Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In some patients with genetic forms of extreme insulin resistance, there is a marked decrease in the number of insulin receptors on the cell surface. We studied an insulin-resistant patient (RM-1) with the Rabson-Mendenhall syndrome. As judged by insulin-binding studies, Epstein-Barr virus-transformed lymphocytes from patient RM-1 exhibit a 90% decrease in the number of insulin receptors. Similarly, with either lactoperoxidase-catalyzed radioiodination of cell surface receptors or biosynthetic labeling of receptors with [3H]glucosamine, we demonstrated an 80-90% decrease in the number of insulin receptors in cells from patient RM-1. Previous studies have shown that the marked decrease in insulin receptors of the Rabson-Mendenhall patient is not due to accelerated receptor degradation. Therefore, we investigated the possibility that a slow rate of receptor biosynthesis might account for the 90% reduction of insulin receptors in cells from this patient. Insulin-receptor biosynthesis proceeds through a glycoprotein precursor with an apparent Mr of 190,000. It undergoes endopeptidase cleavage and further posttranslational processing to yield the mature 135,000- and 95,000-Mr glycoprotein subunits. We studied the biosynthesis of the 190,000-Mr precursor and mature receptor subunits by a pulse-chase labeling technique with [2-3H]mannose. The time course of insulin-receptor biosynthesis appeared normal in cells from patient RM-1, despite a 10-fold reduction in the number of receptors on the cell surface. Parallel pulse-chase experiments with either [2-3H]mannose or [35S]methionine yielded the same results regardless of which label was employed. Thus, the receptor precursor in the Rabson-Mendenhall patient seems to be synthesized at a normal rat.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1986 Jul
PMID:Insulin-receptor biosynthesis in cultured lymphocytes from an insulin-resistant patient (Rabson-Mendenhall syndrome). Evidence for defect before insertion of receptor into plasma membrane. 372 Oct 65

Enzyme activities of erythrocyte superoxide dismutase (SOD), peroxidase and catalase in groups of diabetic children, the duration of the disease and control qualities were compared with respective values obtained for healthy children. Generally the disease duration was clearly found to affect SOD activity, and catalase activity only a little. No similar influence of either diabetes duration or control was noticed in the case of peroxidase. SOD activity was diminished in diabetics when compared with control subjects, and in turn peroxidase and catalase activities were generally elevated. The diminution in SOD activity may constitute a reason for enhanced pancreatic cells susceptibility to deterioration, followed by the augmentation of peroxidase activity with an 'elaborated' mechanism compensating for the loss of erythrocyte SOD activity.
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PMID:Peroxide metabolism enzymes in diabetic children: relationship to duration and control of diabetes. 378 Mar 10

Specific radioimmunoassays for the 7-S domain of type IV collagen and the fragment P1 of laminin were used to quantify these basement membrane proteins in human kidney cortex at different ages and in some patients with diabetes mellitus. The antigens were solubilized by treating the tissue samples with the proteolytic enzymes collagenase, trypsin and pepsin. Total collagen content (as indicated by hydroxyproline concentration) increased with age, and the proportion of the collagen that could be solubilized by any enzyme treatment decreased. The type IV collagen concentration increased significantly with age, whereas the laminin concentration tended to decrease. In the one case of a type I diabetic the amounts of both antigens exceeded those in the age matched controls. In four type II diabetics the results were comparable with those for other aged cases. The distribution of the proteins was studied using the peroxidase-antiperoxidase method. The staining intensity and thickness of both antigens increased with age in the mesangium and Bowmans capsules, the change in type IV collagen staining being more evident. In diabetic patients these changes were more pronounced and other basement membranes appeared thicker in the stainings. These results indicate that basement membrane material accumulates in the kidney cortex during aging and that an alteration takes place in the composition of the basement membranes, the proportion of type IV collagen increasing and that of laminin decreasing.
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PMID:Effect of age and diabetes on type IV collagen and laminin in human kidney cortex. 378 96

A rapid, reproducible enzyme-linked immunosorbent assay (ELISA) for antibody to insulin is characterized and used to study antibodies from insulin-treated diabetic subjects. No radioactivity is involved in the ELISA; rather, peroxidase-conjugated anti-human immunoglobulin is used to detect binding of antibodies to insulin-coated microplates. Color is produced by action of peroxidase on a substrate and an automated reader then measures binding spectrophotometrically. This ELISA was optimized to be at least as sensitive as measurement of antibody by direct 125I-insulin binding. Although detection of IgG directly binding to insulin-coated plates in the ELISA does not reveal species-specific differences, avidity differences are shown in competitive inhibition with insulins from several species. Insulin-binding IgG was purified by affinity chromatography and used to construct a standard curve of the optical density (OD) in the ELISA relative to the concentration of antibody. This assay has been used to quantify and to characterize insulin antibody of sera from a large number of diabetic subjects, ranging from insulin resistant to those who had received only highly purified and human insulins. The assay is shown to be most useful to screen for insulin antibodies in resistant patients.
Diabetes 1985 Jan
PMID:Application of a rapid enzyme-linked immunosorbent microassay (ELISA) to study human anti-insulin antibody. 388 May 49

The insulin receptor and its regulation by insulin was studied in U-937 monocytes, a human cell line with properties similar to those of normal peripheral blood monocytes. Treatment of this cell with insulin for 8-16 h produced an overall loss in the insulin receptor, i.e., a loss of receptors from the cell surface and internal pools. In contrast, short-term insulin treatment (15-30 min) caused a reduction in cell surface receptors but an increase in the internal receptors, as judged by pronase treatment at 4 degrees C to distinguish receptor location. After the removal of insulin and pronase, the internalized receptors were rapidly reinserted back into the cell surface after warming to 37 degrees C. Further studies showed an insulin-mediated increase in fluid-phase pinocytosis as measured by horseradish peroxidase (HRP) uptake. The amount of HRP accumulation and the time course for this stimulation were similar to those for receptor internalization. These features plus other results suggest that the insulin-stimulated internalization of insulin receptors may require an acceleration in the rate of pinocytic vesicle formation.
Diabetes 1985 Apr
PMID:Rapid effects of insulin on the cycling of the insulin receptor in a human monocyte cell line (U-937). 388 3

Utilizing islet amyloid-laden pancreatic tissues from six diabetic cats, we demonstrated substantial immunoreactivity (peroxidase-antiperoxidase technique) of the islet amyloid with antiserum to a B chain-rich insulin fraction, but no reactivity with antisera to insulin, glucagon, or somatostatin. Islet amyloid was purified from two cats and a protein unique to the diabetic and islet amyloid-laden cats was separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis. Immunoreactivity of this protein with antiserum to the B chain-rich insulin fraction was also shown by immunoblotting. Attempts to obtain the amino acid composition of the purified unique protein (represented by a single 25,000 dalton band on gel electrophoresis) were not successful because the amount of protein was too small. These results provide important additional evidence that an insulin-related protein is involved in the formation of islet amyloid. Our study also shows that the diabetic cat provides several advantages for the continued study of the etiopathogenic relationship of islet amyloid and diabetes mellitus.
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PMID:Feline insular amyloid: immunohistochemical and immunochemical evidence that the amyloid is insulin-related. 390 95

Cardiac rupture occurs in 10 per cent of patients who die with acute myocardial infarction, but the pathogenesis remains unclear. Twenty randomly selected patients with cardiac rupture were reviewed retrospectively at autopsy, and the findings were compared with those of 20 age- and sex-matched control subjects who had died of acute transmural myocardial infarction without rupture. The times from the onset of chest pain to death were similar in the two groups (5.7 +/- 5.8 days for patients with rupture versus 4.2 +/- 4.9 days for control subjects), and there were no differences in the incidences of systemic hypertension, diabetes mellitus, hypercholesterolemia, history of myocardial infarction, or angina pectoris. The severity of coronary atherosclerosis was different in the two groups, with 55 per cent of the patients with cardiac rupture having single-vessel disease and 70 per cent of the patients without cardiac rupture having disease in three vessels. Additionally, the incidence of thrombosis was greater in patients with cardiac rupture than in those without. The inflammatory cell response in each patient was quantitated microscopically (number and type of leukocytes) in ten high-power fields. The inflammatory response was greater in patients with cardiac rupture. The number of eosinophils in the inflammatory response was significantly (P less than 0.01) greater in hearts associated with cardiac rupture (29.5 +/- 4 per cent) than in control hearts (11.7 +/- 3.1 per cent). It is postulated that eosinophils rich in arylsulfatase B, peroxidase, glucuronidase, beta-glycerophosphatase, major basic protein, and eosinophilic cationic protein may further weaken the necrotic myocardium and, in part, determine whether acute myocardial infarction will eventually result in cardiac rupture.
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PMID:Association of eosinophils with cardiac rupture. 399 34

The influence of alloxan diabetes on reproductive function and the estradiol-stimulated increase in uterine peroxidase was investigated. Alloxan monohydrate in a dose of 75 mg/kg body weight effectively produced permanent diabetes. In adult rats, 20 days of diabetes resulted in cessation of the estrous cycle and a significant reduction in the gain of body weight, the weights of anterior pituitary gland, ovary, uterus, the level of serum progesterone and the activity of the estradiol-stimulated uterine peroxidase (P less than 0.05). After 10 days of insulin treatment, the ovarian weight, the estrous cycle and the level of ovarian hormones were restored to normal whereas the uterine weight and the estradiol-stimulated uterine peroxidase activity were only partially recovered. Persistent depression of the uterine response in the insulin-treated diabetic rats to both endogenous and exogenous ovarian hormone stimulation suggests that the uterus was directly affected by diabetes. The direct effect of diabetes upon the uterus was further demonstrated in the ovariectomized immature rat in which diabetes depressed the stimulatory action of estradiol on both uterine weight and uterine peroxidase activity.
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PMID:Depression of estrogen-induced uterine peroxidase in alloxan-diabetic rats. 609 85

Parotid gland growth and secretory enzyme levels were studied in male Sprague-Dawley rats following the induction of alloxan diabetes. Diabetes resulted in a retardation of parotid gland, as well as body growth, and in a reduction of parotid gland DNA, RNA, and total protein compared with control rats. Morphologically, parotid glands of diabetic animals were characterized by an intracellular accumulation of lipid within acinar and intercalated ductal cells. Parotid amylase was reduced 40% in diabetic rats compared with control rats. In contrast, peroxidase levels increased by 54%, and DNase was unaffected. Insulin treatment of diabetic rats led to a restoration of gland and body growth. Parotid gland DNA, RNA, total protein, and secretory enzyme levels returned to control values within 7 days. Thus, insulin in vivo may play a major role in the regulation of parotid gland growth and function.
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PMID:Effects of alloxan diabetes and insulin in vivo on rat parotid gland. 619 14

Stereological analysis of electron micrographs of the pigment epithelium of rats with drug-induced diabetes demonstrated an increase of plasma membrane surface area at the basal aspect of the cells. In none of the diabetic animals examined was there any evidence of breakdown of the blood-retinal barrier to the protein tracer, horseradish peroxidase. Statistically significant increases in basal plasma membrane length and surface density (surface area per unit cell volume) were measured in both streptozotocin and alloxan-injected rats after four weeks of diabetes. When hyperglycemia in streptozotocin-injected rats was promptly reversed by transplantation of normal pancreatic islets, the increase of membrane surface area did not occur. We conclude, therefore, that increased basal surface area of pigment epithelial cells is related to the diabetic condition rather than to a toxic action of the diabetogenic agents. Furthermore, increased membrane surface area was present in streptozotocin-diabetic rats killed after six months of diabetes indicating that the structural change is relatively stable. Relation of basal membrane alteration in the pigment epithelium to any functional disturbance of the barrier cell layer or of the retina in diabetes remains to be established.
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PMID:Increase of basal cell membrane area of the retinal pigment epithelium in experimental diabetes. 623 94


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