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)

Glucosyltransferase (UDPglucose: galactosylhydroxylysine-basement membrane glucosyltransferase), an enzyme specifically involved in collagen synthesis, was measured in various kidney fractions of normal, diabetic and underfed rats, using as basis the incorporation of radioactivity into protein during incubation with UDP[U-14C]glucose and alkali-soluble fetal calf-skin collagen. Three criteria of enzyme activity were compared: A, total radioactivity of the washed protein precipitate; B, this figure minus activity incorporated in the absence of the collagen acceptor; and C, radioactivity incorporated into the mixed amino acid fraction, collected by elution with dilute NH4OH from a Dowex 50 resin column after alkaline hydrolysis of the protein. Method A was found satisfactory using whole medulla or isolated glomeruli, since the average proportions of total protein radioactivity recovered in the NH3 fraction were 0.81 and 0.87, respectively, and the deviations were small. There was a larger and variable proportion of nonspecific incorporation using whole cortex. Incubation of a control set of sample without added collagen was found to be unnecessary (Method B). Per mg protein, medulla and glomeruli had more enzyme than did whole cortex. In diabetes, activity was enhanced in the 10,000 X g supernatant fraction of cortex, as previously reported. However, the increase associated with diabetes was even more consistent in the medulla, averaging 3-fold in the 10,000 X g pellet fraction. No increase was found in isolated glomeruli in diabetes. Also, no increase was seen in the kidneys of non-diabetic rats with body weight similar to that of the diabetics.
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PMID:Glucosyltransferase activity in kidney fractions of normal and streptozotocin-diabetic rats. 44 72

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.
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PMID:Platelet coagulant activities in arterial occlusive disease of the eye. 50 1

Alloxan diabetes in Swiss mice induced decreased levels of percent solubility of collagen in bone, skin and tendon both after 4 days (96 h) and 28 days of treatment. In vitro treatment of tissues with alloxan in physiological saline did not influence the cross-linking of collagen. It is suggested that in alloxan diabetes, metabolites formed in the tissues might accelerate aging of collagen.
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PMID:In vivo and in vitro effects of alloxan on collagen characteristics of bone, skin and tendon of Swiss mice. 51 Sep 25

Platelet functions studied in 163 unselected diabetics compared with 163 controls had the following characteristics: hyperagregation induced by ADP (1.2 muM and 0.6 muM), delayed platelet disagregation (ADP: 0.6 muM), normal agregation in the presence of collagen and thrombin. Platelet hyperagregation induced by ADP was marked in both sexes in cases of retinopathy and in women after the age of 50. By contrast, no correlation was demonstrated between the degree of hyperagregation and age, weight, the duration of diabetes, blood glucose control, lipid profile, vascular complications other than retinopathy and the nature of treatment.
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PMID:[Platelet functions in diabetes with angiopathy (author's transl)]. 53 70

This paper reemphasizes that xeromammographic changes in the skin, parenchyma, and vascular structures of the breast may be manifestations of a host of systemic diseases. Xeromammographic examples of such diseases as congestive heart failure, diabetes mellitus, collagen vascular diseases, and endocrine diseases are presented and discussed.
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PMID:The breast as a mirror of systemic diseases. 59 56

An increased sensitivity of platelets to aggregation from ADP and epinephrine is described in diabetics with or without vascular disease. This sensitivity correlates with elevated levels on von Willebrand factor (vWF), which, in turn appears to be influenced by growth hormone. VWF activity correlates with previously described "plasma factor" activity. Platelets from diabetic subjects are more sensitive than platelets from normal subjects to arachidonic acid-induced aggregation. This sensitivity is abolished by aspirin, which is a prostaglandin synthetase (cyclo-oxygenase) inhibitor. Platelets from diabetc subjects synthesize increased amounts of PGE2-like material (iPGE) in response to ADP, epinephrine, collagen, and arachidonic acid. The latter finding suggests that a fundamental mechanism for increased platelet aggregation in diabetes is increased prostaglandin synthetase activity. Therapeutic endeavors that would lower growth hormone levels, vWF activity, and/or prostaglandin synthetase activity may be of benefit in the prophylaxis of diabetic vascular disease. Prospective studies are needed to explore these hypothesis, as are more studies on the precise mechanisms and platelet aggregation in diabetes mellitus.
Diabetes 1976
PMID:Altered platelet function in diabetes mellitus. 82 64

Several aspects of in-vitro cell growth and protein synthesis were assessed in cultures of skin fibroblasts from subjects with juvenile-onset diabetes mellitus (JODM) or adult-onset diabetes mellitus (AODM) and from age-matched nondiabetic controls (C). There was an inverse correlation between increasing age and both the log-phase doubling rate and saturation density at confluence in C fibroblasts. JODM and AODM cells had a reduction in both indices of cell population growth in comparison with age-matched C fibroblasts. Fibroblasts grown in the presence of 0.3 micronM hydrocortisone were stimulated to grow more rapidly and to a greater saturation density. Stimulation of cell division by hydrocortisone accentuated the abnormalities in growth of JODM and AODM fibroblasts. Total protein and collagen synthesis was measured whtn the fibroblasts had grown to confluency in medium with or without hydrocorticone. Hydrocorticone did not produce a significant change in total protein and collagen synthesis per cell by C fibroblasts. Fibroblasts from AODM had a 180 per cent increase in total protein and collagen synthesis in the presence of hydrocortisone. In contrast, total protein and collagen synthesis decreased 40 per cent in fibroblasts from JODM when grown in the hydrocortisone medium. These studies indicate that skin fibroblast cultures from patients with diabetes exhibit abnormalities in cell proliferation. Furthermore, hydrocortisone appears to unmask diffeerences in protein synthesis that distinguish JODM and AODM fibroblasts in culture.
Diabetes 1977 Apr
PMID:Abnormalities in proliferation and protein synthesis in skin fibroblast cultures from patients with diabetes mellitus. 84 9

The macromolecules of the intercellular matrix (MM) : collagen, elastin, proteoglycans and structural glycoproteins) are present in all tissues in variable amount and proportion. Some tissues, particularly rich in MM are designated as "connective tissues". Matrix macromolecules assure the integration of cells in tissues and of tissues in organs and in the whole organism. Differentiation, morphogenesis, maturation and aging are characterized by the variation of the raltiave rates of synthesis of individual MM-s. Several post-transcriptional and post-translational steps play an important role in biosynthesis of MM-S offering a multitude of possibilities for genetic and/or aquired anomalies. Recent progress in the descriptive and dynamic biochemistry of MM-s sheds new light on these anomalies which condition a whole class of diseases (the diseases of the intercellular matrix or matrix pathology). The molecular and cellular mechanisms of several of these diseases start to be understood. As the great majority of the important disease of occidental societies (such as vascular and articular diseases, diabetes, and the pathology of aging) belong to this category, intensive research in matrix biology and pathology as well as of its teaching in the medical curriculum should be considered as first priorities.
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PMID:Matrix biology and pathology, a new branch of biomedical sciences. 86 48

Thickening of the basement membrane and deposition of collagen-like substances in vascular lesions are well-known findings in diabetes mellitus, suggesting altered metabolism of glycoproteins. Glomerular glucosyltransferase activity were measured in normal and diabetic rats. Enzymic activity in diabetic animals did not differ from control. Another mechanism must be involved in the thickening of the B.M., such as increased production of hydroxylysine-rich peptides or decreased breakdown of B.M. materials.
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PMID:Glucosyl transferase activity and diabetic microangiopathy. 89 17

Recent epidemiologic studies have suggested that cardiac disease in common in diabetics and may often have a noncoronary basis. To examine the status of the left ventricle, 17 adult-onset diabetics of familial type without hypertension or obesity underwent hemodynamic study and were compared to 9 controls of similar age. Of the 17, 12 subjects had no significant occlusive lesions by coronary angiography. From this group eight without heart failure had a modest, but significant, elevation of left ventricular end-diastolic pressure. End-diastolic and stroke volumes were reduced, but ejection fraction and mean rate of fiber shortening were within normal limits. The left ventricular end-diastolic pressure/volume ratio was significantly higher than controls. Afterload increments effected a significant increase of filling pressure compared to normals without a stroke volume response, consistent with a preclinical cardiomyopathy. Four patients with prior heart failure had similar but more extensive abnormalities. None had local dyskinesia by angiography, and lactate production was not observed during pacing-induced tachycardia. Left ventricular biopsy in two patients without ventricular decompensation showed interstitial collagen deposition with relatively normal muscle cells. These findings suggest a myopathic process without ischemia. Postmortem studies were performed in 11 uncomplicated diabetics. Nine were without significant obstructive disease of the proximal coronary arteries, and the majority succumbed with cardiac failure. On left ventricular sections, none had evident luminal narrowing of the intramural vessels. All nine exhibited periodic acid-Schiff-positive material in the interstitium. Collagen accumulation was present in perivascular loci, between myofibers, or as replacement fibrosis. Multiple samples of left ventricle and septum revealed enhanced triglyceride and cholesterol concentrations, as compared to controls. Thus, a diffuse extravascular abnormality may be a basis for cardiomyopathic features in diabetes.
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PMID:Evidence for cardiomyopathy in familial diabetes mellitus. 89 79


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