal model-derived insulin sensitivity index to identify a simple and reliable alternative method for assessing insulin sensitivity in cats. In addition, we aimed to determine whether this simpler measure or measures showed consistency of association across differing body weights and glucose tolerance levels. Data from glucose tolerance and insulin sensitivity tests performed in 32 cats with varying body weights (underweight to obese), including seven cats with impaired glucose tolerance, were used to assess the relationship between Bergmans minimal model-derived insulin sensitivity index (SI), and various simpler measures of insulin sensitivity. The most useful overall predictors of insulin sensitivity were basal plasma insulin concentrations and the homeostasis model assessment (HOMA), which is the product of basal glucose and insulin concentrations divided by 22.5. It is concluded that measurement of plasma insulin concentrations in cats with food withheld for 24 h, in conjunction with HOMA, could be used in clinical research projects and by practicing veterinarians to screen for reduced insulin sensitivity in cats. Such cats may be at increased risk of developing impaired glucose tolerance and type 2 diabetes mellitus. Early detection of these cats would enable preventative intervention programs such as weight reduction, increased physical activity and dietary modifications to be instigated.
Journal of Feline Medicine and Surgery | 2002
D. J. Appleton; J. S. Rand; Gregory Dean Sunvold
This study investigated relationships between plasma leptin, insulin concentrations, insulin sensitivity and glucose tolerance in lean and overweight cats. Leptin concentrations were measured in 16 cats during glucose tolerance tests before and after gaining weight, and after feeding a test meal in overweight cats. An important finding of this study is that in both lean (r=-0.79) and overweight (r=-0.89) cats, the higher the leptin concentrations, the more insulin resistant the cat, independent of the degree of adiposity. Leptin concentrations at baseline and after consuming a meal tended to be higher in overweight cats with glucose intolerance, compared to overweight cats with normal glucose tolerance, although the difference was not significant. After feeding the test meal to overweight cats in the early morning, plasma leptin concentrations initially decreased before subsequently rising to peak 15 h later, which coincided with late evening. The leptin peak occurred 9 h after the insulin peak following ingestion of the test meal. Importantly, this study suggests that increased leptin concentrations may contribute to the diminished insulin sensitivity seen in overweight cats. Alternatively, the compensatory hyperinsulinaemia found with insulin resistance in overweight cats could stimulate leptin production.
Journal of Feline Medicine and Surgery | 2002
D. J. Appleton; J. S. Rand; Gregory Dean Sunvold; J Priest
The effect of dietary chromium supplementation on glucose and insulin metabolism in healthy, non-obese cats was evaluated. Thirty-two cats were randomly divided into four groups and fed experimental diets consisting of a standard diet with 0 ppb (control), 150 ppb, 300 ppb, or 600 ppb added chromium as chromium tripicolinate. Intravenous glucose tolerance, insulin tolerance and insulin sensitivity tests with minimal model analysis were performed before and after 6 weeks of feeding the test diets. During the glucose tolerance test, glucose concentrations, area under the glucose concentration-time curve, and glucose half-life (300 ppb only), were significantly lower after the trial in cats supplemented with 300 ppb and 600 ppb chromium, compared with values before the trial. Fasting glucose concentrations measured on a different day in the biochemistry profile were also significantly lower after supplementation with 600 ppb chromium. There were no significant differences in insulin concentrations or indices in either the glucose or insulin tolerance tests following chromium supplementation, nor were there any differences between groups before or after the dietary trial. Importantly, this study has shown a small but significant, dose-dependent improvement in glucose tolerance in healthy, non-obese cats supplemented with dietary chromium. Further long-term studies are warranted to determine if the addition of chromium to feline diets is advantageous. Cats most likely to benefit are those with glucose intolerance and insulin resistance from lack of exercise, obesity and old age. Healthy cats at risk of glucose intolerance and diabetes from underlying low insulin sensitivity or genetic factors may also benefit from long-term chromium supplementation.
22nd Annual American College of Veterinary Internal Medicine Forum | 2004
D. J. Appleton; J. S. Rand
Numerous genes of E. coli encode proteins putatively important to urovirulence,for example, adhesins and protectins. Human, canine, and feline urinary E. coli isolates have been characterized on the basis of their extended urovirulence genotypes in studies that typically test for the presence or absence of about 25 of these genes. It has been reported recently that extended urovirulence genotypes of canine and feline urinary E. coli isolates overlap with, and are essentially indistinguishable from, those of human strains that cause serious extraintestinal infections. On the basis of these and other phylogenetic findings, concern has been expressed that some canine and feline uropathogenic E. coli strains pose a significant human health hazard. However, very few canine isolates and even fewer feline isolates have been adequately studied to date.
Journal of Nutrition | 2004
J. S. Rand; L. M. Fleeman; H. A. Farrow; D. J. Appleton; R. Lederer
Nutrition Research | 2004
D. J. Appleton; J. S. Rand; J Priest; Gregory Dean Sunvold; J.R Vickers
Asia Pacific Journal of Clinical Nutrition | 2003
J. S. Rand; H. A. Farrow; L. M. Fleeman; D. J. Appleton
Journal of Veterinary Internal Medicine | 2013
M. K. Reeve-Johnson; J. S. Rand; S. T. Anderson; D. J. Appleton; D. Vankan; J. Morton