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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth hormone (hGH) reserve following arginine administration and the paradoxical hGH response to thyrotropin-releasing hormone (TRH) were studied in 30 diabetics without evidence of vascular complications. The diabetics were divided into 4 groups according to the type of their disease and to the metabolic condition within the IDDM group (insulin-dependent: IDDM, in acceptable response and in poor metabolic control; non-insulin-dependent: NIDDM, and juvenile diabetics not requiring insulin at least for two years after diagnosing their disease: NIDDY). The results were compared with controls of identical age and normal weight. A paradoxical hGH response to TRH stimulation was found only in IDDM patients in poor metabolic control. In this group the hGH reserve revealed by arginine was significantly larger than in the others. It was shown that the induced hGH release was independent of the sex distribution of the groups and of the basal hGH values. Magnitude of the hGH reserve and appearance of the paradoxical hGH response were not necessarily correlated but the substantial reserve was frequently associated with a paradoxical response. It can be assumed that the unfavorable metabolic condition is of decisive importance in giving rise to these anomalies. Our observations seem to confirm the need for good metabolic control if the pathological hGH secretion in diabetics is to be prevented.
Acta Diabetol Lat
PMID:Arginine induced growth hormone (hGH) response and paradoxical hGH secretion stimulated by TRH in diabetes mellitus. 311 18

Insulin binding to erythrocyte receptors was studied in 36 newly diagnosed male subjects with NIDDM, treated with diet alone (Group I; n = 10) or diet + glibenclamide (Group II; n = 12) or diet + glibenclamide + metformin (Group III; n = 14). Fourteen matched non-diabetic subjects were also studied as controls. Initially, mean (+/- SD) specific insulin binding was lower in NIDDM patients than in controls (p less than 0.001), due to decreased receptor number and affinity. Control of diabetes with short-term therapy (10 +/- 2 days) resulted in significantly increased specific insulin binding in Groups II and III (p less than 0.001). A marginal increase was observed in Group I (p less than 0.01). The improved insulin binding observed in Group II and III patients after short-term therapy was maintained even after long-term therapy (9 +/- 1 months). Analysis of the insulin binding data by Scatchard plots and average affinity profiles indicated increased receptor number and affinity after short-term therapy. However, changes in affinity were reversed with long-term therapy in Groups II and III and the predominant effect appeared to be an increase in the number of binding sites.
Acta Diabetol Lat
PMID:Rapid improvement in insulin binding to erythrocyte insulin receptors in non-insulin-dependent diabetes mellitus during therapy. 314 5

A case of sulindac-induced toxic epidermal necrolysis (TEN) is described; the etiology, symptoms, and treatment of TEN are reviewed; and sulindac's pharmacokinetic characteristics and other adverse effects are discussed. A 62-year-old black woman was given a prescription for sulindac 150 mg twice daily to relieve pain associated with degenerative joint disease. She also had a nine-year history of type II diabetes mellitus that was being managed with tolbutamide 500 mg once daily. After two weeks of sulindac therapy she developed a rash that spread over her entire body. Sulindac therapy was discontinued, and one day later the patient was admitted to the hospital with a temperature of 104.6 degrees F, conjunctivitis, and an erythematous macular rash over 60% of her body. Initially, therapy included prednisone 160 mg orally every day, applications of silver sulfadiazine cream four times daily for two days, and methylcellulose 0.5% ophthalmic solution (two drops four times daily) for the conjunctivitis. She also received intravenous hydration. By the fifth hospital day the patient's skin lesions and conjunctivitis had improved to the point that the prednisone dosage was tapered to 120 mg, then to 80 mg, and then to nothing over the following three days. Her diabetes was managed by short-term treatment with NPH insulin; however, before discharge, tolbutamide therapy was reinstituted, and insulin was discontinued. At follow-up four weeks after discharge, the patient's skin was largely clear. TEN has multiple etiologies, but the basic mechanism of injury is believed to be an immunological reaction directed at the basal cell layer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sulindac-induced toxic epidermal necrolysis. 323 97

In the perfused pancreas from normal SD rats, AD-4610 (0.01-0.1 mM) potentiated biphasic insulin secretion induced by 7.5 mM of glucose. The concentration-response curve of insulin secretion to glucose was shifted leftwards with AD-4610 (0.1 mM) without altering either the threshold concentration of glucose to induce insulin secretion or the maximal insulin response to glucose, indicating increased sensitivity of the pancreatic B-cells to glucose. On the other hand, AD-4610 was 10-fold less effective in altering insulin secretion induced by arginine and glyceraldehyde. The effect of AD-4610 on insulin secretion and glucose metabolism was compared with that of tolbutamide in vivo. AD-4610 (100 mg/kg) potentiated insulin secretion induced by an intravenous glucose load, and also accelerated glucose metabolism without altering basal insulin secretion in normal rats. On the other hand, tolbutamide (20 mg/kg) increased basal insulin secretion, but slightly decreased glucose-induced insulin secretion. In yellow KK mice with hyperglycemia, AD-4610 (10-100 mg/kg) had a dose-dependent hypoglycemic action, but tolbutamide did not. Thus, AD-4610 stimulated insulin secretion in a glucose-dependent fashion and enhanced glucose metabolism in vivo. These results suggest that AD-4610 selectively potentiates glucose-induced insulin secretion by increasing the sensitivity of pancreatic B-cells to glucose and may be useful for treating human NIDDM through a different mechanism than that of tolbutamide.
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PMID:Selective potentiation of 5-methyl-2-(1-methylcyclohexyl)-4-oxazoleacetic acid (AD-4610) on glucose-induced insulin secretion. 329 76

Based on the known action of xanthine derivatives on the insulin secretion, the effect of pentoxifylline on carbohydrate homeostasis of type I (IDDM) and type II (NIDDM) diabetics was investigated. Pentoxifylline is known to exert a favorable influence on hemorheological disturbances in such patients. Twenty-four hour blood glucose pattern and insulin requirements were evaluated in type I and type II diabetics by the use of the artificial pancreas before and after a 14-day treatment with pentoxifylline 400 mg p.o. (Trental 400) t.i.d. During the stabilization period before treatment with pentoxifylline, NIDDM patients required 10.1 +/- 3.8 U of insulin and the IDDM 35 +/- 13.7 U. After 2 weeks on pentoxifylline, NIDDM required only 6.3 +/- 2.8 U (p less than 0.05) and IDDM 28.5 +/- 9.7 U (n.s.). Average blood glucose during the 24h decreased by 15.8 +/- 3.5% in NIDDM and by 10.3 +/- 2.5% in IDDM. Moreover, a significant smoothing of glucose fluctuations during the 24h was noted in both groups. It is concluded that pentoxifylline administered concurrently to any antidiabetic type of treatment leads to better blood glucose control as well as to prevention or delay of vascular complications.
Acta Diabetol Lat
PMID:24-h blood glucose pattern in type I and type II diabetics after oral treatment with pentoxifylline as assessed by artificial endocrine pancreas. 368 11

In order to establish whether obesity alters whole blood filterability, the corrected whole blood filtration (VRBC) was measured in 54 elderly obese women (mean age +/- SE = 67 +/- 2 years) without (n = 15) or with associated cardiovascular risk factors such as impaired glucose tolerance (IGT) (n = 11), non-insulin dependent diabetes mellitus (NIDDM) (n = 14) or hypertension (n = 14). Twenty-two age matched women with normal body weight participated as controls. VRBC values were similar in normal controls and obese women with normal glucose tolerance (NGT), whereas they were significantly lower in obese subjects with hypertension, NIDDM or IGT. When subjects with normal and impaired glucose tolerance were combined, a significant negative correlation was found between glucose incretory areas during OGTT and VRBC values. These data demonstrate that obesity per se does not alter whole blood filterability; furthermore, our results indicate that this modification is a precocious and sensitive index of altered glucose metabolism.
Acta Diabetol Lat
PMID:Whole blood filterability in elderly obese women. 368 12

Electrophysiological evaluation of peripheral neuropathy was done in 16 patients with tropical pancreatic diabetes (TPD) and the data compared with those of a matched group of 16 NIDDM patients. Peripheral neuropathy was present in 6 TPD and 5 NIDDM patients. Abnormal motor conduction velocity in the lateral popliteal nerve was seen in 9 TPD patients and in 8 NIDDM patients and biothesiometry was abnormal in 7 patients in each group. One TPD patient had an abnormal F wave in the lower limb. An abnormal sensory potential was recorded in the sural nerve in 6 TPD and 8 NIDDM patients. The study showed that occurrence of peripheral neuropathy in TPD was similar to that in NIDDM. Subclinical neuropathy could be detected by electromyographic recording in both groups of patients.
Acta Diabetol Lat
PMID:Peripheral neuropathy in tropical pancreatic diabetes. 375 48

Errors in the assessment of glycemic control by clinicians, using the conventional method, based on random blood glucose and clinical parameters other than HbA1, were assessed in 125 non-insulin-dependent diabetic (NIDDM) patients (Group B). The expected mean post-prandial plasma glucose concentrations (y) for these patients were obtained from their HbA1 values (x) using the regression equation y = 39.6 X x - 157.6. This equation was derived using the data from 35 NIDDM patients (Group A), in whom mean post-prandial plasma glucose concentrations (measured twice daily), correlated excellently (r = 0.82; n = 100; p less than 0.001) with mean HbA1 values (measured monthly) determined over a period of 3 months. A comparison of the observed and expected post-prandial plasma glucose concentrations in Group B indicated that only an overall 42% of the total (n = 455) observed values (as against 60% in Group A) fell within the 99% confidence limits of the expected mean value. Fifty-eight % of the observed plasma glucose values fell outside the expected range of which 36% were underestimates and 22% were overestimates. Thus, we concluded that even in patients with stable diabetes the physician's assessment of the overall degree of glycemic control should be based on both plasma glucose and HbA1 concentrations for optimizing therapeutic measures.
Acta Diabetol Lat
PMID:Errors in clinical assessment of glycemic control in patients with non-insulin-dependent diabetes mellitus. 378 7

Ultrasonography was performed in three groups of young diabetics in the tropics, namely MODY, IDDM and tropical pancreatic diabetes (TPD). Several morphological abnormalities of the pancreas such as fibrosis and shrinkage of the gland, increased echogenicity and ductal dilatation were found in patients with TPD. It also helped to localize the site of calculi in the pancreas. MODY and IDDM patients did not show any significant changes except a slight reduction in size of the gland. Ultrasonography is a useful tool in differential diagnosis of young diabetics in tropical countries.
Acta Diabetol Lat
PMID:Ultrasonographic evaluation of the pancreas in tropical pancreatic diabetes. 390 32

Non-insulin-dependent diabetes (NIDDM) was obtained in adult rats following a neonatal streptozotocin injection. Rats with NIDDM exhibited slightly lowered plasma insulin, slightly elevated basal plasma glucose values (less than 200 mg/dl), and low pancreatic insulin stores (50% of the controls). Insulin secretion was studied in this model using the isolated perfused pancreas technique. Insulin response to glucose stimulation over the range 5.5-22 mM was lacking, thus indicating complete loss of B-cell sensitivity to glucose. Even in presence of theophylline, the B-cells remained insensitive to glucose. In contrast, glyceraldehyde elicited an insulin release as important as that obtained in the control pancreata. This could possibly suggest that the B-cell dysfunction in rats with NIDDM involves a block in glucose metabolism in the early steps of glycolysis prior to the triose-phosphate. Mannose stimulated insulin secretion less in the diabetics than in the controls. The insulin secretion obtained in response to isoproterenol indicated that the ability of the adenylcyclase to generate cAMP in the B-cells of the diabetics was not decreased. The insulinotropic actions of acetylcholine and tolbutamide were normal and increased, respectively, as compared with the controls. In the absence of glucose, the B-cells of the diabetics were unexpectedly hypersensitive to arginine and leucine. The alpha-ketoisocaproate effect in the diabetics was not significantly different from that obtained in the controls. The possibility that enhancement of insulin response to leucine in the diabetics might be related to a more active conversion of leucine to ketoisocaproate along the first steps of intraislet leucine metabolism is proposed.
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PMID:Glucose insensitivity and amino-acid hypersensitivity of insulin release in rats with non-insulin-dependent diabetes. A study with the perfused pancreas. 634 Nov 28


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