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Query: UMLS:C0011849 (diabetes)
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Administration of phentholamine or obsidan to rats for 3 weeks sharply diminished the diabetogenic action of alloxan. The insular tissue of the pancreas became less affected, and the percentage of animals with signs of diabetes (polyuria, glucosuria, and hyperglycemia) decreased. Hyperglycemia (averaging 276 and 286 mg%) was revealed in the majority of the animals given alloxan and adrenoblockers. Phentholamine sharply suppressed the development of polyuria in rats with intact pancreas following water load, but obsidan produced no such effect. The mechanism of action of adrenoblockers used on polyuria and glucosuria in animals given alloxan is suggested on the basis of experiments with water load.
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PMID:[Effect of prolonged administration of the adrenergic blockaders, fentolamin and obsidan, on the course of alloxan diabetes in rats]. 70 60

We have recorded clues to the clinical recognition of chronic insulin overdosage in 101 pediatric patients with diabetes mellitus, identified predisposing circumstances, and reconsidered the traditional strategy of slow reduction in insulin dose. Overtreatment occurred in 70%, overall, and in 90% of those referred for instability; mean overdose was 38% of the readjusted dose. The most common findings were frank hypoglycemic episodes, polyuria/nocturia/enuresis despite increasing insulin dosage, excessive appetite, hepatomegaly, weight gain, headaches, exercise intolerance, marked variation in glucosuria, mood swings, and frequence bouts of rapidly developing ketoacidosis. Overtreatment usually developed because of attempts to achieve metabolic control using glucosuria as principal criterion. One fourth of those observed became overtreated during periods of emotional turmoil when need for increased insulin to counter stress-induced hyperglycemia and ketosis led to chronic increase in dosage. Persistent glucosuria/ketonuria and exacerbation of hypoglycemic symptoms were more frequent with slow than with rapid reduction in insulin dosage.
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PMID:Chronic overtreatment with insulin in children and adolescents. 88 3

Very fat people die earlier than people of normal weight because hypertension, diabetes and coronary disease are more frequent among the markedly obese. Most obese subjects, however, are only slightly overweight and their mortality is not elevated. Reasons for dieting are more often psychological than somatic. 2. Reducing diets are ineffective because the obese rarely follow them. Total fasting and intestinal bypass may provide better results, but are more dangerous. 3. Atkins' diet eliminates carbohydrates from food without restricting protein and fat intake. Deprived of carbohydrates, the body uses fat for fuel. A small part of metabolized fat is eliminated in the urine as ketone bodies, and this is why such diets are called "ketogenic". They have been known at least since 1863. 4. Caloric loss due to ketonuria does not exceed 100 Cal/day in the non-diabetic. It is maximal during total fasting and cannot be increased by a ketogenic diet. 5. In the short run, such diets produce rapid weight loss due to polyuria. On the other hand, refeeding carbohydrates causes water retention and weight gain. 6. The diet decreases appetite: patients eat less without feeling severe hunger and without measuring their food intake. 7. Orthostatic hypotension, fatigue, and nausea are frequent, despite what Dr. ATKINS claims. 8. The diet increases plasma cholesterol and uric acid. It may be dangerous in diabetes (anorexia, acidosis) and in heart or kidney failure (hypokalemia). 9. The diet, though far from good, is better than the book. ATKINS' theories are at best half-truths, and the results he claims lack credibility. The obese subject's disappointment with traditional reducing diets and the book's hard-sell style account for ATKINS' success.
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PMID:[Dr. Atkins' dietetic revolution: a critique]. 89 45

Diabetes mellitus was tentatively diagnosed in a black-footed ferret with polyuria, polydipsia, polyphagia, dehydration, and weight loss. Laboratory findings (marked hyperglycemia (724 mg/100 ml), glycosuria, and ketonuria) and the subsequent favorable response to insulin therapy confirmed the diagnosis. Although lesions were not observed in the pancreas, gross and histologic findings concomitant with diabetes mellitus included arteriosclerosis, with calcification of the aorta and other major vessels; mild necrotizing hepatitis; and mild proliferative glomerulonephritis. A perineal adenocarcinoma, with metastasis to an internal iliac lymph node, was an incidental finding. Special stains demonstrated adequate numbers of beta cell granules in the islets of Langerhans. Thus, the diabetes was apparently due to a lack of release of the synthesized insulin or to diminished effectiveness of the secreted insulin.
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PMID:Diabetes mellitus in a black-footed ferret. 92 62

In a study of 66 children with juvenile diabetes symptoms had often present for over a month before diagnosis. Though polyuria, polydipsia, and weight loss were the commonest features, other important symptoms included tiredness lethargy, and malaise. A gradual onset of diabetes was commoner than is generally realised.
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PMID:Mode of presentation of juvenile diabetes. 97 95

A large number of individuals currently diagnosed as having diabetes mellitus are asymptomatic. In order to provide rational therapy for this patient population, it is necessary to focus upon the differences between these patients and the classic prototypes with polyuria and weight loss, who require insulin for survival. Patients with asymptomatic diabetes do not need insulin for survival, and, by definition, they do not need it to alleviate symptoms. They tend to be middle-aged and overweight, but they can be young and thin. Their degree of hyperglycemia is moderate, often indistinguishable from that of normal individuals in their day-to-day existence. Indeed, they can often be differentiated from normal persons only on the basis of their blood glucose response to the stress of a large dextrose challenge; in this regard, the potential problem of over-diagnosing diabetes has been discussed. Since the major problem facing patients with asymptomatic diabetes is accelerated atherogenesis, the therapeutic approach must be based upon efforts to delay or prevent the onset of vascular disease. It has yet to be shown that any therapeutic intervention helps such patients, but an argument has been made in support of the following goals in subjects with asymptomatic diabetes whose fasting blood glucose level is less than 170 mg/100 ml: (1) stop smoking, (2) control hypertension, (3) attain ideal body weight, and (4) maintain blood triglyceride and cholesterol levels well within normal limits. Attempts to lower blood glucose with either insulin or oral agents do not seem indicated in the majority of patients within this defined diabetic population.
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PMID:Treatment of asymptomatic diabetes mellitus. 97 61

The incidence and prevalence of diabetes mellitus in residents of Rochester, Minnesota, for 25 years (1945 to 1970) were determined from available medical records. The over-all incidence rate for diabetes is 133 new cases per 100,000 population per year (age-adjusted to 1970 U.S. white population). The rate increased with age for both men and women and was higher among men over 30 years of age. The average annual incidence rates per five-year period for juvenile-onset diabetes mellitus were low and variable and showed little change. Polyuria, polydipsia, glycosuria, lean habitus, loss of weight, and high levels of fasting hyperglycemia at initial diagnosis occurred more frequently in younger than in older patients. The peak incidence in 1960 through 1964 and the decrease in the following five years may be a reflection of the introduction of the AutoAnalyzer method for blood glucose in 1958. The average annual incidence rates for 1955 through 1959 and 1965 through 1969 were essentially the same. The over-all prevalence for diabetes mellitus is 1.6 per cent, with a higher rate among men than among women over 40 years of age; among school children the rate is 0.1 per cent. Survivorship in the diabetic population is lower than that in the general population. The leading cause of death was coronary heart disease, the death rate from it being higher than for the general population.
Diabetes 1976 Jul
PMID:Diabetes mellitus: incidence, prevalence, survivorship, and causes of death in Rochester, Minnesota, 1945-1970. 108 8

Young, adult, female Sprague-Dawley rats were fasted for 18 h and then given a single s.c. injection of alloxan (10 mg/100 g body weight) which promptly induced a severe state of diabetes. The animals were killed at frequent time intervals during the 7-day study period in order to record the dynamic changes in their capacity for adrenal steroidogenesis and secretion as measured by fluorometric determination of their circulating corticosterone (Cmpd B) levels as well as by thin layer chromatographic identification of cortical lipid moieties used for steroidogenesis. In addition to severe polydypsia, polyuria and polyphagia, these animals manifested super-normal glucose, triglycerides, free fatty acids and cholesterol in their blood, severe hepatic steatosis, adrenal hyperplasia with lipid depletion from the mineralocorticoid producing z. glomerulosa, thymus gland involution and complete degranulation of their insulin producing islet beta cells. Despite an initial high output of Cmpd B and despite progressive cortical hyperplasia, the serum Cmpd B levels became reduced and many of the animals succumbed suddenly, due most likely to inadequate adrenocortical steroidogenesis. Adrenocortical lipids showed a progressive accumulation of free fatty acids, di- and triglycerides, suggesting that some lipid enzymatic defect could be responsible for the lack of conversion of these lipid entities essential for proper steroidogenesis.
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PMID:Adrenal glandular lipids and circulating corticosterone in severely diabetic rats. 117 54

Various biochemical parameters of renal tubular function were examined for a period of up to 12 weeks in rats rendered diabetic by an i.v. injection of streptozotocin. Except for a statistically significant decrease in the urinary excretion of gamma-glutamyl-transpeptidase to 64% of control values, the urinary excretion of beta-N-acetyl-D-glucosaminidase, beta-galactosidase, alanine aminopeptidase, and lactate dehydrogenase significantly increases in diabetic rats to between 154% and 712% of control values. This increased enzymuria is not correlated to the marked polyuria induced by diabetes (r between 0.14 and 0.35, not significant). Enzymuria is also accompanied by a 10-fold increase in the urinary excretion of the low molecular weight protein beta 2-microglobulin while the excretion of albumin is not significantly modified, indicating impairment of tubular reabsorption in diabetic animals. Clearance studies reveal that the clearance of both beta 2-microglobulin and infused egg-white lysozyme are also increased. Finally the histopathologic examination of paraffin sections of the kidney show hydropic degenerescence and pycnosis of the tubular cells. It is concluded that early-stage diabetes results in tubular impairment and that the streptozotocin-rat model appears well suited to the study of these early signs of renal dysfunction.
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PMID:Enzymuria and tubular proteinuria in diabetic rats: a 12-week follow-up study. 134 85

A spontaneously diabetic rat with polyuria, polydipsia, and mild obesity was discovered in 1984 in an outbred colony of Long-Evans rats, which had been purchased from Charles River Canada (St. Constant, Quebec, Canada) in 1982. A strain of rats developed from this rat by selective breeding has since been maintained at the Tokushima Research Institute (Otsuka Pharmaceutical, Tokushima, Japan) and named OLETF. The characteristic features of OLETF rats are 1) late onset of hyperglycemia (after 18 wk of age); 2) a chronic course of disease; 3) mild obesity; 4) inheritance by males; 5) hyperplastic foci of pancreatic islets; and 6) renal complication (nodular lesions). Histologically, the changes of pancreatic islets can be classified into three stages: 1) an early stage (6-20 wk of age) of cellular infiltration and degeneration; 2) a hyperplastic stage (20-40 wk of age); and 3) a final stage (at > 40 wk of age). These clinical and pathological features of disease in OLETF rats resemble those of human NIDDM.
Diabetes 1992 Nov
PMID:Spontaneous long-term hyperglycemic rat with diabetic complications. Otsuka Long-Evans Tokushima Fatty (OLETF) strain. 139 18


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