1/104. insulin resistance caused by massive degradation of subcutaneous insulin.Severe resistance to subcutaneous insulin but sensitivity to intravenous insulin persisted for 15 months in a 17-year-old diabetic girl. Heat-labile insulin-degrading activity was present in the patient's ketotic sera and in the 100,000 g fraction (soluble fraction) of adipose tissue. serum-degrading activity was not inhibited by N-ethylmaleimide. The soluble fraction also degraded glucagon and B chain but not growth hormone or myoglobin. It was inhibited by incubation with the patient's nonketotic sera, normal sera, or Trasylol. glutathione-insulin-transhydrogenase (GIT) activity was 66% of normal. The biopsy of adipose tissue at remission showed a normal level of insulin- and glucagon-degrading activity. The activity was eluted from Sephadex G200 as a single peak and had properties consistent with those of the insulin-specific protease (ISP). The increased degrading activity present during insulin resistance had properties not shared with ISP, suggesting the presence of an uncharacterized protease.- - - - - - - - - - ranking = 1keywords = diabetic (Clic here for more details about this article) |
2/104. Type a syndrome of insulin resistance: anterior chamber anomalies of the eye and effects of insulin-like growth factor-I on the retina.BACKGROUND: The purpose of this work was to describe the anterior chamber and iris anomalies as well as to evaluate the effects of recombinant human insulin-like growth factor-I (rhIGF-I) on the retinal vessels in 2 diabetic patients with type A syndrome of insulin resistance, a rare condition associated with acanthosis nigricans. methods: Ophthalmologic examinations, including photographs and fluorescein angiograms, were performed before, and 2 and 4 weeks after starting subcutaneous rhIGF-I treatment, and 3 months after withdrawal of rhIGF-I treatment. RESULTS: Both patients had goniodysgenesis with mild elevation of the intraocular pressure. Before and after 2 weeks of treatment with rhIGF-I, the fundus and the fluorescein angiograms were mainly normal. After 4 weeks of rhIGF-I treatment both patients' retinas revealed leakage of fluorescein. Three (case 1) and 4 months (case 2) after withdrawal of rhIGF-I, the fundus of all four eyes were again without leakage. CONCLUSIONS: The anterior chamber anomalies found in these patients may be part of the type A syndrome of insulin resistance and could alert clinicians that these patients might not have the usual type of diabetes. Moreover, the data show that exogenous rhIGF-I administration in patients with type A syndrome of insulin resistance alters the permeability of the superficial layer of retinal capillaries which is comparable to the earliest angiographic changes in childhood diabetic retinopathy. Whether this is a direct effect of rhIGF-I, as suggested by experiments in an animal model, or an indirect effect due to the near-normalization of the glucose levels by rhIGF-I warrants further investigations. Finally, this work points to an important caveat regarding the therapeutic use of rhIGF-I in this patient population.- - - - - - - - - - ranking = 2keywords = diabetic (Clic here for more details about this article) |
3/104. insulinoma induced hypoglycemia in a type 2 diabetic patient.insulinoma in a patient with pre-existing diabetes mellitus is extremely rare. We report a case of an insulinoma in a patient with type 2 diabetes mellitus who after 14 years of sulfonylurea treatment experienced recurrent episodes of hypoglycemia. Endogenous hyperinsulinism was confirmed and endoscopic ultrasonography identified a pancreatic tumor, which was positive for insulin by immuno-histological staining. After surgical excision of the tumor, no further hypoglycemic attacks occurred. Loss of body weight after removal of the tumor correlated with a dramatic reduction of insulin resistance to such a degree that diet alone proved sufficient for satisfactory glycemic control.- - - - - - - - - - ranking = 4keywords = diabetic (Clic here for more details about this article) |
4/104. A patient with subcutaneous-insulin resistance treated by insulin lispro plus heparin.Severe resistance to subcutaneous insulin but sensitivity to intravenous insulin persisted for 11 years in a 23-year-old diabetic woman. Several therapeutic trials revealed that (1) intravenous regular insulin improved her metabolic control; (2) continuous subcutaneous infusion (CSII) treatment with regular insulin or insulin lispro caused hyperglycemic period with hypoinsulinemia and hypoglycemic period with hyperinsulinemia alternately; (3) adding heparin to insulin lispro in CSII resulted in dramatic increase of serum insulin level and improvement of glycemic control; and (4) regular insulin plus heparin in CSII could not increase serum insulin level and thus the glycemic values was not improved. From these results, the patient followed the insulin lispro plus heparin protocol and obtained a better glycemic control without any adverse events. Effectiveness of this therapy may lead us to further understanding of pathophysiology of this syndrome.- - - - - - - - - - ranking = 1keywords = diabetic (Clic here for more details about this article) |
5/104. Normalization of insulin and glucagon secretion in ketosis-resistant diabetes mellitus with prolonged diet therapy.Glucose tolerance and insulin and glucagon secretion were examined sequentially during 6 months of calorie and carbohydrate restriction in an obese, recent-onset, ketosis-resistant diabetic adult. The subject was then followed for 9 additional months, during which some weight was regained. fasting plasma glucose levels returned to normal after 6 week of calorie restriction and remained normal during periods of carbohydrate refeeding. Normalization of 2-h plasma glucose concentrations after a standard oral carbohydrate load required 5 months, and glucose disposal after an iv glucose load did not return to normal until the end of the study. Insulin secretion in response to oral glucose reached maximal levels during the first months of weight reduction and then decreased as glucose tolerance continued to improve. Acute phase insulin release in response to iv glucose gradually increased throughout the study. glucagon stimulation by iv arginine and suppression by iv glucose also returned to normal levels slowly over several months. Abnormalities in glucose tolerance and glucoregulatory hormone secretion of ketosis-resistant diabetes are totally reversible with prolonged dietary therapy. Reduction in tissue resistance to the action of insulin also appeared to be of major importance in the recovery of normal glucose tolerance in this subject.- - - - - - - - - - ranking = 1keywords = diabetic (Clic here for more details about this article) |
6/104. Sulphonylureas and insulin resistance.This is a case report of a diabetic who required 750-1000 units of insulin per day when gangrene of the leg developed, whereas previously he had needed no insulin. After amputation of the leg, the patient remained asymptomatic for 9 weeks without insulin. This was clearly related to an increased concentration of circulating antibody-bound insulin. Despite healing at the site of amputation, diabetic symptoms and insulin resistance reappeared. chlorpropamide treatment reduced the insulin requirement to zero, which was unrelated to a change in insulin antibody concentration.- - - - - - - - - - ranking = 2keywords = diabetic (Clic here for more details about this article) |
7/104. Rosiglitazone treatment of patients with extreme insulin resistance and diabetes mellitus due to insulin receptor mutations has no effects on glucose and lipid metabolism.BACKGROUND: Rosiglitazone, a thiazolidinedione (TZD), increases insulin sensitivity by reducing levels of plasma NEFA, triglycerides (TG), glucose and serum insulin. Rosiglitazone treatment decreases insulin resistance in type 2 diabetic patients, but no data exist concerning rosiglitazone treatment of patients with syndromes of extreme insulin resistance. OBJECTIVES: To evaluate whether hyperglycaemia in two lean patients with primary severe insulin resistance due to insulin receptor (IR) mutations and diabetes mellitus could be reduced by supplement of rosiglitazone for 180 days and secondary, to evaluate the effects on plasma NEFA, TG, Apo B, PAI-1 and serum insulin. SUBJECTS: Both patients (brothers) have known mutations in the IR gene localized to the tyrosine kinase domain and a deletion of exon 17 in part of their IR mRNA. Prior to the study the HbA1c values were higher than 10% in both patients for more than 12 months during treatment with insulin and metformin. RESULTS: After 180 days of rosiglitazone supplement (8 mg day(-1)), no changes were observed in fasting plasma glucose and HbA1c. Incremental plasma glucose areas under the curves during a 75-g oral glucose tolerance test (OGTT) were unchanged. Likewise, no improvements were seen in either first or second phase insulin secretion during a 0.3 g kg(-1) intravenous glucose tolerance test (IVGTT). fasting plasma VLDL and HDL cholesterol, TG and Apo B levels were unchanged, whereas a small increase was seen in total and LDL cholesterol levels. fasting plasma NEFA increased by 51% in KC after 90 days of treatment, and after 180 days plasma NEFA was still 26% higher, when compared with pretreatment levels. In BC an initial 16% decrease was seen in plasma NEFA after 90 days of treatment. plasma NEFA was increased 14% after 180 days of treatment, when compared with pretreatment levels, but 35% when compared with day 90. plasma PAI-1 decreased in both patients after 45 and 90 days of treatment but the decrease was only maintained in KC (47%). CONCLUSIONS: Rosiglitazone treatment, in combination with insulin and metformin, of patients with severe primary insulin resistance due to IR mutations and diabetes mellitus, had no impact on the measured estimates of glucose and lipid metabolism. These findings may suggest that the effect of rosiglitazone on glucose and lipid metabolism are dependent on the presence of intact IR protein.- - - - - - - - - - ranking = 1keywords = diabetic (Clic here for more details about this article) |
8/104. Familial insulin-resistant diabetes, multiple somatic anomalies, and pineal hyperplasia.West, R. J., Lloyd, J. K., and Turner, W. M. L. (1975). archives of disease in Childhood, 50, 703. Familial insulin-resistant diabetes, multiple somatic anomalies, and pineal hyperplasia. A syndrome comprising unusual facies, dry skin, acanthosis nigricans, thickened nails, hirsutism, dental precocity and dysplasia, abdominal protuberance, and phallic enlargement is described in 2 sibs. Both have developed diabetic ketoacidosis with insulin resistance. The elder child, a girl, had recurrent septic episodes and died at the age of 7-8 years. At necropsy the pineal gland was hyperplastic, weighing 900 mg. Investigation of the younger sib over a 4-year period has shown decreasing glucose tolerance, and he was frankly diabetic with ketoacidosis by the age of 6-8 years. serum insulin concentrations have always been grossly raised. Though the mechanism for insulin resistance has not been definitely established, a functional abnormality of the hypothalamus or pituitary is postulated to explain the many endocrine features of the syndrome.- - - - - - - - - - ranking = 2keywords = diabetic (Clic here for more details about this article) |
9/104. Measurement of accidental urinary insulin loss from a dislocated intraperitoneal insulin catheter.We report the case of a type-2 diabetic woman who received continuous intraperitoneal insulin infusion and developed deterioration of metabolic control by accidental insulin loss into urine (54 U per day) as a consequence of catheter migration which probably resulted in bladder wall injury. Due to iodine allergy of this patient, an analyte addition procedure for insulin quantification in urine had to be applied to allow proof of insulin loss from the catheter tip before as well as reversal to zero insulin excretion after implantation of a new intraperitoneal port and a shorter catheter. The lost fraction of insulin accounted nearly completely for the difference between pre- and postoperatively required insulin doses (146 versus 88 U per day).- - - - - - - - - - ranking = 1keywords = diabetic (Clic here for more details about this article) |
10/104. Evaluation of insulin resistant diabetes mellitus in alstrom syndrome: a long-term prospective follow-up of three siblings.alstrom syndrome is a rare cause of diabetes mellitus. We studied two generations of a Turkish family in whom four members were affected by alstrom syndrome. The natural course of the syndrome in three sisters was followed for 13 yr. The three sisters had short stature and truncal obesity, and developed complete blindness due to retinitis pigmentosa at 10, 5 and 13 yr of age. Two had sensorineural hearing loss and mild mental retardation, while the other developed diabetic ketoacidosis (DKA) at 14 yr and was treated with insulin from onset of diabetes. In the second case, diagnosis of diabetes was made by an OGTT at age 20 yr, and controlled with diet alone for 11 yr, then with a sulphonylurea for 2.5 yr, then with insulin. The third case developed acute hyperglycaemia at 20 yr, and required insulin from onset. Moreover, transitional features of impaired carbohydrate and fat metabolism (severe hyperinsulinaemia and insulin resistance progressing to islet beta cell failure, and hypertriglyceridaemia with fatty liver) were demonstrated, in accord with the literature. Previously unreported findings characteristic of nephro-uropathy with early-onset hypertension were also detected, and included in all cases proteinuria, glomerulopathy, and abnormal locations of the kidneys, narrowed uretero-renal junctions and dilated ureters.- - - - - - - - - - ranking = 1keywords = diabetic (Clic here for more details about this article) |
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