Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of HLA-DR 3 was analysed in 745 patients with Type 1 (insulin-dependent) diabetes with age at diagnosis between 1-19 years. HLA-DR 3 and/or 4 was found in 678/745 (91%) of the patients. Presence of DR2 with neither DR 3 nor 4 was demonstrated in 15 patients. Patients with HLA-DR 3 without DR 4 presented with Type 1 diabetes more evenly over the year; they also presented without incidence peaks at 7 years or 10-11 years, as seen especially in DR 3/4 patients. The DR 3 patients more often had mild disease with less ketonuria at diagnosis, less often ketoacidotic symptoms and more often a subsequent partial remission. The apparently more severe disease among diabetic girls may, at least to some extent, be explained by their higher prevalence of HLA-DR 4. The differences found were similar in North America and Europe. The results suggest that Type 1 diabetes is a genetically heterogeneous disease and that HLA-typing may be a useful marker of this heterogeneity.
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PMID:HLA-DR 3 is associated with a more slowly progressive form of type 1 (insulin-dependent) diabetes. 348 90

It has been postulated that glucose regulation is secondary to maintenance of normal basal insulin secretion. Serum glucose, insulin, and C-peptide levels were measured at fasting in 209 consecutive non-insulin-dependent diabetic patients and after glucose stimulation in 193 patients. The basal serum insulin C-peptide levels were not significantly different in control subjects (mean 22 +/- 8.8 microU/ml) and in patients with varying severity of diabetes (mean 24 +/- 9.6 microU/ml) except in the most severely diabetic group [fasting serum glucose greater than 350 mg/dl (19.4 mmol/L), mean 19 +/- 7 microU/ml]. In 39 patients who developed ketonuria without acidosis during follow-up, the mean basal serum insulin was 22 microU/ml during the episode of ketonuria, 21 microU/ml during the glucose tolerance test, and 25 microU/ml after glucose stimulation (statistically nonsignificant differences). Our data suggest that hyperglycemia compensates for beta-cell impairment so that basal insulin secretion usually stays above the threshold for ketoacidosis unless there is marked beta-cell impairment. Patients who fail to increase insulin in response to nutrient challenge are at risk of developing ketosis.
Diabetes Care
PMID:Maintenance of basal insulin secretion in severe non-insulin-dependent diabetes. 352 54

Physicians routinely order urinary ketone testing for most patients with diabetes mellitus upon hospitalization, even in the absence of a history of diabetic ketoacidosis. To determine whether testing for urinary ketones is clinically useful in patients with non-insulin-dependent diabetes mellitus (NIDDM), a retrospective review was undertaken of 152 charts of patients admitted to the hospital during a 6-mo period with the diagnosis of diabetes mellitus. Of the 135 patients with NIDDM, 96% had routine testing performed for urinary ketones. Surprisingly, 26% of the patients with NIDDM had positive urine ketones at some time during hospitalization, and the degree of ketonuria was markedly greater did not reflect diabetic ketoacidosis. Ketonuria was accompanied by significant hyperglycemia and most likely reflects relative insulinopenia. Only 23% of the episodes of ketonuria were acknowledged in the progress notes. Although NIDDM patients who had ketonuria in the hospital were more likely to be transiently treated with insulin than patients without ketonuria, in no instance did the progress notes state that a diagnostic test or change in therapy was ordered because of the presence of a positive test for urinary ketones. The primary goal for therapy of patients with NIDDM should remain good control of blood glucose. In the hospitalized patient in whom frequent blood glucose determinations are made, it is not clear that urinary ketone testing needs to be routinely done.
Diabetes Care
PMID:Ketonuria in hospitalized patients with non-insulin-dependent diabetes mellitus. 354 54

Diabetes mellitus uncommon in the newborn infant. There are two entities: a transient form and a permanent one. Differenciation is difficult. Transient diabetes, apparently the more common of the two, results in complete recovery. Permanent diabetes requires continued insulin therapy. The clinical presentations of these patients in the first days to weeks of life are similar in that the infants are small for gestational age, hyperglycemic, dehydrated and only rarely have ketonemia or ketonuria. However, the aetiology of the syndrome is unknown. The authors report two cases of permanent diabetes mellitus identified in the first two months of life, and still treated at thirty months of life.
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PMID:[Neonatal diabetes. Apropos of 2 cases]. 354 6

Pregnancy in diabetic mothers is associated with intrauterine death, perinatal mortality, and birth weight greater than that of infants born of normal mothers. The use of rodents made diabetic by alloxan or streptozotocin as an animal model for human diabetic pregnancy has been controversial because of the severity of the diabetes as well as the direct effect of diabetogenic drugs on the developing organism. Among our female NOD (nonobese diabetic) mice, insulin-dependent diabetes occurs spontaneously in 9% by 12 weeks and in 80% by 29 weeks of age. Offspring born within 21 days of conception to mildly hyperglycemic NOD pregnant mice between 26 and 52 weeks of age, and prior to the onset of maternal ketonuria are macrosomic with an average of 31% increase in body weight and 44% increase in kidney weight, in comparison to controls. Besides organomegaly, the macrosomic offspring have significantly higher pancreatic insulin content which was elevated 80% when compared with that of controls, and litter sizes are significantly 50% smaller. These results suggest that the mildly hyperglycemic pregnant NOD mouse represents a promising model for the study of pregnancy complicated by diabetes.
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PMID:The offspring of the female diabetic "nonobese diabetic" (NOD) mouse are large for gestational age and have elevated pancreatic insulin content: a new animal model of human diabetic pregnancy. 354 10

Although lipoprotein lipase (LPL) is believed to be rate limiting in the catabolism of triglyceride-rich lipoproteins, LPL activity has not correlated with plasma triglyceride concentrations in experimental rat diabetes. To gather more information about this enzyme system in diabetes, LPL activities were measured in representative tissues from control and streptozocin-induced diabetic rats fed fat-free chow and in 48-h-starved animals. The DNA content of each tissue was determined so that LPL activity could be expressed in a way that was unaffected by tissue wasting. Diabetic animals lost approximately 20% of their body mass. Adipose tissue and soleus muscle cell masses were reduced, and there was marked fat atrophy at necropsy. Adipose tissue LPL was decreased in both starved and diabetic animals, whereas skeletal muscle activities were variably affected. Lipase content and distribution among the individual organs were calculated with published data for rat carcass composition. In diabetic rats, total LPL (adipose tissue, muscle, and parenchymal organs) was reduced by nearly two-thirds so that skeletal muscle became the predominant source of LPL. Ketonuria was less frequent in diabetic than in starved rats (P less than .018) despite their severe wasting. Serum triglyceride concentrations were higher in ketonuric than nonketonuric diabetic animals, and severe hypertriglyceridemia was seen exclusively in heavily ketonuric animals. These observations together with published information suggest that plasma triglyceride concentrations in the rat model are determined by a complex interplay between very-low-density lipoprotein synthesis, the capacity of the LPL removal system, properties of the lipoprotein substrate, and other unidentified factors.
Diabetes 1987 Apr
PMID:Relationship of organ lipoprotein lipase activity and ketonuria to hypertriglyceridemia in starved and streptozocin-induced diabetic rats. 381 3

In an attempt to explain the rarity of ketonuria in Indian diabetics, plasma glucose, insulin and free fatty acid (FFA) levels were measured in 35 non-obese patients with non-insulin-dependent diabetes in the young and 35 matched controls during a 100 g oral glucose tolerance test. Compared with the controls, the patients had a severe degree of hyperglycaemia, fasting hyperinsulinism, and an attenuated and delayed insulinaemic response. However, in addition to the fasting plasma FFA levels being similar in the two groups, the decrement in the FFA responses was equivalent. Thus, the hormone-sensitive lipase of the adipose tissue appeared to be sensitive to inhibition by insulin. Also, the fasting insulin:glucagon molar ratios were computed and found to be no different in the two groups. The normal fasting FFA levels, relative sensitivity to insulin of lipolysis in the adipocyte and normal insulin: glucagon molar ratios may help to explain in part the general rarity of ketosis-prone diabetes in the South African Indian population.
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PMID:A plausible explanation for the aketonuria of young Indian non-insulin-dependent diabetics. 392 67

Diabetic ketoacidosis is usually associated with marked secondary hyperaldosteronism. Plasma levels of renin, angiotensin II, and aldosterone are markedly raised before treatment in most patients, with values falling rapidly toward normal as metabolic control is restored. In a few patients, mostly those with long-term complications of diabetes, plasma levels of renin, angiotensin II, and aldosterone before treatment remain within the normal range. In moderately hyperglycemic patients who have glycosuria but not ketonuria, plasma levels of all three substances are significantly higher than when control is improved. Occasionally, moderately hyperglycemic patients have mild secondary hyperaldosteronism. Improved metabolic control in such patients causes a rise in plasma volume and a rise in total exchangeable sodium, the latter to levels significantly above normal. Plasma catecholamine levels are markedly elevated in diabetic ketoacidosis, probably as a consequence of the ketoacidotic state. In nonketotic patients with moderate hyperglycemia, basal plasma norepinephrine levels are normal; catecholamine responses to exercise may be exaggerated, however. Epidemiological and animal studies suggest a relationship between blood pressure and blood glucose levels. There are few clinical studies of the effects of altering metabolic control of diabetes on blood pressure, and this is an important area for further study.
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PMID:Diabetic control and the renin-angiotensin system, catecholamines, and blood pressure. 393 82

The relationship between the dose of intravenously administered streptozotocin (a N-nitroso derivative of glucosamine) and the diabetogenic response has been explored by use of the following indices of diabetogenic action: serum glucose, urine volume, and glycosuria, ketonuria, serum immunoreactive insulin (IRI), and pancreatic IRI content. Diabetogenic activity could be demonstrated between the doses of 25 and 100 mg/kg, all indices used showing some degree of correlation with the dose administered. Ketonuria was only seen with the largest dose, 100 mg/kg. The most striking and precise correlation was that between the dose and the pancreatic IRI content 24 hr after administration of the drug, and it is suggested that this represents a convenient test system either for both related and unrelated beta cytotoxic compounds or for screening for modifying agents or antidiabetic substances of a novel type. Ability to produce graded depletion of pancreatic IRI storage capacity led to an analysis of the relationship between pancreatic IRI content and deranged carbohydrate metabolism. Abnormal glucose tolerance and insulin response were seen when pancreatic IRI was depleted by about one-third, while fasting hyperglycemia and gross glycosuria occurred when the depletion had reached two-thirds and three-quarters, respectively. The mild yet persistent anomaly produced by the lowest effective streptozotocin dose, 25 mg/kg, exhibits characteristics resembling the state of chemical diabetes in humans and might thus warrant further study as a possible model. Finally, the loss of the diabetogenic action of streptozotocin by pretreatment with nicotinamide was confirmed and was shown to be a function of the relative doses of nicotinamide and streptozotocin and of the interval between injections.
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PMID:Diabetogenic action of streptozotocin: relationship of dose to metabolic response. 424 8

Briscoe, H. Frances (University Medical Center, Jackson, Miss.), and Fred Allison, Jr. Diabetes and host resistance. I. Effect of alloxan diabetes upon the phagocytic and bactericidal efficiency of rat leukocytes for pneumococcus. J. Bacteriol. 90:1537-1541. 1965.-Chronic diabetes mellitus was induced in rats with alloxan monohydrate. Glycosuria persisted for the 6 weeks of study, but ketonuria was never encountered. The cellular composition of peritoneal exudate recovered from diabetic rats after starch aleuronat administration was the same as that obtained from normal rats. The quantity of exudate recovered from the diabetic rats was thought to be less than that obtained from normal rats subjected to the same irritant. Phagocytosis was found to be essentially the same for both diabetic and normal cells when suspended in normal saline. The killing efficiency of harvested peritoneal phagocytes suspended in saline from both diabetic and normal rats for type 1 pneumococcus was compared and no difference between the groups was found.
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PMID:Diabetes and host resistance. I. Effect of alloxan diabetes upon the phagocytic and bactericidal efficiency of rat leukocytes for Pneumococcus. 437 43


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