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

A survey of ketonuria in insulin-treated diabetics showed that its significance might vary according to the time of day at which the test was performed. Some of the patients had uncontrolled diabetes in the early morning, when severe hyperglycaemia and hyperketonaemia occurred together, while later during the same day or night an episode of hypoglycaemia caused hyperketonaemia, indicating that too much insulin had been given. Correct assessment of the significance of ketonuria is obviously important, because some patients would probably require a decrease rather than an increase of insulin dosage. Ketonuria does not necessarily indicate impending ketoacidosis.
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PMID:Interrelationships of blood sugar and ketones in insulin-treated diabetics. 498 85

The aim of this study was to examine the long-term effects of synthetic chow diet on the metabolic pattern of diabetic syndrome in a large group of sand rats. Few animals had a fulminating reaction with markedly decreased glucose tolerance, low plasma insulin levels and death within 3-4 weeks. But the most of sand rats developed obesity and elevated plasma insulin levels. From the third month, 40% of sand rats presented a diabetic syndrome with hyperinsulinemia, hyperglycemia, markedly decreased glucose tolerance and insulin resistance. Plasma lipids were increased; the lipid and glycogen accumulation in the liver was high. So this diabetic syndrome can be compared to maturity onset diabetes. If this synthetic chow diet lasted more than 6 months, the most of animals lost considerable weight with a strong lipid depletion of fat stores. Serum immunoreactive insulin levels fall and the blood glucose rose over 500 mg/100 ml with glycosuria and ketonuria . The elevated triglyceride content of plasma and the lipid deposits in the liver were exaggerated; glycogen had disappeared. Animals developed an overtly insulin- dependent diabetes, the latter phase of the disease. The sand rat appears to us as a potentially interesting model for investigation both maturity onset and ketotic-type diabetic syndrome.
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PMID:[Appearance and metabolic development of diabetes mellitus in the sand rat, Psammomys obesus]. 623 80

It has been reported that sand rats, naturally feeding on low-caloric-value plants containing a high concentration of salt, become obese and develop hyperglycemia when fed on a standard laboratory diet. The aim of this study was to examine the long-term effects of a synthetic-chow diet on the metabolic pattern of the diabetic syndrome in a large group of sand rats. While a few animals had a fulminant reaction with markedly decreased glucose tolerance, low plasma insulin levels, and death within 3-4 wk, most sand rats developed obesity and elevated plasma insulin levels. From the third month and forward, 40% of sand rats presented with a diabetic syndrome with hyperinsulinemia, hyperglycemia, markedly decreased glucose tolerance, and insulin resistance. This diabetic syndrome can be compared with maturity-onset (type II) diabetes. When this synthetic-chow diet was given for more than 6 mo, the majority of animals lost considerable weight and showed a major depletion of fat stores. Serum immunoreactive insulin levels fell, while blood glucose rose to above 500 mg/dl with glycosuria and ketonuria. The elevated triglyceride content of plasma and the lipid deposits in the liver were greatly augmented, and no glycogen was present. Animals developed frank insulin-dependent diabetes, and diabetic animals not treated with insulin died in diabetic coma with presumed ketoacidosis. The disease was essentially confined to sand rats showing abnormal glucose tolerance, even before eating laboratory chow. This observation suggests a genetic factor. Thus, the sand rat appears to be a potentially interesting model for investigation of both maturity-onset and insulin-dependent diabetes.
Diabetes 1984 May
PMID:Diabetes mellitus in sand rats (Psammomys obesus). Metabolic pattern during development of the diabetic syndrome. 637 52

We studied the occurrence of diabetes mellitus in 6 children receiving corticosteroid therapy after renal transplantation. The first hyperglycemic episode occurred in all cases before the fortieth day of treatment but other episodes were observed thereafter. All children were glycosuric, without ketonuria. The diabetes has always been transient, and easily managed with insulin treatment and usual diabetic diet. A glucose tolerance test was performed 3 to 6 months after these episodes; glycemic response to glucose was abnormal in 2 of 6 children; in all cases, the insulin response to the glucose load was inadequate. In 2 children, the fasting blood glucose is still abnormal after a follow-up of 3 years. The other patients have recovered despite sustained corticotherapy. No specific background (genetics, HLA groups) or specific circumstances of treatment were identified. Therefore, we recommend to follow closely glycemia in children after renal transplantation, with a daily glycemic determination especially during the first 3 weeks.
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PMID:[Diabetes induced by corticoids in 6 children after renal transplantation]. 638 52

Patients with type II diabetes mellitus (type II DM patients) are characteristically obese, hyperinsulinemic, and non-ketosis prone. Recently, we have encountered several obese type II DM patients with either diabetic ketoacidosis or significant ketonuria after insulin withdrawal. There was no evidence of infection, stress, or starvation to explain their ketonuria. Therefore, we assessed serum connecting peptide (C-peptide) response to oral glucose in 14 obese, insulin-treated type II DM patients: 6 with and 8 without episodes of spontaneous ketonuria. The group presenting with ketonuria had low to absent basal and stimulated serum C-peptide responses. The nonketonuric group had higher basal C-peptide (P less than 0.01) concentrations that increased significantly (P less than 0.001) after oral glucose compared with those of the ketonuric group. Clinical characteristics and biochemical control were similar in both groups. Our findings confirm that obese type II diabetes mellitus is a heterogeneous disease with variable fasting and stimulated C-peptide responses. Spontaneous ketonuria could be a feature in the clinical presentation of the patients especially in the presence of both low fasting and stimulated C-peptide levels. The significance of these findings is unclear but suggests individualization in the management of type II DM patients and cautious withdrawal of insulin therapy in such patients. Furthermore, serum C-peptide levels alone cannot be recommended to classify patients into either type I or type II diabetes mellitus.
Diabetes Care
PMID:Significance of spontaneous ketonuria and serum C-peptide levels in obese type II diabetic patients. 638 58

A patient with a history of diabetes mellitus and congestive heart failure was taking furosemide and metolazone as diuretics. Diabetic ketoacidosis developed, and the patient became lethargic and confused. Initial biochemical determinations showed an alkalemic pH, serum and urine ketones with an anion gap, and hyperventilation. The hyperventilation was appropriate for the degree of ketoacidosis but it was grossly inappropriate for the alkalemia. This could be explained by a direct effect of ketones on the respiratory center or a sudden increase in hydrogen ion concentration superimposed on previously chronic alkalemic pH due to the potent combination of furosemide and metolazone.
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PMID:Alkalemia in diabetic ketoacidosis. 643 81

The absence of ketoacidosis is thought to be characteristic of generalized lipoatrophic diabetes. It is widely believed that lipoatrophic diabetic patients are able to tolerate starvation and therapeutic insulin withdrawal, due to absence of subcutaneous body fat, the substrate essential for ketogenesis. In this article, we document nine episodes of acidosis and accelerated ketone body formation in a 24-yr-old woman whose deterioration followed episodes of dietary excesses without evidence of intercurrent infection or other identifiable forms of metabolic stress. Serum C-peptide measurements demonstrated that an absolute insulin deficiency did not exist. During short-term, experimental, dietary manipulations, excess dietary calories worsened the hyperglycemia and hyperlipidemia but did not reproduce the ketoacidotic state. Excess fat added to the diet was the most poorly tolerated of the food groups, causing ketonuria, hypertriglyceridemia, and abdominal pain. Our experience with this patient suggests that increased food consumption, insufficient insulin relative to an insulin-resistant state, and increased amounts of insulin counterregulatory hormones (stress), acted in concert to cause acidosis and increased ketone body formation.
Diabetes Care
PMID:Recurrent ketoacidosis in acquired, total lipodystrophy (lipoatrophic diabetes). 643 2

Myocardial membranes from rats rendered diabetic with streptozotocin were used to determine muscarinic receptors with 3H-quinuclidinyl benzilate. In the acute state of diabetes, four days after induction, the density of receptors were equal in controls, insulin (glucosuria) and non insulin-treated (glucosuria and ketonuria) diabetic animals. In myocardial membranes from diabetic rats agonist binding to the muscarinic receptor was shifted to higher affinity than in controls. Computer modeling revealed that guanine nucleotides transformed agonist binding from two sites to a site of low affinity in controls. In membranes from insulin-treated diabetic animals the shift to lower affinity occurred but two receptor sites remained. In non insulin-treated membranes the nucleotides failed to exert any effect. Inhibition of adenylate cyclase by the muscarinic agonist oxotremorine was amplified in diabetic membranes. This indicates that the function of the inhibitory nucleotide binding protein (NI), as reflected by agonist binding to the receptor and adenylate cyclase inhibition, is sensitive to the hormonal status.
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PMID:Effects of acute ketotic and non-ketotic diabetes on the myocardial muscarinic receptors. 644 90

A rapid paper-strip test for the semiquantitating 3-hydroxybutyrate (3-OHBA) has been developed. The color develops within 5 min after applying the serum to the paper strip, and the purple color was read either visually or by reflectance meter. This can detect 3-OHBA levels as low as 0.1 mmol/L up to 2.0 mmol/L. The more concentrated sample can be measured on serial dilution. Clinical usefulness has been tested in a summer camp for insulin-dependent diabetic children as well as in a routine diabetes clinic. Serum 3-OHBA levels ranged from greater than 100 mumol/L to 4 mmol/L in all the subjects before breakfast in a summer camp. In four subjects, 3-OHBA was elevated to the level of 2-4 mmol/L, and only one of these four subjects exhibited ketonuria by nitroprusside test. In a diabetes clinic, a new paper-strip test for 3-OHBA has revealed ketonemia in 34 (74%) of 46 diabetic subjects, while nitro-prusside test revealed ketonemia in only 4 (13%). The present paper-strip test for 3-OHBA is sensitive enough to detect levels as low as 0.1 mmol/L and is clinically useful for rapid detection of ketosis proneness as well as for monitoring of diabetes control.
Diabetes Care
PMID:Development of paper-strip test for 3-hydroxybutyrate and its clinical application. 649 40

Insulin binding to monocytes was assessed before and after plasma insulin suppression by diazoxide in 14 obesity-related diabetic subjects. Four of the five patients with mild carbohydrate intolerance (FBS less than 150 mg%) and hyperinsulinism exhibited low monocyte insulin binding. Despite an increase in insulin binding after 7 days of diazoxide therapy, no improvement in carbohydrate tolerance could be demonstrated. Lack of improvement may have been related to persistent diazoxide effect. An additional group of 4 patients with low plasma insulin values and more severe carbohydrate intolerance (FBS greater than 150 mg%) had high monocyte insulin binding. This group, as well as a group of patients with intermediate insulin responses, tolerated diazoxide poorly and developed moderate ketonuria or severe hyperglycemia (plasma glucose greater than 350 mg%) necessitating discontinuation of the drug after 3-6 days. The studies in these patients suggest that obesity-related diabetes may be characterized early by mild elevation of plasma glucose, hyperinsulinism and impaired monocyte insulin binding. As beta cell exhaustion occurs, more severe hyperglycemia intervenes and insulin binding to monocytes increases.
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PMID:Role of insulin receptors in obesity-related diabetes. 675 56


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