Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Diabetic renal disease is a clinical syndrome in which proteinuria is followed by the development of renal failure, and is commonly associated with the concomitant development of hypertension. In insulin-dependent diabetic (IDDM) patients, hypertension often first appears in the microalbuminuric phase of diabetic nephropathy whereas in non-insulin-dependent diabetic (NIDDM) patients, hypertension often antecedes nephropathy and may precede the diagnosis of diabetes. Antihypertensive regimens including diuretics, vasodilators such as hydralazine, beta-blockers and ACE inhibitors reduce proteinuria and delay the decline in renal function in IDDM patients with established nephropathy. No such data are as yet available for calcium antagonists. In microalbuminuric diabetic patients with hypertension, conventional antihypertensive agents, ACE inhibitors and calcium antagonists have been shown to decrease urinary albumin excretion. In the diabetic patient with normal blood pressure and microalbuminuria, there is much less information. It appears likely that ACE inhibitors reduce or retard the rate of increase in albuminuria in these patients. The effect on ultimately delaying or preventing renal failure remains unknown although the preliminary evidence is encouraging. Data on calcium antagonists remain inconclusive with some reports suggesting an increase in proteinuria with the dihydropyridine calcium antagonists. However, a recent longer term study suggested that nifedipine may prevent the rise in albuminuria which is generally observed in the untreated normotensive microalbuminuric subject.
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PMID:The management of diabetic proteinuria. Which antihypertensive agent? 150 44

24-hour ambulatory blood-pressure measurements were obtained according to criteria of the German Hypertension League in 61 non-insulin-dependent diabetic patients after admission to hospital under clinical routine conditions. 30 patients had no signs of nephropathy; 15 patients showed signs of proteinuria of more than 0.5 g/d and/or renal insufficiency, and 16 patients were on chronic hemodialysis renal replacement therapy. Despite antihypertensive therapy, the majority of NIDDM patients with nephropathy and/or dialysis therapy were hypertensive. Hypertension of non-nephropathic patients showed a better response to therapy. About 50% of all patients with nephropathy had a higher mean arterial blood pressure at night than during the daytime. In about 25% of all diabetics with nephropathy, we found, during night time, an especially pronounced increase of both systolic and diastolic blood pressure of more than 5% above the daytime values. Diabetic patients without nephropathy already show a reduced night/daytime variation of blood pressure, however, inverse circadian rhythm as a sign of prognostically non-favorable autonomic neuropathy was found almost exclusively in the nephropathic diabetic patients.
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PMID:[24-hour blood pressure measurement in type-2 diabetic patients with and without nephropathy]. 151 18

The prevalences of risk factors and angiopathy were studied in 260 diabetic patients, 100 females and 160 males, 35-54 years old, in Uppsala. The prevalence, in females and males separately, of hypertension (WHO-criteria) was 46-34%, of hypercholesterolaemia (greater than or equal to 6.7 mmol.l-1) 32-29%, and of obesity (relative BMI greater than or equal to 120%) 25-20%. Those smoking greater than 15 cigarettes/day were 11-20%. Mean HbA1 was 10.6-10.5%. The prevalence of angina pectoris was 11-6%, of possible infarction 4-6%, and of major ECG abnormalities 6-4%. Large vessel (cardiovascular) disease was independently related to HbA1 (strongly), hypertension, cholesterol, age and familial NIDDM. The prevalence of severe retinopathy (blindness, new vessels or large hemorrhage) was 0% with 7-13 years of diabetes duration, and 26% with greater than or equal to 14 years of duration. The prevalence of severe proteinuria was 4% with 7-13 years of diabetes duration, and 15% with greater than or equal to 14 years of duration. Small vessel (retinopathy and nephropathy) disease was independently related to diabetes duration (strongly), HbA1 and hypertension. The data were discussed related to data from the London, Berlin and Tokyo centres of the WHO Multinational Study of Vascular Disease in Diabetics, using the same study protocol in the present study.
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PMID:Prevalences of risk factors and angiopathy in diabetic patients in Uppsala. 152 37

A review of the putative risk factors associated with the development of coronary heart disease in diabetes is presented. Emphasis is given to the effect of nephropathy (persistent proteinuria) and hypertension on cardiovascular mortality in IDDM. Risk factors associated with CHD in NIDDM are also reviewed. Finally, possible reasons to explain the increased incidence of CHD associated with proteinuria in IDDM patients, including lipoprotein abnormalities, increased fibrinogen levels, increased platelet adhesiveness, and altered hemostatic variables, are discussed.
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PMID:Risk factors for coronary heart disease in diabetes mellitus. 152 26

Diabetes mellitus and hypertension are common diseases that coexist at a greater frequency than chance alone would predict. Hypertension in the diabetic individual markedly increases the risk and accelerates the course of cardiac disease, peripheral vascular disease, stroke, retinopathy, and nephropathy. Our understanding of the factors that markedly increase the frequency of hypertension in the diabetic individual remains incomplete. Diabetic nephropathy is an important factor involved in the development of hypertension in diabetics, particularly type I patients. However, the etiology of hypertension in the majority of diabetic patients cannot be explained by underlying renal disease and remains "essential" in nature. The hallmark of hypertension in type I and type II diabetics appears to be increased peripheral vascular resistance. Increased exchangeable sodium may also play a role in the pathogenesis of blood pressure in diabetics. There is increasing evidence that insulin resistance/hyperinsulinemia may play a key role in the pathogenesis of hypertension in both subtle and overt abnormalities of carbohydrate metabolism. Population studies suggest that elevated insulin levels, which often occurs in type II diabetes mellitus, is an independent risk factor for cardiovascular disease. Other cardiovascular risk factors in diabetic individuals include abnormalities of lipid metabolism, platelet function, and clotting factors. The goal of antihypertensive therapy in the patient with coexistent diabetes is to reduce the inordinate cardiovascular risk as well as lowering blood pressure.
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PMID:Diabetes mellitus and hypertension. 156 57

Diabetic nephropathy is the most important complication of diabetes, because it is a major cause of morbidity and mortality for diabetic subjects. Since not all subjects with diabetes are at risk of developing this complication, we conducted a study to determine if heredity might be a possible risk factor for diabetic nephropathy in non-insulin dependent diabetes. Twenty-one factors including inheritance of nephropathy and hypertension were investigated in 109 individuals with NIDDM: 50 patients without proteinuria (Group I), 20 patients with intermittent proteinuria (Group II), and 39 patients with continuous proteinuria (Group III) matched for age and duration of diabetes. Of those patients, 55 patients with inheritance of diabetes were also divided into three groups: 29 patients without proteinuria (Group I), 9 patients with intermittent proteinuria (Group II), and 17 patients with continuous proteinuria (Group III). Individuals in Groups II and III has significantly higher frequency of inheritance of diabetic nephropathy than those in Group I, and also individuals with inheritance of diabetic nephropathy had significantly higher frequency of diabetic nephropathy than those without it. Frequency of hypertension, retinopathy and body mass index in the past were significantly higher in subjects in Groups II or Group III than in those in Group I. There were no significant differences between subjects in Groups II and III. These findings suggest that susceptibility to diabetic nephropathy in NIDDM may be hereditary, although hypertension and obesity may also be important risk factors for diabetic nephropathy.
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PMID:[The possibility of hereditary factors in the susceptibility to diabetic nephropathy in NIDDM]. 163 29

Kidney disease is a primary cause of morbidity and mortality in diabetic patients. Factors that predetermine development of nephropathy remain unknown. Poor glycemic control, insulin requirement, duration of diabetes and family history of hypertension appear to be associated with an increased risk. Arterial hypertension, which is twice as common in diabetic patients as in the normal population, accelerates the progression of diabetic nephropathy. The pathophysiologic mechanisms responsible for hypertension appear to be different in IDDM and NIDDM. In IDDM, hypertension occurs usually as a consequence of diabetic renal disease. Conversely, the pathogenesis in NIDDM appears to be multifactorial. In either condition, aggressive blood pressure control is the single most important intervention proven to retard the progression of nephropathy. A stepped-care approach similar to that for essential hypertension with slight modifications is indicated in the treatment of the hypertensive diabetic patient with nephropathy. Nonpharmacological therapy, including dietary protein restriction, should be used as first step. Selection of the ideal antihypertensive must be based not only on efficacy but also on its side effect profile. Angiotensin converting enzyme inhibitors and calcium antagonists have a low incidence of side effects and do not induce metabolic disturbances. Therefore, they are the agents of choice for patients who do not respond to nonpharmacological therapy alone. Thiazide diuretics and beta-blockers should be used as first line therapy only for specific indications. Antihypertensive therapy combined with good glycemic control and dietary protein restriction constitute the standard of care for diabetic patients with hypertension and renal disease.
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PMID:Hypertension and kidney disease of diabetes mellitus. 176 55

Type 2, non-insulin-dependent diabetes mellitus accounts for 60% of the end-stage renal disease attributed to diabetes in the United States, yet little is known about glomerular function or the development of renal disease in this type of diabetes. The Diabetic Renal Disease Study (DRDS) is a longitudinal study designed to elucidate the natural history of renal disease and to characterize glomerular function throughout the course of renal disease in type 2, non-insulin-dependent diabetes mellitus. The study is being conducted among the Pima Indians from the Gila River Indian Community in Arizona because they experience a very high rate of type 2 diabetes mellitus, which often develops at a young age and which is frequently associated with the development of renal disease. Glomerular filtration rate, renal plasma flow, albumin and IgG excretion, level of vasoactive hormones, retinal damage, and glomerular capillary permeability to dextrans of different sizes will be assessed at regular intervals over 48 months in six groups of subjects representing a range of glucose tolerance from normal to diabetes, and among the diabetic subjects, a range of proteinuria from normal to overt diabetic nephropathy. The DRDS is designed to provide new information on the functional determinants of renal disease in type 2, non-insulin-dependent diabetes mellitus and will serve as the basis for designing intervention strategies.
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PMID:Renal function in non-insulin-dependent diabetes mellitus: purposes and design of the Diabetic Renal Disease Study. 177 50

It has been suggested previously that a decrease in urinary dopamine output might be related to a decrease in the urinary sodium excretion in subjects with diabetic nephropathy suffering from type 2 diabetes. To investigate the renal dopamine status in children with type 1 (insulin-dependent) diabetes mellitus, we measured the 24-hour urinary excretion of dopamine, norepinephrine and sodium in 12 patients with incipient nephropathy (group A, 24-hour albumin excretion rate 70-200 micrograms/min), in 20 age matched patients with normal microalbuminuria (group B, AER less than 20 micrograms/min) and in 8 healthy controls (group C). The mean values for urinary excretion of dopamine and norepinephrine were significantly lower in group A compared to groups B and C (25.6 +/- 14.8 vs. 65.9 +/- 25.5 and 73.3 +/- 18.0 micrograms/day, p less than 0.001 and 11.8 +/- 4.6 vs. 25.1 +/- 12.1 and 28.4 +/- 8.9 micrograms/day, p less than 0.01, respectively). The mean value for the urinary excretion of sodium was also significantly lower in group A than in groups B and C (98.4 +/- 24.1 vs. 206.2 +/- 59.5 and 198.1 +/- 42.8 mEq/day, p less than 0.01). The 24-hour urinary excretion of dopamine correlated significantly with the sodium excretion (r = 0.65, p less than 0.001). Arterial blood pressure was elevated in group A compared to group C (p less than 0.01). Our results suggest that a decrease in endogenous dopamine could play a role in the low urinary sodium excretion thereby resulting in sodium retention which may in turn lead to the development of higher blood pressure in diabetic children with incipient nephropathy.
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PMID:Decreased urinary excretion of dopamine and sodium in diabetic children with incipient nephropathy. 179 93


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