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 assess the changes of calcium metabolism and osteopathy in patients with diabetes. Serum Ca, P, AKP, PTH, CT, plasma fasting blood glucose (FBG) and HbA1 as well as X-ray film of the lumbar spine were measured in 30 diabetes patients; 11 were IDDM and 19 were NIDDM as compared to controls matched for age and sex. There were no significant differences in Ca, P, and CT values in serum between the IDDM and NIDDM patients and controls, whereas the serum levels of PTH and AKP were significant increased in IDDM patients. The incidence of osteoporosis which was shown by X-ray film in NIDDM patients was higher than in those of controls. No correlation between PTH value and osteoporosis or clinical control of diabetes was observed.
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PMID:Calcium metabolism and osteopathy in diabetes mellitus. 195 49

Abnormalities of plasma lipid and lipoprotein concentrations are common in both insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. In general, individuals with IDDM who are untreated or inadequately treated have elevations in both postprandial and fasting triglyceride levels in association with reduced activity of lipoprotein lipase. Low-density lipoprotein (LDL) cholesterol levels can rise when insulin deficiency impacts on LDL-receptor function. When patients with IDDM are treated and plasma glucose levels well controlled, plasma very-low-density lipoprotein (VLDL) triglyceride and LDL cholesterol levels are usually normal. In addition, plasma high-density lipoprotein (HDL) cholesterol levels are normal or elevated in well-controlled IDDM subjects. In NIDDM, increased VLDL triglyceride and reduced HDL cholesterol concentrations are common and are only partially related to glycemic control. Overproduction of VLDL leads to hypertriglyceridemia, which can be exacerbated if lipoprotein lipase activity is also reduced. The regulation of LDL levels is complex; catabolism can be reduced if significant insulin deficiency exists or increased if significant hypertriglyceridemia is present. The reduced levels of HDL cholesterol in NIDDM appear to be related to increased exchange of HDL cholesteryl esters for VLDL triglycerides, although other mechanisms may exist. The roles of insulin resistance, obesity, and independently inherited abnormalities of lipoprotein metabolism in the etiology of dyslipidemia of NIDDM are complex and require further investigation. Finally, the effects of diabetes on glycosylation of apoproteins; on other lipid enzymes, particularly hepatic triglyceride lipase; on lipoprotein surface lipids; and on hepatic uptake of remnants have only just begun to be defined. In view of the marked increase in atherosclerotic cardiovascular disease in individuals with diabetes mellitus, prompt attention to and aggressive therapy for dyslipidemia should be a central component of care for these patients.
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PMID:Lipoprotein physiology in nondiabetic and diabetic states. Relationship to atherogenesis. 195 76

The pathophysiological basis of microalbuminuria is outlined. In a preliminary study (n = 71) and a comprehensive retrospective study over 4 years in type I diabetics (IDDM) (n = 1470) and type II diabetics (NIDDM) (n = 2112), clinical and anamnestic data were compared and the blood pressure, protein excretion, and albumin concentration in the urine were recorded. Early recognition of microalbuminuria in diabetic nephropathy permits successful therapeutic intervention and thus a significant postponement of terminal renal failure.
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PMID:[Microalbuminuria--an early marker of diabetic nephropathy]. 196 88

Insulin deficiency is a prominent feature of non-insulin-dependent (NIDDM) and insulin-dependent (IDDM) diabetes mellitus that could result from defects in the insulin gene. Cloning of this gene has permitted molecular-genetic studies including the definition of multiple-DNA-sequence polymorphisms detected with restriction endonucleases, or restriction-fragment-length polymorphisms (RFLPs), and the mapping of the insulin gene to the short arm of chromosome 11 adjacent to the insulinlike growth factor II (IGF-II) and tyrosine hydroxylase genes. The combined RFLPs for the insulin, IGF-II, and tyrosine hydroxylase genes make this a highly informative locus for genetic studies of the insulin gene in diabetes. Early studies of an RFLP consisting of variable-number tandem repeats (VNTR) of DNA near the insulin gene suggested an association of certain alleles with approximately 170 copies of the repeat unit with NIDDM. Although subsequent studies in NIDDM did not confirm this association, an association of different alleles defined by approximately 40 copies of the repeat unit in this VNTR region with IDDM has been demonstrated in multiple studies. This VNTR region and the multiple other RFLPs for this region have been used in linkage analysis to study the segregation of insulin genes in families. These studies have failed to demonstrate a major significant role for insulin-gene defects in NIDDM, maturity-onset diabetes of the young, or IDDM in American Blacks and Whites and under various models of inheritance. Several pedigrees with diabetes and defects of the insulin gene have been described, however, and a minor role for this gene in NIDDM cannot be eliminated from available studies. Similarly, the association studies of the insulin gene and IDDM suggest a minor modifying role undetectable in pedigree studies. The role of defects in or near the insulin gene in a small subset of NIDDM or in IDDM must await direct investigation of the insulin gene in diabetic individuals with the most recent methods for gene amplification and sequence analysis.
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PMID:Insulin gene in diabetes. Analysis through RFLP. 196 74

NIDDM and hypertension are both characterized by insulin resistance and/or hyperinsulinemia. In IDDM, factors associated with nephropathy produce hypertension. To avoid exacerbation of the metabolic condition, and to prevent further deterioration in glycemic control, treatment of hypertension in the diabetic patient should include the administration of medication with the fewest adverse effects on glucose homeostasis. If diuretics are to be used, it appears that loop diuretics may be preferable to the thiazides or potassium-sparing compounds. Among the remaining classes of antihypertensive drugs, ACE inhibitors may be the agents of choice because of their potential positive effects on insulin sensitivity and renal function, and their lack of severe adverse side-effects.
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PMID:Insulin sensitivity and blood lipids during antihypertensive treatment with special reference to ACE inhibition. 197 44

This study was undertaken to investigate pancreatic changes associated with phasic insulin dependent diabetes mellitus (PIDDM). Twelve PIDDM patients were studied. They were compared with groups of patients, 10 insulin dependent (IDDM), 10 non-insulin dependent (NIDDM), and 10 normal controls. Each group was matched for age, sex, and body mass index. For the study, the mean age was 56.7 +/- 2.5 years, mean body mass index 24.0 +/- 0.8, and mean duration of diabetes 14.2 +/- 2.2 years. Flat abdominal radiograph and ultrasonography were performed on each participant. The results suggest an increased echogenicity of the pancreas in the phasic insulin dependent group of patients.
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PMID:Radiological evaluation of the pancreas in malnutrition-related (phasic insulin dependent) diabetes mellitus. 199 67

White diabetic patients are at high risk of developing coronary artery disease (CAD). The natural history of CAD in insulin-dependent (ID) and noninsulin-dependent (NID) diabetes mellitus (DM) is reviewed to gain insight into the mechanisms responsible for the development of premature or accelerated atherosclerosis in diabetic patients. In both IDDM and NIDDM, the risk of CAD increases with lengthening duration of diabetes; the risk, however, does not grow as a constant multiple of the nondiabetic risk of CAD, suggesting that the cumulative exposure to diabetes plays a significant role as a risk factor for CAD only in a subset of patients. This is consistent with the hypothesis that the diabetic milieu has an impact on the progression of atherosclerotic lesions but not on their initiation. This hypothesis is corroborated further by the observation that CAD does not occur in diabetic patients in populations with a low risk of CAD among nondiabetic patients. The component of the diabetic milieu responsible for promotion of atherosclerotic lesions is unknown. There is evidence, however, of a direct or indirect role of hyperinsulinemia in this process.
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PMID:Evolving natural history of coronary artery disease in diabetes mellitus. 199 19

IDDM and NIDDM are classifications of Diabetes Mellitus (DM) but should be recognized as having related but different treatment regimens; different problems, but the same desired outcome. That outcome is maintenance of normal blood glucose levels and prevention of acute and chronic complications. Nurses who care for patients with diabetes and who provide diabetes education need to continually assess patients' understanding about DM and its treatment. As a result, patient independence is fostered, the likelihood of adherence is increased, and optimal outcomes of the management of diabetes are promoted.
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PMID:Diabetes mellitus. Types I and II. 199 59

While exercise has not been shown to provide long-term improvements in blood glucose control, it has been shown to delay or prevent secondary conditions associated with diabetes. Exercise also offers significant psychological gains by allowing both IDDM and NIDDM patients to participate in normal recreational or competitive activities. A properly designed exercise prescription begins with the education of the patient, including a thorough understanding of the effects of exercise, the demand it places on the metabolic processes, and the necessary adjustments that must be made to maintain normoglycemia. A stress test is a recommended preliminary.
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PMID:A brief overview of diabetes mellitus and exercise. 201 24

Lytic changes to the mesangium and subendothelial area in diabetic glomerulosclerosis were studied by electron microscopy with an emphasis on the mechanism of nodule formation. Renal biopsy specimens were obtained from 30 diabetics (11 males, 19 females; 27 NIDDM, 3 IDDM; mean age, 52.2 years) with renal involvement. Evaluations were made of the glomerular lesions, particularly the ultra-structural findings contributing to nodule formation, mainly by electron microscopy. Varying degrees of lytic change, such as a loose and edematous mesangial matrix, widening of the subendothelial space, followed by endothelial detachment, and destruction of anchor points, were observed in close association with progression of the diffuse lesions. Plasma proteins were found to infiltrate into the widened subendothelial space. Mesangial cells also protruded into the same space and encroached around the whole capillary wall. The interposed mesangial cells were occasionally separated from the basement membrane. Monocytes identified from their ultrastructure were frequently present noticed in the lytic areas, suggesting a reaction to lytic changes. These processes may occur repeatedly with direct expansion of the mesangial matrix, subsequently revealing a nodular appearance.
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PMID:Early mesangiolysis and monocyte influx observed in diabetic glomerulosclerosis: relation to nodule formation. 203 30


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