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Adrenal function was assessed by a combined dexamethasone suppression-ACTH stimulation test in 18 healthy cats, 17 diabetic cats, and 19 sick nondiabetic cats. In all groups, plasma cortisol concentrations decreased after dexamethasone was administered and increased after ACTH was administered. There were no significant (P greater than 0.05) differences among groups in time trend changes in cortisol concentration. There was considerable variation in adrenal response between cats in each group. Diabetic cats had more variation in base-line and postdexamethasone plasma cortisol concentrations (P less than 0.05) than did other groups. In sick, nondiabetic cats, cortisol concentrations tended to be higher in cats with hyperthyroidism (P = 0.06) than in cats with other diseases.

In four cases of diabetes mellitus in juvenile dogs, clinical and clinicopathologic findings were similar to those of juvenile onset diabetes mellitus in man. However, histopathologic findings varied from the usual findings in the human disease, and lack of plasma insulin was not proved in the canine cases.

Pituitary-adrenal function was assessed by a combined dexamethasone suppression-ACTH stimulation test in 15 diabetic and 9 healthy dogs. In both groups, plasma cortisol concentrations decreased (P less than 0.001) after dexamethasone administration and increased (P less than 0.001) after ACTH administration. Differences between groups (P greater than 0.05) and group-by-time interactions were not significant (P greater than 0.05). Seemingly, adrenal function was not altered in well-regulated diabetic dogs.

A new congenic strain of genetically obese rat, SHR/N-corpulent (cp), was studied. Young male corpulent (cp/cp) and lean (cp/+ or +/+) rats approximately 5 wk of age were fed a diet containing 54% carbohydrate as either sucrose or cooked cornstarch for 9 wk. A phenotype effect was observed with body weight, fasting levels of serum insulin, triglyceride and total cholesterol, levels of serum insulin and glucose after an oral glucose load, and level of urine glucose (corpulent greater than lean), and with systolic blood pressure (corpulent less than lean). Only lean rats were hypertensive. Corpulent rats were hyperinsulinemic, hyperlipidemic, exhibited glycosuria, and were hyperglycemic after an oral glucose load. Lean rats were hyperinsulinemic, but normoglycemic. A diet effect (sucrose greater than starch) was observed with body weight, level of serum glucose after an oral glucose load, and urine volume in both corpulent and lean rats, and with levels of serum insulin and total urine glucose in corpulent rats. Corpulent rats fed sucrose had 20 to 40% higher levels of serum glucose and insulin after an oral glucose load, and twice the amount of total urine glucose, than did corpulent rats fed starch. The data demonstrate that corpulent rats have metabolic characteristics associated with insulin-independent diabetes in humans and that sucrose is more diabetogenic than starch. Manifestation of hyperglycemia in this model may be the result of superimposing obesity on an insulin-resistant genetic background.

The IV glucose-tolerance test was performed in 71 diabetic dogs (fasting glycemia greater than 6.70 mmol/L) and in 20 healthy dogs. All diabetic dogs were characterized by various degrees of glucose intolerance as expressed by an abnormal glucose disappearance coefficient. On the basis of the fasting plasma insulin concentration (Io), insulin peak response (IPR), the insulinogenic index (delta I/delta G), and the total insulin secretion (TIS), the diabetic dogs were classified, as follows: Type I dogs (n = 32) which had the severe clinical signs of diabetes and an absence of certain diagnostic responses: Io, IPR, delta I/delta G, and TIS. Type II dogs (n = 15) which also had marked diabetic signs and an absence of IPR, delta I/delta G, and TIS responses. The dogs were further subdivided into obese and nonobese groups; the Io was within acceptable limits in the nonobese group (n = 8), but was markedly increased in the obese group (n = 7). Type III dogs (n = 24) had no diabetic signs and a fasting plasma glucose less than 12 mmol/L. They were also subdivided into obese and nonobese groups. The nonobese dogs (n = 13) had Io values within acceptable limits and decreased IPR, delta I/delta G, and TIS. In contrast, the obese dogs had increased Io, IPR, delta I/delta G, and TIS. Statistical analyses indicated that the TIS and IO were highly significant linear functions of obesity.(ABSTRACT TRUNCATED AT 250 WORDS)

The most commonly available primate models of diabetes mellitus are of the insulin-dependent type and are attained through beta cell ablation techniques. Noninsulin-dependent primate models are less common since the animals must have a genetic predisposition to diabetes. Few studies have been conducted on lipid or vascular abnormalities associated with diabetes in primates. Diabetes develops spontaneously in Macaca nigra as the result of a lesion in the islets of Langerhans. As secretory cells are gradually lost, mild to moderate hyperglycemia, impaired glucose clearance, acute insulin release, hyperglucagonemia, and chronic hypoinsulinemia develop. Overtly diabetic monkeys require insulin therapy and thus alternate between hypoinsulinemia and hyperinsulinemia. The development of aortic atherosclerosis correlates positively with the severity of metabolic impairment. Lipid deposition is primarily extracellular and there is a paucity of foam cells. The very low density and intermediate-density lipoprotein fractions increase significantly, the low-density lipoprotein fraction increases slightly, and the high-density lipoprotein fractions remain essentially unchanged. Because these monkeys are maintained on a nonatherogenic chow ration, the effects of diabetes, per se, on vascular sclerosis can be evaluated.