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

Eighteen patients with non-insulin dependent diabetes mellitus and hypertension were treated during two 4 week periods with the calcium antagonist felodipine or placebo in a double-blind, randomised, cross-over study. Mean systemic blood pressure was significantly lower on felodipine, without producing a deleterious effect on diabetic control. Felodipine was associated with an increment in plasma renin concentration but plasma aldosterone and the renal outputs of sodium and dopamine were similar on both treatments. Plasma atrial natriuretic peptide levels were significantly reduced following felodipine treatment.
Br J Clin Pharmacol 1990 Sep
PMID:Effects of felodipine on atrial natriuretic peptide in hypertensive non-insulin dependent diabetes mellitus. 214 57

Coagulation-fibrinolytic system is known to be one of the exacerbating factors in patients with diabetic nephropathy. The aim of the present study was to evaluate whether coagulation-fibrinolytic system in patients with diabetic nephropathy were significantly correlated with the development of this disease using new parameters of plasma thrombin antithrombin III complex (TAT) and plasmin alpha 2 plasmin inhibitor complex (alpha 2PIC). Fifty-six patients with NIDDM were examined. None of these patients showed more than 1.3 mg/dl of serum creatinine levels. These patients were divided into three groups according to the levels of albumin creatinine ratio (ACR) in urine as follows: 1) group I had ACR of less than 30 mg/g.Cr; 2) group II had ACR of greater than 30 mg/g.Cr and less than 100 mg/g.Cr; 3) group III had ACR of greater than 100 mg/g.Cr. Correlations of levels of plasma TAT and alpha 2PIC, levels of HbAlc, duration of diabetes, and presence of retinopathy were determined in these groups. The levels of plasma TAT and alpha 2PIC increased as the levels of urinary ACR increased regardless of presence of retinopathy. The levels of TAT and alpha 2PIC with retinopathy increased compared with those without retinopathy. There was a significantly positive correlation between plasma TAT and alpha 2PIC (r = 0.52, p less than 0.01). The levels of HbAlc and duration of diabetes did not significantly correlate to plasma TAT and alpha 2PIC. These data suggest that the existence of increase in coagulation-fibrinolytic system seem to be one of the exacerbating factors in patients with diabetic nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)
Nihon Jinzo Gakkai Shi 1990 Sep
PMID:[Studies on coagulation-fibrinolytic system in diabetic nephropathy--with reference to plasma TAT and alpha 2PIC]. 214 99

Non-insulin-dependent diabetic (NIDDM) subjects exhibit abnormalities in their plasma lipid and lipoprotein profiles that increase the risk of ischemic heart disease. This study was designed to examine the metabolic behavior of very-low-density (VLDL), intermediate-density (IDL), and low-density (LDL) lipoproteins in NIDDM patients before treatment and after 4 wk of insulin therapy. Basal turnover studies of 131I-labeled VLDL1 (svedberg units [Sf] 60-400) and 131I-labeled VLDL2 (Sf 20-60) apolipoprotein B (apoB) were conducted in a group of seven NIDDM patients who had been off oral therapy for 1 wk. The subjects exhibited higher than normal transport rates for VLDL1 and a diminished input of apoB into the VLDL2 density range. These observations are concordant with the hypothesis that NIDDM patients overproduce VLDL triglyceride but not apoB. VLDL1 and VLDL2 were converted to IDL and ultimately to LDL at approximately normal rates, although the delipidation pathway by which apoB-containing particles were processed exhibited different properties from that seen in control subjects. Insulin therapy reduced plasma triglyceride by 38%, and this was associated with a 41% fall in VLDL1 mass (P less than 0.01). VLDL2 was less affected (19% reduction, P less than 0.05), IDL was unchanged, and LDL fell 17% (P less than 0.05). Repeat metabolic studies revealed that the major effects of insulin were to reduce VLDL1-apoB transport (from 811 to 488 mg/day) and increase the direct input of VLDL2 into the plasma (from 182 to 533 mg/day, P less than 0.05). These alterations in VLDL production led to normalization of apoB kinetics in IDL and LDL. The fractional catabolic rate of LDL increased 19% (P less than 0.05), whereas direct input into this fraction, which had been high before treatment, was reduced. Postheparin plasma lipoprotein lipase (LPL) and hepatic lipase levels were unaffected by insulin, although the hormone did increase LPL in adipose tissue. This lack of effect on lipase activities correlated well with the observation that the rates of catabolism of apoB in VLDL1, VLDL2, and IDL were not significantly affected by insulin therapy.
Diabetes 1990 Sep
PMID:Effect of insulin therapy on metabolic fate of apolipoprotein B-containing lipoproteins in NIDDM. 220 Jul 27

The present study was carried out to see if either the volume of water or the duration of ingestion time influence the postprandial blood glucose and insulin responses in non-insulin-dependent diabetic (NIDDM) subjects. Small test meals containing 40 g carbohydrate as rye bread (100 g) with butter (10 g) and tomatoes (75 g) were given to 10 NIDDM subjects. The meals were taken in random order with either 90 or 600 mL tap water. The meal with 90 mL tap water was ingested over 10 and 30 min. The glycemic responses to isocaloric meals of large and small volumes were similar (338 +/- 56 vs 384 +/- 67 mmol/L.240 min) as were the insulinemic responses (29,424 +/- 6512 min vs 27,140 +/- 6548 mumol/L.240 min). An extension of eating time from 10 to 30 min did not alter the glycemic (384 +/- 67 vs 370 +/- 54 mmol/L.240 min) or the insulinemic response (27,140 +/- 6548 vs 35,670 +/- 10,245 mumol/L.240 min) in the NIDDM patients.
Am J Clin Nutr 1990 Sep
PMID:Water volume and consumption time: influence on the glycemic and insulinemic responses in non-insulin-dependent diabetic subjects. 220 55

Glycemic and hormonal responses to two breakfast mixed meals were studied in six obese subjects with NIDDM. The study evaluated a high-glycemic-effect (HGE) and a low-glycemic-effect (LGE) meal, each with approximately 600 kcal and 12% protein, 15% fat, and 73% carbohydrate. Plasma insulin and counterregulatory hormones were measured at baseline and at 30-min intervals for 5 h after meals. Mean fasting plasma glucose and insulin concentrations were similar before both studies: for the LGE meal, 11.9 +/- 1.8 mmol/L and 261.9 +/- 50.1 pmol/L; for the HGE meal, 11.9 +/- 2.0 mmol/L and 262.6 +/- 43.1 pmol/L. Peak plasma glucose concentrations were approximately 25% lower with the LGE meal and the area under the glucose curve was 63% of that obtained for the HGE meal (p less than 0.05). Although the integrated insulin responses of the two meals did not differ, the peak occurred 60 min earlier in the LGE meal (p less than 0.05). The LGE meal may produce a lower glycemic response, in part because of earlier insulin secretion.
Am J Clin Nutr 1990 Sep
PMID:Insulin response and glycemic effects of meals in non-insulin-dependent diabetes. 220 56

Patients with non-insulin dependent diabetes mellitus have an increased incidence of coronary artery disease which may, in part, be associated with abnormalities in plasma lipids. In a double-blind, parallel, randomized study, lovastatin and gemfibrozil were compared in 102 diabetic patients with primary hypercholesterolemia; two-thirds of the patients were treated with oral hypoglycemic agents and one-third received diet therapy alone for their diabetes. Mean pretreatment total and low-density lipoprotein (LDL) cholesterol values were 273 and 193 mg/dl, respectively. Lovastatin significantly reduced total, LDL and very low density lipoprotein cholesterol (20, 26 and 28%, respectively) and raised high-density lipoprotein (HDL) cholesterol (14%). Gemfibrozil significantly reduced triglycerides and very low density lipoprotein cholesterol (36 and 41%, respectively) and, to a lesser extent, total cholesterol (9%); it also increased HDL cholesterol (21%). Lovastatin therapy was not associated with a significant change in triglycerides, and gemfibrozil did not significantly lower LDL cholesterol. The decrease in the ratio of total to HDL cholesterol tended to be greater with lovastatin than with gemfibrozil (26.5 and 20.4%, respectively; p = 0.053). Changes in lipid profiles with both agents were of a degree similar to those reported in nondiabetic patients. Neither agent had a clinically important effect on fasting glucose or hemoglobin A1c. Both drugs were well tolerated with the exception of 2 patients treated with gemfibrozil who developed symptoms of cholecystitis.
Am J Cardiol 1990 Sep 18
PMID:Comparison of the effects of lovastatin and gemfibrozil on lipids and glucose control in non-insulin-dependent diabetes mellitus. 220 32

Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by insulin resistance and beta-cell dysfunction. This review focuses on the beta-cell, what defects occur when and why. Two major anatomic observations have been made in NIDDM. The beta-cell mass is mildly reduced, especially when obesity is taken into account. Also, amyloid deposits are frequently observed in the islets. It is unclear whether these changes are genetically mediated or result secondary to the loss of glucose homeostasis. Many studies have looked at some aspect of insulin secretion in NIDDM, and two types of distinct abnormalities have been described. Early on, there is a marked disruption in pulsatile insulin delivery, which is potentially an important contributor to the insulin resistance. It is unclear whether the loss of pulsatile delivery is acquired or genetically induced. Later, after glucose intolerance has started, several other secretory abnormalities develop coincident with loss of beta-cell glucorecognition. The net result is further deterioration in timing of insulin delivery and postprandial hyperglycemia. A second important consequence of the glucose blindness is that the inherent compensatory beta-cell mechanisms that guard against hyperglycemia are bypassed. We propose that the loss of glucose responsiveness is a direct result of an elevated glucose concentration (so-called glucotoxicity) and have generated substantial data in rat models that support this idea. The logical conclusion is that beta-cell function in NIDDM can be maximized by achieving the best metabolic control possible.
Diabetes Care 1990 Sep
PMID:Natural history of beta-cell dysfunction in NIDDM. 222 13

In order to examine sex differences in the association of obesity with the risk of non-insulin dependent diabetes mellitus (NIDDM) when using the body mass index (BMI), we compared unisex body mass index classifications with sex-specific categories, as defined by the Metropolitan Life Tables, based on their utility in predicting the 12-year incidence of NIDDM in men and women. The present analysis included all 747 men and 969 women from a defined older caucasian population in Rancho Bernardo, California, who were 40 years of age or older at the baseline examination in 1972-1974 and who had complete diabetes-related data available then and between 1984-1987. The 12-year age-adjusted incidence rates for NIDDM increased with increasing BMI among women (all steps significant), but was significantly increased only in the most obese category of men (relative risk (RR) = 2.3, P less than 0.05 for men; RR = 3.8, P less than 0.001 for women). Men and women had nearly identical rates of NIDDM in this obese category. When identical (unisex) BMI cutpoints were used, results were the same; (RR = 2.4, P less than 0.05 for men; RR = 3.1, P less than 0.01 for women). These data indicate that unisex and sex-specific cutpoints for BMI identify the same sex-specific patterns of association between obesity and risk of NIDDM.
Int J Obes 1990 Sep
PMID:Sex-specific vs. unisex body mass indices as predictors of non-insulin dependent diabetes mellitus in older adults. 222 11

The serum values of para-amino-benzoic acid in subjects affected by type II diabetes mellitus, were measured hourly for 6 hours, after oral ingestion of B-T-PABA. These values were compared with those of a control group. The results demonstrate that at 1, 2, 4 and 5 hours, the mean values of the two groups were significantly different: p less than 0.01, p less than 0.002, p less than 0.0001 and p less than 0.005 respectively. Comparing the area under the curve the data did not differ significantly, indicating that at the end of the sixth hours the quantity of PABA absorbed is very similar in the two groups. These results indicate that patients with diabetes seem to have an altered exocrine pancreatic function, which may be due to a reduction in the zymogen stocked in the acinar cells or a lower secretory response to physiological stimulus. This impairment does not affect the digestion and the nutritional state of the patients.
Recenti Prog Med 1990 Sep
PMID:[Serum PABA test in diabetes mellitus]. 226 55

Alterations in Relative Plasma Viscosity (RPV) and Plasma Fibrinogen Concentration (PFC) were compared in 24 insulin-dependent (IDDM) and 33 non-insulin-dependent (NIDDM) black Nigerian diabetics, during the course of treatment. Both PFC and RPV were significantly (p less than 0.001) increased in the diabetics, as a group, compared to a non-diabetic control group. PFC and RPV showed consistently marginal, though insignificant, increases in the IDDM vs NIDDM. Hypertensive diabetics, as a group, had significantly greater PFC (p less than 0.025), and RPV (p less than 0.025) than normotensive diabetics. Although PFC was significantly (p less than 0.05) raised in hypertensive IDDM, there was no marked change in RPV, compared to normotensive IDDM. Neither PFC nor RPV revealed a significant change between hypertensive and normotensive NIDDM. The implication of the present findings is that insulin-dependent diabetics may be more prone than non-insulin-dependent diabetics to develop haemorheological and hence circulatory disorders.
West Indian Med J 1990 Sep
PMID:Comparison of plasma viscosity and fibrinogen concentration in African insulin-dependent and non-insulin-dependent diabetics with and without hypertension. 226 27


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