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

Insulin resistant, Type II diabetes mellitus (NIDD) in a rat animal model results in profound changes in basal and insulin-stimulated membrane (Ca2+ +Mg2+)-ATPase activity in kidney basolateral membrane (BLM) preparations. We find that NIDD in these animals does not result in similar changes in membrane (Na+ +K+)-ATPase activity. Basal enzyme activity was the same in diabetic and control animals. Insulin treatment of diabetic animals in vivo resulted in hyperinsulinemia and increased BLM (Na+ +K+)-ATPase, while food restriction for 18 hr resulted in lowered enzyme activity. There was no direct effect of insulin on (Na+ +K+)-ATPase activity in isolated membranes from any of the animal groups. Thus, physiologic perturbations which alter insulin sensitivity and glucose homeostasis are accompanied by altered levels of (Na+ +K+)-ATPase activity. Lower levels of this membrane enzyme activity appear to be associated with optimal insulin action.
Biochem Biophys Res Commun 1986 Sep 30
PMID:(Na+ +K+)-ATPase activity in kidney basolateral membranes of non insulin dependent diabetic rats. 302 Nov 55

To determine whether differences in the metabolic response to two common starches could be eliminated by altering the physical form of food, 12 normal and 6 noninsulin-dependent diabetic (NIDDM) subjects were studied after consumption of test loads of whole and blended rice and potato. In normal and NIDDM subjects the lower postprandial glycemia and insulinemia of whole rice was eliminated and became similar to that of whole potato, which was unaffected by blending. The glucagon responses were unchanged and similar in both groups under all study conditions. In both normal and NIDDM subjects the glucose and insulin response to a particular starch is not a stable feature dependent on the unique characteristics of the starch molecule but is affected by food processing and the form in which it is presented to the gastrointestinal tract.
Am J Clin Nutr 1988 Sep
PMID:Postprandial metabolic responses to the influence of food form. 304 97

This study tests the hypothesis that improved glycemic control decreases the postprandial plasma triglyceride (TG) response to ingestion of a saturated fat load. Fifteen normotriglyceridemic subjects with insulin-dependent diabetes mellitus (IDDM, group I) and six hypertriglyceridemic subjects with non-insulin-dependent diabetes mellitus (NIDDM, group II) were studied. Each subject was studied before and after 12 days of continuous subcutaneous insulin infusion (CSII). Each subject ingested identical meals on both study days. Plasma glucose was determined in all patients before and two hours after each meal and at 3 AM, and a mean value was calculated for each patient. CSII reduced mean plasma glucose from 252 to 140 mg/dL in group I, and from 209 to 120 mg/dL in group II (P less than .001 in both groups, paired t test). Plasma TG levels were measured before and 1.5, 3, 4.5, 6, and 7.5 hours after a breakfast which contained 50 g of mostly saturated fat. A repeated-measures ANOVA was performed to assess the effects of glycemic control (factor A) and TG response (factor B) to fat ingestion. In both groups plasma TG levels increased significantly after fat ingestion (P less than .001), and were significantly reduced during improved glycemic control (P less than .001). The reduction was observed in 14 of 15 patients in group I and in all patients in group II. In group I the lowering of the postprandial plasma TG levels after CSII was secondary to a decrease in the fasting plasma TG levels, as shown by the unchanged mean percent TG elevation over the baseline.(ABSTRACT TRUNCATED AT 250 WORDS)
Metabolism 1988 Sep
PMID:Effect of improved glycemic control on the response of plasma triglycerides to ingestion of a saturated fat load in normotriglyceridemic and hypertriglyceridemic diabetic subjects. 304 21

A synthetic peptide formed from residues 20-29 of the pancreatic islet amyloid protein has the confirmation of a twisted beta-pleated sheet protein suggesting it is a potential contributor toward amyloid fibril formation in the islets of Langerhans in Type 2 diabetes mellitus.
Biochem Biophys Res Commun 1988 Sep 15
PMID:Amyloid fibrils formed from a segment of the pancreatic islet amyloid protein. 304 59

Non-insulin-dependent diabetes mellitus patients are those patients who do not require insulin for survival and do not have gestational, secondary, or malnutrition-related diabetes. They may require insulin to maintain good health. Therapy in NIDDM should attempt to reverse the coexisting defects of insulin deficiency and insulin resistance that lead to hepatic glucose over-production and diminished glucose tissue utilization. Both sulfonylureas and insulin can achieve near normal FPGs and HbA1c concentrations in mild to moderately severe NIDDM. Both can reduce insulin resistance and both increase insulin availability. Evidence exists, however, showing that prevention of post-prandial hyperglycemia, whose significance is unknown, may require soluble preprandial insulin. Treatment goals should be realistic and discussed with the patient. In younger patients, the aim should be to achieve normoglycemia, while in those who have other significant medical or social problems, or who are of advanced age, diabetic control may, out of necessity, need to be relaxed. At presentation a diet and exercise program should be initiated and the patient observed if clinically well. If diet fails to reduce the FPG below 108 mg/dl, additional therapy should be used. In mild to moderate NIDDM, sulfonylurea or basal insulin (given as once daily long- or intermediate-acting insulin) can be equally successful without the need for rigid dietary habits. More severe degrees of NIDDM or patients with sulfonylurea failure not caused by dietary indiscretion will require more complex insulin regimens. The socially dependent patient requiring insulin should have as simple a regimen as possible. The insulin-resistant patient undergoing surgery or with an intercurrent illness is most easily managed with a variable rate insulin infusion that allows prediction of subsequent subcutaneous insulin requirements. Combination insulin-sulfonylurea therapy should be reserved for patients failing to achieve acceptable glycemic control when insulin and sulphonylurea are used separately. It may improve control or lessen insulin requirements.
Prim Care 1988 Sep
PMID:Insulin: either alone or combined with oral hypoglycemic agents. 305 69

The one advantage a physician has in designing a regimen to control glucose values in a patient with IDDM is that the physiologic mechanism underlying IDDM is homogeneous: All patients are deficient in insulin and tend to be responsive to physiologic amounts of exogenous insulin. Although patients with NIDDM are inherently more stable, the optimal therapy is less clear and physiologic abnormalities must be considered on a case-by-case basis. Maintaining a balance between food intake, exercise, emotions, hormonal changes, and insulin, however, is an ongoing challenge. Only a fraction of IDDM patients are able to achieve excellent control over a long period of time, but it is generally not possible to predict which patients will be able to achieve these goals. Physicians must be patient and persistent in helping patients adhere as closely as possible to a strict diabetic regimen. Psychological, social, and emotional factors must be considered at every visit. Concern over high glucose levels may cause physicians to overlook important emotional events or a family upset that is causing the patient to be less concerned about blood glucose values. If a patient is having trouble adhering to a regimen, the physician should do a complete history and physical examination, with an appropriate differential diagnosis to help address the broad scope of the problem. For most diabetic persons who administer insulin, split, mixed doses given several times throughout the day allow the patient to use a lower total dose and minimize risk of hypoglycemia while improving the potential for glucose control.(ABSTRACT TRUNCATED AT 250 WORDS)
Compr Ther 1988 Sep
PMID:Meticulous glucose control in diabetic persons using insulin. 306 59

The role of epinephrine in platelet activation and the effect of an alpha 2-adrenoceptor antagonist, midaglizole, during insulin-induced hypoglycaemia in Type 2 (non-insulin-dependent) diabetes mellitus were examined. The action of midaglizole as a platelet alpha 2-antagonist was confirmed by in vitro studies using platelet-rich plasma and washed platelet suspension. Hypoglycaemia was induced by a bolus injection of short-acting insulin in 24 diabetic patients. They were divided into two groups, a control group (n = 12) and an alpha 2-group (n = 12), and midaglizole was administered orally 60 min before insulin injection in the latter. Blood glucose and plasma C-peptide levels were significantly decreased (p less than 0.005) by insulin injection in both groups. Counter-regulatory hormones, including epinephrine, and arginine vasopressin were similarly increased at the hypoglycaemic nadir compared with the levels at 0 min in both groups. Plasma beta-thromboglobulin was increased at the hypoglycaemic nadir (165.5 +/- 12.6 ng/ml) compared with the level at 0 min (121.0 +/- 11.5, p less than 0.005) in the control group, whereas no significant increase was demonstrated in the alpha 2-group. These results suggest that plasma epinephrine plays an important role in platelet activation during hypoglycaemia in Type 2 diabetes mellitus, and that the platelet activation is prevented by alpha 2-adrenoceptor antagonist.
Diabetologia 1988 Sep
PMID:Effect of alpha 2-adrenoceptor antagonist on platelet activation during insulin-induced hypoglycaemia in type 2 (non-insulin-dependent) diabetes mellitus. 306 33

In 97 patients with type I diabetes mellitus, 155 patients with type II diabetes mellitus, and two matched control groups, serum concentrations of laminin P1, a non-collagenous component of basement membranes, were determined by radioimmunoassay to see whether laminin P1 might be a valuable indicator of microangiopathic complications in diabetics. Independent of the type of diabetes, serum laminin concentrations in patients without nephropathy or with early renal damage as assessed by microalbuminuria were comparable with those of the control subjects. Patients with macroproteinuria or with renal insufficiency had significantly increased serum laminin P1 concentrations. Diabetic retinopathy was not found to influence serum laminin P1 concentrations. These data indicate that serum laminin P1 concentrations are increased in advanced diabetic nephropathy.
J Clin Pathol 1988 Sep
PMID:Serum concentrations of laminin P1 in diabetics with advanced nephropathy. 319 51

One hundred ninety-three patients 50 to 89 years of age had cataract surgery between January 1, 1979, and December 31, 1980, at West Virginia University Medical Center, Morgantown. In comparison with 182 patients who elected one of three other surgical procedures, cataract surgery patients had a significantly higher mortality rate (P = 0.0005) than control group patients, according to life-table analysis estimates adjusted for age and sex. Patients with adult onset diabetes mellitus had slight increased survival and did not alter relative mortality. The authors' results support the hypothesis that senile cataracts may reflect systemic factors in addition to localized ocular disease.
Ophthalmology 1988 Sep
PMID:Increased mortality rates after cataract surgery. A statistical analysis. 321 6

To elucidate the mechanism of impaired insulin release in case of non-insulin-dependent diabetes (NIDDM), we investigated insulin release and 45Ca++ efflux from perifused islets obtained from neonatal streptozotocin diabetic model rats. The model rats were prepared by the intraperitoneal administration of 65 mg/kg streptozotocin (STZ) to neonatal males. Rats treated with STZ did not differ from controls in body weight from 1 week to 16 weeks. The model rats had significant hyperglycemia both in the fasting state and after intraperitoneal administration of 2 g/kg glucose. Although the diameter of the islets from the model rats was not significantly different from that of controls, immunoreactivity to anti-insulin was slightly diminished, and degranulation was slightly observed in B-cells. Insulin content was reduced to 45.6% of the control. Insulin release from the perifused islets of STZ-treated rats responded little to 16.7 mmol/L glucose, but normally to 20 mmol/L arginine in the presence of 5.5 mmol/L glucose. In experiments to test the 45Ca++ efflux from the perifused islets prelabeled with 45Ca++, a rise of 45Ca++ efflux concomitant with the second phase of insulin release from the islets of the model rats was inhibited although a sharp increase of 45Ca++ efflux concomitant with the first phase of insulin release was maintained. 45Ca++ uptake for 30 minutes was reduced in the islets from the model rats in the basal and stimulated state of insulin secretion although the incremental 45Ca++ uptake was similar. It is possible that the abnormal calcium handling in pancreatic B-cells may be one of the causes of defect in insulin release in our model rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Metabolism 1987 Sep
PMID:Abnormal calcium handling by perifused pancreatic islets from neonatal streptozotocin diabetic model rats. 330 76


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