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Query: UMLS:C0162275 (ketonuria)
 553 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic effects of Somatostatin (SRIF) added to insulin were studied in five diabetic subjects with ketonuria induced by insulin withdrawal. In the same patients ketonuria was induced twice and they were randomly treated with insulin alone (10 units as a bolus + infusion 1 U/hr) until euglycemia was reached or with insulin (same criteria) + cyclic SRIF (100 micrograms/ hr i.v.) for ten hours. Treatment with insulin + SRIF significantly reduced both peak and cumulative hGH levels in contrast to insulin alone. Moreover, the percent decrease of glucagon was significantly greater during insulin + SRIF than with insulin alone. On the other hand, the beta-OH levels fell significantly more during insulin + SRIF than during insulin alone. Finally the prolactin plasma levels fell considerably when combined treatment was given but not when just insulin was administered.
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PMID:Effects of somatostatin on established induced ketosis. 612 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

We succeeded in inducing different severities of diabetic state in C3H male mice by repeated intraperitoneal injections of various doses of SZ. SZ-induced diabetic mice were divided into four groups as follows: Group A, B, C and D. SZ, respectively, 3, 5 doses of 45 mg/kg, 5 doses of 60 mg/kg on consecutive days and one of a dose of 200 mg/kg BW. The degree of hyperglycemia and glycosuria were mild in group A and D. Group B was moderate and group C severe with ketonuria and loss of body weight. We investigated the immune response to anti-sheep red blood cells (SRBC) and the phagocytic activity of macrophages in the above mentioned various SZ-induced mice. Antibody forming activities (values of anti-SRBC plaque-forming cells (PFC) and serum agglutinin) were markedly depressed in all of SZ-diabetic groups. The degree of the suppression of antibody response to SRBC in SZ-diabetic mice corresponded with the severity of the diabetic state (C greater than B greater than A = D). However, the phagocytic activity of peritoneal macrophages in SZ-diabetic mice was as high as or higher than that in normal controls, using both latex beads and immune complex as test particles. Moreover, we observed that insulin treatment reversed the defect in the immune response in SZ-diabetic mice. These results indicate that the phagocytic activity of peritoneal macrophages was retained but the antibody response was impaired in the SZ-diabetic mice, and this suggested that the impaired antibody response may be a contributing cause of increased susceptibility to infections in a diabetic state.
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PMID:Immune responsiveness and phagocytic activity of macrophages in streptozotocin (SZ)-induced diabetic mice. 623 61

Fifteen children with severe diabetic ketoacidosis (pH less than 7,10) were treated according to two protocols. Protocol I used in 7 patients, consisted in a low dose insulin therapy by intravenous and intramuscular injections. Protocol II consisted in a low dose continuous intravenous insulin therapy, with insulin added to the rehydration solution at constant concentration (22 U/l). Rehydration and potassium supplementation were similar in both methods. The fall of glucose concentration, rise in venous pH, fall of diuresis, glycosuria, ketonuria were similar in the two groups. With protocol I three hypoglycemias (greater than 4 mM) and three hypokalemias (greater than 3 mEq/l) did occur. With protocol II no hypoglycemia and only one moderate hypokalemia was observed. Thus, continuous infusion of insulin added to the rehydration solution, including isotonic bicarbonate, isotonic saline, glucose and electrolytes is as effective as discontinuous insulin infusion, but with a lower incidence of complications. In addition, this method has the advantage of being easy and applicable everywhere.
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PMID:[Treatment of severe diabetic ketoacidosis in children. A comparative study of two methods (author's transl)]. 627 10

Interruption of a continuous subcutaneous insulin infusion, most often due to technical problems occurring during the night, is a not uncommon event whose metabolic consequences have received relatively little attention until now. We have therefore investigated the changes in blood glucose, plasma non-esterified fatty acids, 3-hydroxybutyrate, glucagon and free insulin in eight C-peptide negative Type 1 diabetic patients whose pumps were deliberately stopped between 23.00 h and 05.00 h. A control test with the pump functioning normally was carried out in each patient and the studies were randomized. Considering the values at 23.00 h as reference, interruption of the insulin infusion resulted in (1) a rapid decrease in plasma free insulin significant after 1 h and reaching a nadir of 6 +/- 2 mU/l after 6 h; (2) a rise in blood glucose which was significant at hour 3 and reached 17.4 +/- 1.9 mmol/l at hour 6; (3) a moderate increase in plasma nonesterified fatty acids which remained in the range of 700-800 mumol/l; (4) an early and linear rise in plasma 3-hydroxybutyrate, significant after 1 h and averaging 1290 +/- 140 mumol/l after 6 h; (5) a late increase (hour 5) in plasma glucagon. The second aim of our study was to provide for the patient a precise scheme of insulin supplements administered via the pump and based on blood glucose monitoring (Dextrostix - Glucometer) and semi-quantitative evaluation of ketonuria (Acetest). Resetting the pump at its basal rate at 05.00 h and giving insulin supplements (2-8 U) at 06.45 h (with the usual breakfast dose) and again at 10.00 h have proved efficacious in restoring satisfactory metabolic control by noon the day after starting the experiment. These results form practical recommendations to patients undergoing this type of accident.
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PMID:A 6-hour nocturnal interruption of a continuous subcutaneous insulin infusion: 1. Metabolic and hormonal consequences and scheme for a prompt return to adequate control. 634 79

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.
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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.
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PMID:Significance of spontaneous ketonuria and serum C-peptide levels in obese type II diabetic patients. 638 58

Phlorizin and 1,3-butanediol were used to determine effects of glucosuria and ketonemia on concentrations of metabolites in blood plasma and on kinetics of glucose metabolism. Four steers received four treatments (control; control plus dietary 1,3-butanediol; control plus phlorizin injections; and control plus phlorizin and 1,3-butanediol) in a Latin square design. Treatments lasted 14 days. All steers received a 30% grain, 70% forage ration in equal meals every 2 h. Metabolite concentrations in blood plasma and urine and glucose kinetics were measured on each of the last 3 days of each treatment period. Phlorizin caused glucosuria; decreased plasma glucose, glucose total entry rate, and glucose recycling; and increased plasma free fatty acids and glucose irreversible loss. Glucose pool size was increased by 1,3-butanediol. Phlorizin plus 1,3-butanediol caused glucosuria and ketonuria; decreased plasma glucose; and increased blood ketone bodies, plasma free fatty acids, glucose irreversible loss, and glucose pool size. Growth hormone, insulin, and glucagon were not affected by treatment. Physiological perturbations in these steers were characteristic of some of those in ketotic cows.
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PMID:Glucose kinetics, plasma metabolites, and endocrine responses during experimental ketosis in steers. 638 28

We present case histories of two young children with episodes of hypoglycemia, elevation of SGOT, low insulin levels, increased urinary excretion of psi-hydroxy fatty acids (5-hydroxyhexanoic, 7-hydroxyoctanoic and 9-hydroxydecanoic), traces of the corresponding psi-ketoacids and elevations of urinary adipic, suberic, and sebacic acids. The ratio of psi-hydroxy fatty acids to 3-hydroxybutyric in the urine of these patients is higher than in patients of similar ages with similar illnesses. These acids persisted while the patients were well. Increased urinary psi-hydroxy fatty acids could be reproduced by a load of medium chain triglycerides without precipitating other clinical symptoms. Three children with hypoglycemia were found not to excrete measurable amounts of these unusual acids while ill. A medium chain triglyceride load in one of these children after recovery failed to elicit psi-hydroxy acid excretion. Small amounts of urinary 5-hydroxyhexanoic acid only were found in two patients with acute Reye's syndrome and in three of five severely ill children with starvation ketonuria. In this last group, no urinary psi-hydroxyacids could be detected after recovery. Normal children do not excrete measurable amounts (less than 1 mg/g creatinine) of these psi-hydroxyacids.
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PMID:Episodic hypoglycemia with psi-hydroxy fatty acid excretion. 640 54


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