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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperadrenocorticism was diagnosed in 7 cats with concurrent diabetes mellitus. Four cats had pituitary adenoma with bilateral adrenocortical hyperplasia, 1 cat had pituitary carcinoma with bilateral adrenocortical hyperplasia, 1 cat had adrenocortical carcinoma, and 1 cat had adrenocortical adenoma of the left adrenal gland. One year later, adrenocortical adenoma involving the right adrenal gland also was diagnosed in this cat. Clinical signs included polyuria and polydipsia (n = 7), development of pot-bellied appearance (n = 5), dermatologic alterations (n = 5), lethargy (n = 3), weight loss (n = 3), dyspnea/panting (n = 2), and recurrent bacterial infections (n = 2). In 6 cats, the diagnosis of hyperadrenocorticism was established before death on the basis of results of the ACTH stimulation test (n = 3) and the dexamethasone screening test (n = 5). Pituitary-dependent hyperadrenocorticism was differentiated from adrenocortical neoplasia on the basis of results of the dexamethasone suppression test (n = 4), endogenous ACTH concentration (n = 3), results of abdominal radiography and ultrasonography (n = 3), and exploratory celiotomy (n = 1). Four cats died or were euthanatized without treatment attempts. Treatment with mitotane followed by 60Co teletherapy was ineffective in one cat with pituitary adenoma. One cat with pituitary carcinoma died one week after bilateral adrenalectomy. Bilateral adrenocortical adenomas were removed surgically in the affected cat.
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PMID:Hyperadrenocorticism in cats: seven cases (1978-1987). 284 Dec 69

Pituitary-dependent hyperadrenocorticism was diagnosed in a 9-year-old, male castrated cat that had polyuria, polyphagia, pendulous abdomen, truncal hair loss, congestive heart failure, and insulin-resistant diabetes mellitus. Results of pituitary-adrenal function testing revealed inadequate serum cortisol suppression following dexamethasone administration, exaggerated serum cortisol responses after exogenous ACTH stimulation, and high plasma ACTH concentrations. The pathologic findings of bilateral adrenocortical hyperplasia and a pituitary adenoma that immunostained well for ACTH-related peptides confirmed pituitary-dependent hyperadrenocorticism.
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PMID:Pituitary-dependent hyperadrenocorticism in a cat. 301 73

The nomenclature of human diabetes mellitus (DM) has been revised, and this classification has been accepted throughout the medical world and literature. The major categories of diabetes are: insulin-dependent DM, type I or IDDM; noninsulin-dependent DM, type II or NIDDM; secondary DM or type S; impaired glucose tolerance, IGT; gestational diabetes; and previous abnormality of glucose tolerance, PrevAGT. A review of the literature has shown that over half of the documented diabetic dogs, with a single medical diagnosis, appear to be type I, IDDM, with a substantial proportion being type S, and the remainder being type II, NIDDM. Obesity is frequently associated with IGT and NIDDM. Diabetic cats most commonly have pancreatic islet destruction associated with pancreatic amyloidosis; they are insulin deficient, IDDM. The commonest causes of secondary diabetes in dogs are pancreatic damage, hyperadrenocorticism and hypersomatotropism secondary to persistent progesterone influence. Progestogen therapy is the most frequently reported cause of secondary diabetes in cats. Diabetes in horses is type S, usually secondary to a functional pituitary tumor but occasionally following chronic pancreatitis. The blood glucose ranges for normal, IGT and diabetic animals, and the normal serum insulin values of various species is tabulated.
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PMID:Definition of diabetes mellitus. 351 69

A diabetic cat with hyperadrenocorticism had polydipsia, polyuria, ventral abdominal alopecia, thin dry skin, and a pendulous abdomen. Results of laboratory testing indicated persistent resting hypercortisolemia, hyperresponsiveness of the adrenal glands (increased cortisol concentration) to ACTH gel, and no suppression of cortisol concentrations after administration of dexamethasone at 0.01 or 1.0 mg/kg of body weight. Necropsy revealed a pituitary gland tumor, bilateral adrenal hyperplasia, hepatic neoplasia, and demodicosis. Adrenal gland function was concurrently assessed in 2 cats with diabetes mellitus. One cat had resting hypercortisolemia, and both had hyperresponsiveness to ACTH gel (increased cortisol concentration) at one hour. After administration of dexamethasone (0.01 and 1.0 mg/kg), the diabetic cats appeared to have normal suppression of cortisol concentrations. The effects of mitotane were investigated in 4 clinically normal cats. Adrenocortical suppression of cortisol production occurred in 2 of 4 cats after dosages of 25, 37, and 50 mg/kg. Three cats remained clinically normal throughout the study. One cat experienced vomiting, diarrhea, and anorexia.
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PMID:Hyperadrenocorticism in a cat. 355 96

Generalized demodicosis with concurrent diabetes mellitus was diagnosed in 2 cats. Both cats had generalized alopecia and a bilateral brown aural exudate. Mites were seen microscopically in skin scrapings and ear swab specimens. Histologic examination of the skin showed the follicular orientation of the mites. Abnormal results on oral dexamethasone suppression tests, clinical findings, and bilateral adrenal hyperplasia found on necropsy of one of the cats suggested concurrent hyperadrenocorticism.
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PMID:Generalized demodicosis associated with diabetes mellitus in two cats. 365 22

Indirect immunofluorescence on normal canine pancreatic tissue fixed in Bouin's solution was used to detect islet cell antibodies in dogs with diabetes mellitus, other endocrine diseases, and pancreatitis. 18 of 25 dogs with diabetes mellitus alone, 2 of 8 dogs with diabetes mellitus and concurrent pancreatitis, and 2 of 2 dogs with diabetes mellitus and concurrent pancreatic exocrine insufficiency were positive for autoantibody. 2 of 12 dogs with hypoadrenocorticism, 3 of 6 dogs with hyperadrenocorticism, 6 of 28 dogs with hypothyroidism and one of 19 dogs with pancreatitis alone were also antibody positive. None of 20 healthy dogs or 20 dogs with disorders other than those of the pancreas or endocrine organs were antibody positive. Islet cell antibodies were demonstrated in dogs with diabetes mellitus and other endocrine disorders. The possibility of autoimmune involvement in the development of diabetes mellitus in the dog should be considered.
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PMID:Autoantibodies to pancreatic islet cells in canine diabetes mellitus. 388 43

Young Obese/SHR, genetically destined to become obese were made to run three times daily, averaging 2740 ft/day. Siblings of these young Obese/SHR which were allowed to remain sedentary, developed voracious appetites, massive obesity, hyperlipidemia, diabetes, hypertension, hyperadrenocorticism, muscle wasting, kidney stones, thin skin, and accelerated aging. The Obese/SHR that exercised did not become obese, their blood lipid, glucose, BUN, blood pressure, and hyperadrenocorticism were reduced, but their testes and ovaries became prematurely atrophic.
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PMID:Jogging reduces obesity and hypertension in obese/SHR. 631 Jun 22

Insulin resistance is evident in several clinical conditions such as obesity, diabetes type II, hypercortisolism. The mechanisms behind this resistance at the level of the target cell can be evaluated with measurements of insulin sensitivity with techniques both in vitro and in vivo. In this review various techniques used to evaluate insulin action are discussed and also some clinical conditions associated with insulin resistance.
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PMID:Insulin sensitivity and responsiveness in vitro and in vivo. 634 68

Male, 5 months old, massively obese, spontaneously hypertensive rats (Obese/SHR) were given 10 mg alloxan/100 g b.w., s.c., to induce diabetes. Control Obese and non-obese/SHR were given saline. Insulin therapy was withheld. All of the animals were killed at 6 months of age. Alloxan caused a slight but statistically significant increase in blood pressure, pituitary and adrenal glandular hyperplasia, hyperlipidemia, hyperglycemia, and increased BUN levels. The giant sized islets of Langerhans in Obese/SHR showed only partial degranulation of the insulin-producing beta cells concomitant with residual but apparently adequate blood insulin levels, whereas the islets of non-obese/SHR exhibited virtually total beta cell degranulation and only trace amounts of blood insulin. The alloxanized, non-obese rats were severely emaciated; the alloxanized Obese/SHR maintained their obesity. Alloxan-treated, Obese and non-obese/SHR manifested gross and microscopic degenerative changes suggesting acceleration of the normal aging process. The genetically-programmed pathogenesis of diabetes, obesity, hypertension, and Cushingoid pathophysiology of Obese/SHR may be due to hyperadrenocorticism.
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PMID:Resistance of obese and non-obese, spontaneously hypertensive rats to alloxan-induced diabetes. 635 Jul 80

Alterations in carbohydrate metabolism were evaluated in 60 dogs with untreated hyperadrenocorticism by measuring basal concentrations of plasma glucose and insulin and performing glucose and insulin tolerance tests. The 60 dogs could be divided into four groups based on paired glucose and insulin concentrations. Eight dogs had normal concentrations of both glucose and insulin. Twenty-four dogs (40 per cent) were euglycaemic with mild to moderate hyperinsulinaemia whereas 23 (38 per cent) had moderate hyperglycaemia with moderate to severe hyperinsulinaemia. The five dogs (8 per cent) with overt ketoacidotic diabetes mellitus had relative insulin deficiency. Of eight dogs tested, six had intravenous glucose intolerance; all of the dogs had increased total insulin secretion during glucose tolerance testing. Resistance to the hypoglycaemic effect of exogenous insulin was demonstrated in six of the seven dogs tested. In 20 dogs that had basal glucose and insulin again determined after correction of hyperadrenocorticism, mean concentrations of both glucose and insulin decreased into the normal range.
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PMID:Decreased insulin sensitivity and glucose tolerance in spontaneous canine hyperadrenocorticism. 637 57


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