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Biomedical subjects

D W Hamar

Publications and source records attributed to D W Hamar.

54 records · Page 3Linked to original sources

Prevention of oxalate urolithiasis by some compounds.

Male Wistar rats were fed a basal diet, Purina Laboratory Chow, and an oxalate calculi-producing diet (CPD). The CPD was the basal diet containing 3 per cent glycolic acid. Sodium pyruvate, DL-alanine, alpha-keto glutaric acid, thiamine pyrophosphate, and L-glutamic acid were added to the CPD to determine their effectiveness in preventing calculi formation. The effectiveness of methyl glyoxal was determined by adding it to the drinking water. Rats fed CPD for 4 weeks developed calculi in the ureters, bladder, renal tubules, and/or renal pelvis and papilla. Rats in groups fed alanine and/or pyruvate had no calculi in their renal tubules or ureters; additionally, these rats had a significant reduction in incidence and amount of deposits in the renal pelvis and bladder. Rats in groups fed alpha-keto glutaric acid, thiamine pyrophosphate, L-glutamic acid, and methyl glyoxal developed equally or more severe oxalate urolithiasis than those on CPD alone. Results of this study show that either pyruvate or alanine at appropriate levels may be beneficial in preventing oxalate urolith formation.

Alanine↗

Control of oxalate urolithiasis by DL-alanine.

Oxalate urolithiasis in male rats was experimentally induced by feeding a basal diet composed of Purina laboratory chow and 3 per cent glycolic acid. When this basal oxalate calculus-producing diet containing 10 per cent alanine was fed to rats, the incidence of oxalate urolithiasis was markedly reduced. Moreover, when Purina laboratory chow containing 10 per cent alanine was fed to rats which had been on the calculi-producing basal diet for 4 weeks, it appeared that most uroliths were dissolved. Excess intake of alanine increased the concentration of alanine in urine and this apparently aided in the prevention and treatment of urolithiasis.

Administration, Oral↗

Effects of neutering on bodyweight, metabolic rate and glucose tolerance of domestic cats.

Few controlled studies have been made of the possible mechanisms and physiological consequences of weight gain after cats have been neutered. In this study, six male and six female cats were gonadectomised and compared with five entire male and six entire female cats, before they were neutered and one and three months later. The neutered males gained significantly more weight (mean [SEM] per cent) than the entire males (30.2 [5.2] v 11.8 [2.3]) and the entire females gained 40.0 (7.3) v 16.1 (3.3) per cent, (P < 0.05). The castrated males gained more weight as fat than the sexually intact males (22.0 [3.3] v 8.8 [4.5] per cent, P < 0.05). There was a significant increase (P < 0.05) in daily food intake after neutering. Spayed females underwent a significant decrease in fasting metabolic rate (83.7 [5.5] v 67.2 [2.3] kcal/kg bodyweight0.75/day P < 0.05). Gonadectomy had minimal effects on serum thyroid hormone concentrations, the resting or fasting metabolic rates in males, or on indices of glucose tolerance.

Adipose Tissue↗

Effects of weight gain and loss on metabolic rate, glucose tolerance, and serum lipids in domestic cats.

Weight gain is a common problem in domestic cats, but little is known about its metabolic effects. The purpose of this study was to determine the effects of diet-induced weight gain and subsequent weight loss on metabolic rate, body composition, and glucose tolerance. Gain of approximately 20 per cent body weight (divided approximately equally between fat and fat-free mass) over three months resulted in insulin resistance in females, indicated by increases in basal insulin concentration (68.2+/-7.9 to 119+/-16.5 pmol litre(-1), P<0.05), insulin peak response to glucose (241.1+/-31.6 to 315.0+/-23.0 pmol litre(-1), P<0.05), and deltaI/deltaG (14.2+/-2.6 to 18.1+/-1.3 pmol mmol(-1), P<0.05) compared with pre-gain values. The same numerical trend was noted in male cats, however, changes were not significant (P>0.05). Alterations in serum lipids included significant (P<0.05) elevations in triglyceride concentrations in male cats and decreased beta-lipoprotein concentrations in both genders. Weight loss over three months normalised basal insulin, insulin response to glucose, and serum triglyceride concentrations, and resulted in significant (P<0.05) decreases in serum concentrations of beta- and prebeta-lipoproteins, cholesterol, and triiodothyronine. Diet-induced weight gain of three months' duration, followed by three months' maintenance of increased body weight did not affect fasting or resting metabolic rate. Development and severity of impaired glucose tolerance, insulin resistance, and other changes may be affected by duration and possibly severity of weight gain.

Adipose Tissue↗

Serum zinc, chromium, and iron concentrations in dogs with lymphoma and osteosarcoma.

We compared serum concentrations of zinc, chromium, and iron in dogs with cancer to those of normal dogs. Dogs with lymphoma (n = 50) and osteosarcoma (n = 52) were evaluated. Dogs with lymphoma had significantly lower (P = .0028) mean serum zinc concentrations (mean +/- SD; 1.0 +/- 0.3 mg/L) when compared to normal dogs (1.2 +/- 0.4 mg/L). Dogs with osteosarcoma also had lower mean serum zinc concentrations (1.1 +/- 0.4 mg/L), but this difference was not significant (P = .075). Serum chromium concentrations were significantly lower in dogs with lymphoma (2.6 +/- 2.6 microg/L, P = .0007) and osteosarcoma (2.4 +/- 3.1 microg/L, P = .0001) compared to normal dogs (4.7 +/- 2.8 microg/L). Serum iron concentrations and total iron-binding capacity were significantly lower in dogs with lymphoma (110.8 +/- 56.7 microg/dL, P < .0001, and 236.6 +/- 45.6 microg/dL, P < .0001, respectively) and osteosarcoma (99.6 +/- 49.3 microg/dL, P < .0001, and 245.0 +/- 43.8 microg/dL, P = .0011, respectively) when compared to normal dogs (175.1 +/- 56.7 microg/dL and 277.1 +/- 47.4 microg/dL). Mean ferritin concentration was significantly higher in dogs with lymphoma (1291.7 +/- 63.0 microg/L) than in normal dogs (805.8 +/- 291.1 microg/L, P < .0001) and dogs with osteosarcoma (826.5 +/- 309.2 microg/L, P < .0001). Further investigation is needed to explore the clinical significance of these mineral abnormalities in dogs with cancer.

Animals↗