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

Peripheral insulin resistance is suggested to play an important role in the pathogenesis of type II diabetes mellitus. In this study we investigated insulin receptor binding, D-glucose transport under equilibrium conditions for insulin and the activation kinetics of insulin stimulated D-glucose transport in isolated human adipocytes from type II diabetics and healthy controls. While the insulin receptor binding affinity was not significantly different between both groups, basal and insulin stimulated glucose transport rates were reduced in adipocytes from type II diabetics compared to normal controls. The activation of D-glucose transport was significantly delayed in the diabetics, the time to achieve maximal transport rates was 7.7 +/- 1.1 vs. 4.2 +/- 1.4 min, respectively (p < 0.05). Thus a reduced velocity of glucose transport activation by insulin appears to be a further factor contributing to peripheral insulin resistance in type II diabetics.
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PMID:Delayed activation of D-glucose transport in type II diabetes mellitus. 149 Jun 87

The effect of islet surface antibodies (ICSA) on in vitro insulin release was studied. Isolated rat islets were incubated in the presence of immunoglobulin preparations from patients with insulin-dependent and non-insulin-dependent diabetes mellitus (IDDM, NIDDM) and healthy subjects, and stimulated with D-glucose, L-arginine or tolbutamide. After incubation, the amount of insulin release from the rat islets was determined. The immunoglobulin preparations from 5 newly diagnosed IDDM patients who were positive for ICSA, and from 5 age-matched healthy subjects were examined. Even in the absence of complement or lymphocytes, immunoglobulin fractions positive for ICSA significantly inhibited low and high concentrations of glucose-stimulated insulin release compared with normal control (P less than 0.02), but had little influence on insulin release after stimulation with tolbutamide. Arginine-stimulated insulin release was almost the same in ICSA-positive immunoglobulin fractions and the control. Immunoglobulin fractions negative for ICSA either from four patients with recently diagnosed IDDM or from four newly diagnosed NIDDM patients had only negligible effect on insulin release after stimulation with glucose. These results suggest that ICSA in IDDM patients, even in the absence of complement or lymphocytes, may preferentially interfere with the mechanisms of glucose-stimulated insulin release in the pancreatic B cells.
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PMID:Islet cell surface antibodies preferentially inhibit glucose-stimulated insulin release in vitro. 219 Jul 82

To assess if a dehydrated extract of nopal stems retains the effect on glycemia of the entire nopal stems two experiments were performed. A. Six patients with type II diabetes mellitus in fasting condition received 30 capsules containing 10.1 +/- 0.3 g of the extract, and serum glucose levels were measured hourly from 0 to 180 minutes. B. Six healthy volunteers received 30 capsules with the extract followed by 74 g of dextrose orally. Serum glucose measurements were made in a similar fashion. In each experiment a control test with empty capsules was performed. Nopal extract did not reduce fasting glycemia in diabetic subjects. Nevertheless, the extract diminished the increase of serum glucose which followed a dextrose load. Peak serum glucose was 20.3 +/- 18.2 mg/dl (X +/- SD) lower in the test with nopal than in the control one (P less than 0.025). Dehydrated extract of nopal (Opuntia ficus-indica Mill) did not show acute hypoglycemic effect, although could attenuate postprandial hyperglycemia.
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PMID:[Effect of a dehydrated extract of nopal (Opuntia ficus indica Mill.) on blood glucose]. 256 Dec 56

Myocardial dysfunction in diabetes mellitus is reversed by proper correction of metabolic changes. To assess the role of hyperglycemia on cardiac dysfunction, 50 g of dextrose were intravenously infused to 15 subjects with stable type 2 diabetes. Echocardiographic measurements were made at 0, 60, 120, 180, and 240 minutes. In spite of the high levels of blood glucose reached in diabetics, left ventricular ejection fraction, fractional shortening, and stroke volume did not experience significant changes. Moreover, cardiac output significantly (p less than 0.01) increased in diabetics secondary to an increase in heart rate. No cardiac changes were noticed in 7 healthy subjects studied in a similar fashion. However, their induced hyperglycemia was not as elevated as in the diabetic patients. These results suggest that acute induced hyperglycemia per se does not appear to impair left ventricular contractility in diabetics at resting conditions.
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PMID:Influence of acute hyperglycemia on left ventricular function in diabetics assessed by echocardiography. 366 17

In a retrospective study, glycaemic control on the day of surgery in 68 diabetic patients, managed by a diabetes team (group A), was compared with that in 44 managed by the surgeon and/or anaesthetist alone (group B). Group A insulin dependent patients and NIDDM undergoing major operations were treated by glucose-insulin-potassium infusion (16 units rapid-acting insulin + 10 mmol potassium chloride/500 ml 10% dextrose at 100 ml/h) modified according to blood glucose values (59 cases); well controlled NIDDM undergoing minor operations received no specific therapy (9 cases). Group B patients were treated by a wide variety of regimens. Blood glucose was measured on average 5 times on the operative day in team-managed patients and only twice in the other patients. One-third of the latter group had no glucose measurements at all. Blood glucose values were lower in team-managed patients. Adequate diabetic control, defined as mean blood glucose on the operation day below 216 mg/dl, without hypoglycaemia, was obtained in 82% of team patients but only in 58% of non-team patients. Control was particularly poor in NIDDM under-going major operations and not treated with GIK. Mortality and morbidity were similar in the two groups. We conclude that better glycaemic control was obtained in patients managed by a diabetic team using a glucose insulin potassium infusion. This approach is suitable for any general hospital which offers a diabetic service.
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PMID:Management of diabetes during surgery. A retrospective study of 112 cases. 637 86

The most common metabolic complications of total parenteral nutrition (TPN), glucose intolerance and abnormal liver function, can be significantly reduced when 30% of the glucose calories are replaced by fat. We gave 88 patients either conventional TPN (CON-TPN, 25% dextrose and 4.25% amino acids) or modified TPN (MOD-TPN, 15% dextrose, fat, and 5% amino acids). The treatment groups were as follows: group A, no surgery with TPN only; group B, postoperative TPN; and group C, preoperative and postoperative TPN. Serial blood samples were analyzed for glucose, albumin, triglycerides, and insulin, and for liver function values. Nine patients manifested hyperglycemia and were removed from the study; seven patients had received CON-TPN and two had received MOD-TPN. In group A, the insulin level rose 50% less with MOD-TPN. There was a 50% smaller rise in the triglyceride, SGOT, and SGPT levels in patients who received MOD-TPN. Replacing one third of the TPN glucose calories with fat leads to better glucose tolerance and fewer hepatic complications.
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PMID:Amelioration of metabolic complications of conventional total parenteral nutrition. A prospective randomized study. 643 72

The usual treatment of diabetic patients during surgery with general anesthesia owes little to logic, common sense, or knowledge of requirements, and mortality and morbidity remain high in many centers. In the nondiabetic patient, surgery is accompanied by a rise in secretion of catabolic hormones, insulin-resistance and loss of protein. Therapy of the diabetic patient should be designed to account for these changes and to avoid hypoglycemia, hyperglycemia, and hyperketonemia. It is suggested that for major operations for well-controlled non-insulin-dependent diabetic (NIDDM) persons and for all minor and major operations for insulin-dependent diabetic (IDDM) persons and poorly controlled NIDDM, a combined insulin (3.2 U/h), glucose (10 g 10% dextrose/h), and potassium infusion should be used until oral feeding recommences. The insulin dose should be modified periodically according to bedside glucose monitoring. Fluids should be used as in nondiabetic patients, except that lactate-containing solutions should be avoided. Insulin requirements will be increased (1) by infection, (2) in patients with hepatic disease, (3) in obese patients, (4) in steroid-treated patients, and (5) during cardiovascular surgery. A diabetes-care team should preferably be responsible for the care of the diabetic pre-, per-, and postoperatively.
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PMID:Insulin delivery during surgery in the diabetic patient. 676 22

(+/-)-5-([4-[2-Methyl-2(pyridylamino)ethoxy]phenyl]methyl) 2,4-thiazolidinedione (BRL 49653) is a new potent antidiabetic agent that improves insulin sensitivity in animal models of NIDDM. In C57BL/6 obese (ob/ob) mice, BRL 49653, included in the diet for 8 days, improved glucose tolerance. The half-maximal effective dose was 3 mumol/kg diet, which is equivalent to approximately 0.1 mg/kg body wt. Improvements in glucose tolerance were accompanied by significant reductions in circulating triacylglycerol, nonesterified fatty acids, and insulin. The insulin receptor number of epididymal white adipocytes prepared from obese mice treated with BRL 49653 (30 mumol/kg diet) for 14 days was increased twofold. The affinity of the receptor for insulin was unchanged. In the absence of added insulin, the rates of glucose transport in adipocytes from untreated and BRL 49653-treated obese mice were similar. Insulin (73 nmol/l) produced only a 1.5-fold increase in glucose transport in adipocytes from control obese mice, whereas after BRL 49653 treatment, insulin stimulated glucose transport 2.8-fold. BRL 49653 did not alter the sensitivity of glucose transport to insulin. The increase in insulin responsiveness was accompanied by a 2.5-fold increase in the total tissue content of the glucose transporter GLUT4. Glucose transport in adipocytes from lean littermates was not altered by BRL 49653. To establish the contribution of changes in glucose transporter trafficking to the BRL 49653-mediated increase in insulin action, the cell-impermeant bis-mannose photolabel 2-N-[4-(1-azi-2,2,2-trifluoroethyl)benzoyl]-1,3-bis-(D-mannos++ +-4-yloxy) -2-[2-3H]-propylamine was used to measure adipocyte cell-surface-associated glucose transporters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Repeat treatment of obese mice with BRL 49653, a new potent insulin sensitizer, enhances insulin action in white adipocytes. Association with increased insulin binding and cell-surface GLUT4 as measured by photoaffinity labeling. 765 33

The monomethyl ester of succinic acid (SME) was recently proposed as a novel tool for stimulation of proinsulin biosynthesis and insulin release in animal models of non-insulin-dependent diabetes mellitus. In the present study, either saline or SME (14 mmol/day) was infused for 3 days to control rats, animals injected with streptozotocin during the neonatal period, and Goto-Kakizaki rats with inherited diabetes. The infusion of SME failed to correct the anomalies found in the islets of diabetic rats, namely, a decreased activity of the mitochondrial FAD-linked glycerophosphate dehydrogenase, a low insulin content, and an impaired secretory response to various nutrient secretagogues including D-glucose, 2-ketoisocaproate, and the combination of L-leucine and L-glutamine. These findings raise the question of whether a more prolonged administration of SME is required to raise the insulin store and improve the secretory potential of the endocrine pancreas in animals with type 2 diabetes.
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PMID:Enzymatic and secretory activities in pancreatic islets of non-insulin-dependent diabetic rats after short-term infusion of succinic acid monomethyl ester. 771 Jul 67

The present study deals with the insulinotropic action of the dimethyl ester of succinic acid (SAD), considered as a potential tool for the treatment of non-insulin-dependent diabetes mellitus. In the perfused pancreas prepared from either euglycemic rats or animals first infused for 48 hours with a solution of D-glucose, SAD (10 mM) markedly enhanced insulin output evoked by a high concentration of D-glucose (16.7 mM), whether in the absence or presence of glimepiride (0.5 microM). The succinate ester failed, however, to affect glucagon secretion. Thus, SAD indeed displays favourable attributes for stimulation of insulin release in type 2 diabetes, with emphasis on its insulinotropic efficiency at high concentrations of D-glucose in an animal model of B-cell glucotoxicity.
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PMID:Enhancement by succinic acid dimethyl ester of insulin release evoked by D-glucose and glimepiride in the perfused pancreas of normoglycemic and hyperglycemic rats. 818 62


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