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

Ten noninsulin dependent diabetic patients (NIDDM) without baseline hyperkalemia and with normal aldosterone levels when given 100 g of glucose orally revealed heterogeneous responses in serum potassium changes. Six diabetics had paradoxical increases in serum potassium levels averaged 0.44 mEq/L (range, 0.1 to 1.1 mEq/L) and were accompanied by increases in plasma aldosterone levels. On the contrary, four other noninsulin dependent diabetics and four nondiabetic control subjects had gradual decreases in serum potassium levels with simultaneous decreases in plasma aldosterone levels. These rises and falls in serum potassium concentrations coincided with changes in serum osmolality related mostly to the degree of increases in serum glucose following oral glucose administration. pH of venous blood didn't show any relevant and significant changes with changes of serum potassium levels following oral glucose load. This finding suggests that osmotic mechanisms with various degree of well known abnormal insulin secretion and resistance to insulin action in target tissues in NIDDM patients may account for these heterogeneous responses in serum potassium changes after glucose load, and normal aldosterone levels may not be sufficient to prevent glucose induced increases in serum potassium in NIDDM patients.
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PMID:Heterogeneous changes of serum potassium levels in NIDDM patients on oral glucose load. 147 29

To assess the quality of screening for diabetic retinopathy by 19 general practitioners (GPs) using ophthalmoscopy, the GPs' performance was compared with the performance of ophthalmologists. The GPs had received special training in retinal examination. Direct ophthalmoscopy was performed after mydriasis of both eyes. Later, one of the ophthalmologists at the local hospital performed ophthalmoscopy in the same way as the GP. The ophthalmologist's diagnosis was used as the criterion for retinopathy. 252 NIDDM patients were analysed. The ophthalmologists found 23 cases of retinopathy, of which one patient was referred immediately for photocoagulation. The GPs diagnosed 12 and missed 11 of these 23 cases (false negatives): sensitivity 52%. In 37 of the 229 negative cases the GPs reported a retinopathy: specificity 84%. Of the 11 missed cases, 7 had stage I retinopathy and four showed more serious abnormalities (hard and soft exudates, macular oedema) Further training of GPs in the art of ophthalmoscopy is recommended.
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PMID:Screening for diabetic retinopathy by general practitioners. 148 Aug 72

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

Prevalence of non-insulin-dependent diabetes (NIDDM) in India was reported to be 2.3% in the urban and 1.5% in the rural areas in the early 1970s by the Indian Council of Medical Research (ICMR). Recent studies both in the migrant Indians and in the native Indians have shown the prevalence to be much higher than the above values. Similar prevalence of NIDDM in the migrant and native Indians in affluent areas suggests that Indians as an ethnic group have a high genetic risk for diabetes. Our recent study in South India showed a high prevalence of diabetes in the urban area (8.2%) versus a low prevalence of 2.4% in the rural area. Age, urban-rural factor, body mass index (BMI) and the waist:hip ratio (WHR) were positively associated with diabetes. Interestingly, the prevalence of impaired glucose tolerance (IGT) was similar in urban and rural areas (8.7% and 7.8%, respectively) despite a four-fold lower prevalence of diabetes in the latter. The ratio of new to known diabetes was 1:2 in the urban and 3:1 in the rural areas. There was a male preponderance among Indian diabetic patients. Migration from rural to urban environment with changes in dietary habits and physical inactivity may have contributed to the increased prevalence of diabetes. A high rate of familial aggregation is noted in NIDDM in India and the genetic risk of NIDDM increases with increasing family history of diabetes. In the adult offspring of diabetic parents, hyperinsulinaemia and decreased insulin sensitivity are observed before the development of glucose intolerance.
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PMID:Genetic epidemiology of NIDDM among Asian Indians. 148 45

Six months monotherapy with Acarbose vs. glibenclamide led to a marked improvement of BG and HbA1 in NIDDM, insufficiently controlled with diet. Beneficial effects of these distinct principles of action were statistically not different.
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PMID:Efficacy of 6 months monotherapy with glucosidase inhibitor Acarbose versus sulphonylurea glibenclamide on metabolic control of dietary treated type II diabetics (NIDDM). 149 Jun 92

To investigate the frequency and etiology of diabetic osteopenia, we measured spinal bone mineral density (SBMD), total body bone mineral density (TBBMD), total body fat and lean body mass in 69 female diabetic patients (14 IDDMs and 55 NIDDMs). SBMD decreased with age in both IDDM and NIDDM, but when expressed as a percentage of age-matched normal Japanese females, some had lower SEMD, but others had normal or increased SBMD. Postmenopausal IDDM patients had lower SBMD than postmenopausal NIDDM patients. Thirteen out of 69 (18.8%) had an SBMD lower than 90% of age-matched controls. SBMD correlated positively with TBBMD. Those with lower SBMD had poor glycemic control, but there was no relation between SBMD and either duration of diabetes or presence of retinopathy and/or nephropathy. IDDM patients had lower 1.25 (OH)2D, osteocalcin than NIDDMs. SBMD correlated negatively with urinary pyridinoline and deoxypyridinoline excretion. SBMD correlated positively with body weight, and those with lower SBMD had significantly lower body mass index, body weight, fat weight and lean body mass than those with normal or increased SBMD. These results suggest that IDDM patients may be at higher risk of losing bone postmenopausally, and diabetic patients with lower SBMD have characteristics of poor diabetic control, lean habitus, low serum 1.25 (OH)2D.
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PMID:[Spinal bone mineral density in the female diabetic patients]. 149 83

60 NIDDM patients, mean age (68 +/- 3 years), BMI (25 +/- 5.1 kg/m2), fasting blood glucose (FG) (170 +/- 10 mg/dl), mean daily blood glucose (MDBG) (180 +/- 10 mg/dl), daily glycosuria (GLU) (15.6 +/- 9 g/24 hours), HbA1c (7.9 +/- 0.6%), basal (1.2 +/- 0.2 ng/ml) and stimulated (3.89 +/- 1.3 mg/ml) C peptide (CP) treated by ASS (7.5 +/- 75 mg), after a strict 4 months follow-up period, were assigned to G + M treatment (7.5 +/- 1.500 mg) during a 4 months period. During G+M treatment FG (171 +/- 13 at t0 to 165 +/- 11 mg/dl: p < 0.01 at t4) varied significantly. MDBG (180 +/- 10 at t0 to 175 +/- 12 mg/dl at t4:p < 0.05), GLU (16 +/- 9 at t0 to 11 + 6 g/24 hours at t4; p < 0.01), HbA1c (8.1 +/- 0.4 at t0 to 7.6 +/- 0.3% at t4; p < 0.01). Basal CP remained unchanged in G+M period and varied significantly during ASS period (1.3 +/- 0.3 ng/ml at t4; p < 0.01) and stimulated CP (unchanged during ASS) was reduced during G+M (4.19 +/- 0.4 to 4.04; p < 0.05). Highly significant variations were observed for LAC (28.4 +/- 2.1 at t0 to 14.9 +/- 0.6 mg/dl: p < 0.01 during G+M treatment). G+M therapy was found to be more effective and safer than ASS therapy in regard to glucose metabolism and lactate production in a selected group of NIDDM patients.
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PMID:[Median-term (4 months) treatment with glibenclamide + metformin substituting for glibenclamide + fenformin lowers the lacticemia levels in type-2 diabetics (NIDDM)]. 149 70

The acetylator phenotype was determined in 31 insulin-dependent (IDDM) and 110 noninsulin-dependent (NIDDM) Jordanian diabetics, and was compared to that of 160 healthy volunteers of the same ethnic group. Dapsone was used as the test drug. The rapid acetylator phenotype was slightly less frequent in IDDM and slightly more frequent in NIDDM. Neither of the differences was significant. When acetylator status in the two types of diabetes mellitus was compared, there was a significant difference among the two groups. Patients with IDDM had a higher percentage of the slow acetylator phenotype when compared to NIDDM patients. The association between acetylator status and IDDM in Jordanians, which agrees with that reported for the Saudi Arabian population, is the reverse of what is found in European populations. The results demonstrate ethnic differences in acetylator status among IDDM patients.
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PMID:Acetylator phenotypes of Jordanian diabetics. 149 43

The term X syndrome involves several dilemmas. The terminological dilemma is that this term is used to describe microvascular angina pectoris, as well as Reaven's metabolic-hormonal syndrome and our 5H syndrome [association of hyperinsulinism with arterial hypertension, hyperlipoproteinaemia, hyperglycaemia (NIDDM) and hirsutism]. It is probable that the coronary X syndrome is frequently conditioned by the hormonal-metabolic X syndrome. The pathogenetic dilemma is that it is not clear why in microvascular angina pectoris the coronary circulation does not possess an adequate reserve for vasodilatation during exercise or in response to some pharmacological stimuli. This could condition hyperinsulinism in hypertonic subjects with NIDDM with an early disorder of paracrine endothelial relaxation mechanisms (EDRF-NO), with a predominance of vasoconstrictor mechanisms (endothelin-1). In Reaven's syndrome X it is not clear whether insulin resistance of the postreceptor type is a primary inborn phenomenon which is compensated by insulin hypersecretion or whether it is a secondary phenomenon, which develops ex post and by which the target tissues defend themselves against an excessive effect of insulin (e.g. down regulation receptors) in primary disorders of its secretion.
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PMID:[The dilemma of syndrome X]. 149 65

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


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