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

A study was conducted on 50 cases comprising 25 patients of non-insulin dependent diabetes mellitus and 25 age and sex matched normal individuals. The diabetic state of the patients was controlled by glibenclamide, a sulphonylurea. The levels of serum total cholesterol and high density lipoprotein cholesterol were measured at the start and 15 and 30 days after glibenclamide therapy. There was a significant (p < 0.001) decrease in the levels of serum total cholesterol from initial 222.96 +/- 31.04 mg% to 218 +/- 28.99 mg% after 15 days and to 211.8 +/- 28.42 mg% after 30 days of therapy. In no case there was increase in serum total cholesterol level. There was a significant (p < 0.001) increase in the levels of serum high density lipoprotein cholesterol from initial 20.96 +/- 4.59 mg% to 21.8 +/- 4.78 mg% after 15 days to 23.72 +/- 5.07 mg% after 30 days of glibenclamide therapy and no case showed a fall in serum high density lipoprotein cholesterol level. This favourable alteration in serum total cholesterol and high density lipoprotein cholesterol was observed in patients of non-insulin dependent diabetes mellitus having ischaemic heart disease as well.
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PMID:The effect of sulphonylurea therapy on serum total cholesterol and high density lipoprotein cholesterol. 128 82

The traditional role of twin studies has been to assess the relative role of genetic factors as a first step in defining the genetic architecture of complex traits. This has been based on the realization that monozygotic pairs (MZ) share all their genes, while dizygotic pairs (DZ) share 50% of their genes on average. Thus, greater similarity of MZ pairs compared to DZ pairs has been taken as prima facie evidence of the role of genetic factors. This is true provided the environmental similarity of MZ pairs is not greater than for DZ pairs for effects relevant to the trait in question. This first step in genetic studies was carried out long ago in many research areas, but not in others. More detailed knowledge of the genetic architecture of traits is then obtained by other means. In this paper, we give a brief overview of some results for metabolic diseases (ischaemic heart disease, hypertension, subarachnoid haemorrhage, NIDDM and IDDM) using the classical twin approach in a large, unselected population-based twin cohort. We also outline approaches to using twins that we believe will continue to be useful, particularly for the study of environmental effects.
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PMID:Twin studies in metabolic diseases. 141 22

In 50 normotonic patients with type 2 diabetes (NIDDM) and controls matched for sex and age with NIDDM and hypertension a statistically significant difference was found as regards S-peptide values on fasting, cholesterol, triglycerides, BMI and atherogenic index (cholesterol/HDL, p < 0.01). C-peptide values correlated positively with values of the systolic and median BP and the atherogenic index in both groups. In normotonic diabetics there was also a positive correlation with the BMI and in hypertonic subjects with the triglyceride levels. The results confirm the hypothesis that in NIDDM there is a direct relationship between arterial hypertension, unfavourable lipid parameters and insulin resistance and compensatory hyperinsulinism resp. The authors discuss possible mechanisms by which hyperinsulinism mediates a rise of BP, hyperlipoproteinaemia, hyperglycaemia and hirsutism (hormonal metabolic syndrome X and 5H resp.). These phenomena are the main risk factors of cardiovascular diseases and lead via heart attacks and cerebrovascular attacks (IHD and stroke) to a high cardiovascular morbidity and mortality in our population. The morbidity and mortality is steadily increasing and thus we are among civilized countries among those with the highest morbidity and mortality.
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PMID:[Insulin resistance and arterial hypertension. Hyperinsulinism as a basic etiopathogenic factor in essential arterial hypertension and associated phenomena]. 148 85

Obesity and impaired glucose tolerance (IGT) are risk factors for non insulin dependent diabetes mellitus (NIDDM) and for ischemic heart disease. Long term treatment of IGT subjects with diet and tolbutamide prevents progression of IGT to NIDDM. We have evaluated the lowest dose of glipizide, a second-generation sulfonylurea, able to improve glucose tolerance in response to oral glucose in 31 obese subjects, 12 with NIDDM, 9 with IGT and 10 with normal glucose tolerance (NGT). All subjects underwent four OGTTs, preceded by placebo and by different doses of glipizide (0.5, 1.0, 2.5 mg). Glucose tolerance was progressively improved by increasing glipizide doses in all groups, probably by peripheral mechanism and by enhanced insulin release.
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PMID:Improvement of glucose tolerance by minimal doses of glipizide in obese subjects with different degrees of glucose intolerance. 149 Jun 90

In one third of patients who suffered an infarction NIDDM and arterial hypertension are present. In the absolute majority of patients with IHD, as apparent from the IRI and C-peptide response after a glucose load, hyperinsulinism is present. The blood sugar response can have the character of diabetes or of impaired glucose tolerance, the curve may be very flat or normal while the IRI and C-peptide response are excessive. Hyperinsulinism has a hypersecretory origin as suggested by the concurrently elevated C-peptide level but also reduced insulin utilization in the liver and peripheral target organs. Hyperinsulinism is thus a regular associated phenomenon of IHD and is a special risk factor independent on hyperglycaemia and associates with the other main risk factors of IHD such as arterial hypertension, HPLP (android obesity), hyperglycaemia (NIDDM) and hirsutism as a manifestation of a hyperandrogenic state in the female organism with the syndrome of polycystic ovaries. Hyperinsulinism plays an indirect role in the pathogenesis of coronary syndrome via the main risk factors (5H syndrome--hyperinsulinism, hypertension, HPLP, hyperglycaemia, hirsutism) and also directly by its action on endothelial paracrine mechanism of the coronary circulation where in the early stage vasoconstrictor factors predominate (endothelin-1, PGF2-alpha) over physiological vasodilatating factors (EDRF-NO, PGE2, PGI2) and this leads then to functional spasms. It seems that also the coronary X syndrome develops very frequently on the background of the hormonal metabolic X syndrome or the 5H syndrome.
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PMID:[Hyperinsulinism and the coronary syndrome]. 149 68

In a study over one year, it was observed that mortality amongst hospitalised patients with non insulin dependent diabetes mellitus (NIBDM) was nearly 20%. Those dying within 24 hr were classified as group A, between one day and one week as B, between one week and one month as C, and those after one month as D. There were 31 patients each in groups A and B, 14 in C, and 4 in D. The mean age at death was 61 years in the first three groups. The prevalence of cerebro-vascular accident as a terminal event was similar i.e. 32.2, 35.5 and 35.7 per cent in groups A, B and C respectively; 48% of patients in group A suffered from ischaemic heart disease. Diabetic ketoacidosis was equally prevalent amongst groups A, B and C. Infection was significantly more common in group B (45.2%) than A (P less than 0.05). Nephropathy was observed in 57% of patients in group C as compared to 22.5% in A (P less than 0.02). Cerebrovascular accident and infection were the major causes of mortality in groups B and C (80.7% and 71.4%), whereas ischaemic heart disease and cerebrovascular accident accounted for 80% of deaths in group A.
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PMID:Mortality events amongst non insulin dependent diabetes mellitus patients in Orissa. 180 Apr 90

The activity of free tissue plasminogen activator (f-tPA) and plasminogen activator inhibitor (PAI) in the plasma of 82 noninsulin-dependent diabetics (NIDDM) was measured by bioimmunoassay of the euglobulin fraction obtained from the plasma, and the levels were compared with those of age- and gender-matched normal subjects. Comparison of these levels in both groups revealed that the f-tPA activity tended to be lower in NIDDM than in the controls, although the differences were not significant. Normal activity of PAI was seen, but f-tPA in NIDDM, when accompanied by macroangiopathy such as ischemic heart disease, was significantly depressed. When glycosylated hemoglobin levels were in excess of 10%, the f-tPA activity was significantly decreased, but no reduction was found in PAI activity as compared with controls. When NIDDM is associated with either macroangiopathy or high glycosylated hemoglobin levels, a decreased f-tPA activity, rather than an increased PAI activity, may contribute to the development of a defective fibrinolytic state.
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PMID:Activity of tissue plasminogen activator and plasminogen activator inhibitor in noninsulin-dependent diabetes mellitus. 214 33

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.
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PMID:Effect of insulin therapy on metabolic fate of apolipoprotein B-containing lipoproteins in NIDDM. 220 Jul 27

We examined clinical and laboratory features retrospectively in 402 patients at the start of chronic hemodialysis in order to define better the "uremic syndrome" in the dialysis era. The information gathered included demographic data, renal diagnoses, uremic symptoms, biochemical values, and prevalences of hypertension (69%), diabetes mellitus (23%) and ischemic heart disease (16%). Unexpected findings were the wide ranges of serum creatinine levels (3.5 to 35 mg/dl) and blood urea nitrogen levels (35 to 345 mg/dl), and the frequency of hyponatremia (27%), hypoalbuminemia (52%), and anion gaps above 25 mg/dl (5%). There were higher hematocrits in males and diabetics, lower serum creatinine levels in females, diabetics and older patients, and lower blood urea nitrogen levels in blacks. The time interval from diagnosis of diabetes mellitus to initiation of dialysis in patients with diabetic nephropathy due to juvenile-onset diabetes mellitus (20.6 +/- 6.8 years) was twice that in adult onset diabetes mellitus (10.3 +/- 8.3 years).
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PMID:Clinical and laboratory features of patients with chronic renal disease at the start of dialysis. 292 Apr 71

Diabetic nephropathy, a rarely listed cause of end-stage renal failure (ESRF) among patients starting renal replacement therapy (RRT) in the early seventies, has progressively gained in importance and become one of the major reasons for the continuous growth of the patient population on RRT in most European countries. Amongst new patients commencing RRT in 1985, the acceptance rate varied between 3 and 12 per million population for type I diabetes mellitus and between one and four per million population for type II diabetes mellitus. Nordic countries, particularly Sweden and Finland, had the highest acceptance rate of young patients with type I diabetes mellitus whose median ages were 38-42 years. In most central and southern European countries the median age of patients with type I diabetes mellitus varied between 50 and 58 years. The high number of young patients with type I diabetes mellitus and ESRF in Nordic countries point to a different natural history of this disease. It cannot be excluded, however, that the higher median age in other countries might result from doctors mistakenly diagnosing type I disease in patients with type II disease who need insulin treatment. Patients with type II diabetes mellitus had a similar age distribution at start of RRT throughout Europe and their median ages clustered around 60 years in most countries. The contribution of haemodialysis, peritoneal dialysis and renal transplantation was analysed for diabetic compared to non-diabetic ESRF. Despite large geographical differences in the proportional use of methods of treatment, a general trend to apply CAPD more frequently in diabetic as compared to non-diabetic patients was observed, and this was true for countries with both predominant haemodialysis and predominant transplant programmes. Transplantation without prior dialysis was performed in 17% of Swedish and 30% of Norwegian patients with type I diabetes mellitus. In order to better explain the mortality of patients with diabetic ESRF, the proportional distribution of causes of death was analysed. Myocardial ischaemia and infarction was confirmed to be the leading cause of death in patients with diabetes mellitus on RRT. The coronary death rate was estimated to be 10 times greater in young patients with type I diabetes mellitus as compared to their non-diabetic counterparts. Other cardiovascular as well as infectious causes were recorded in a similar proportion of deaths in diabetics as in non-diabetics. Cancer deaths, however, appeared to be definitely less frequent in patients on RRT due to diabetic nephropathy.
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PMID:Renal replacement therapy in patients with diabetic nephropathy, 1980-1985. Report from the European Dialysis and Transplant Association Registry. 314 13


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