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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exocrine pancreatic function was studied in 20 juvenile-onset diabetics, seven maturity-onset diabetics, and five patients with diabetes secondary to chronic pancreatitis. The results were compared with 13 non-diabetic controls. The outputs of bicarbonate, trypsin, and amylase were reduced in the diabetic patients in response to intravenous secretin and CCK-PZ. In the juvenile-onset group, exocrine pancreatic secretory capacity was reduced in 80% of the patients, and the severity of the reduction was related to the duration of the diabetes. The reduction in pancreatic secretory capacity must be taken into consideration when interpreting pancreatic exocrine function in patients with diabetes.
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PMID:Exocrine pancreatic function in juvenile-onset diabetes mellitus. 97 8

A conspicious renal change associated with diabetes is the thickening of the basement membranes. This was generally considered diffuse and little attention was paid to its nodular character. In the present study of the nodules, their topo-optical reation, electron microscopic fine structure as well as their trypsin digestibility after periodic acid-sulphatation revealed their basement membrane character. The increased basophilia obtained by the aldehyde-bisulphite-toluidine blue reaction indicated an increased amount of sugar components, whereas the decreased double refraction and the red polarization colours a decrease of the micellary arrangement. The change is mostly observed in diabetics; the specific localization around the Henle loops may refer eventual hyperosmolar effects, whereas the nodular character points to the role of local factors.
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PMID:Nodular thickening of peritubular basement membranes in diabetic kidneys. 103 74

In 11 juvenile diabetics and 13 control subjects, the secretin-pancreozymin test was performed. Duodenal-volume losses were corrected by use of radioactive vitamin B12 as marker substance. As compared to normal subjects, juvenile diabetics had significantly decreased pancreatic outputs of amylase, trypsin, chymotrypsin, and to a lesser degree, of bicarbonate. Clinical evidence of disease of the exocrine pancreas was missing. There was no discernible relationship between the abnormality of external pancreatic function and the duration of diabetes mellitus or the dose of insulin required. Possible factors that may be responsible for the exocrine deficiency of the pancreas in juvenile diabetics are discussed.
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PMID:Exocrine pancreatic function in juvenile diabetics. 113 Mar 59

The aim of the present study was to investigate whether or not alterations of the plasma proteinase-antiproteinase system were present in type 1 (insulin-dependent) diabetic patients and, if so, whether or not they were related to sex, age at onset and duration of the disease as well as to short- and long-term diabetic control. The plasma concentration of trypsin-like activity and two of the most important plasma serine proteinase inhibitors, alpha 1-antitrypsin and alpha 2-macroglobulin, were determined in 95 type 1 diabetic and 67 control subjects. The plasma concentration of alpha 1 antitrypsin was found to be markedly decreased (P < 0.001), whereas plasma alpha 2-macroglobulin and trypsin-like activity were increased in diabetics compared to controls (P = 0.009 and < 0.001, respectively). Sex also influenced the values of both proteinase inhibitors in diabetics, women showing higher values of plasma alpha 1-antitrypsin (P = 0.004) than men. In women, HbA1c was also positively correlated with blood glucose (P < 0.001), daily insulin dosage (P < 0.001), and trypsin-like activity of plasma (P = 0.02). On the contrary, in men, HbA1c appeared to be negatively correlated with plasma alpha 2-macroglobulin (P = 0.02). In addition to sex, age at onset (but not duration) of the disease revealed differences in plasma alpha 1-antitrypsin among diabetics, the lowest mean value of this inhibitor being present in men with age at onset below 15 years, who also showed a significant negative correlation between this inhibitor and HbA1c (P = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res Clin Pract 1992 Oct
PMID:Alteration of plasma proteinase-antiproteinase system in type 1 diabetic patients. Influence of sex and relationship with metabolic control. 128 Jan 91

To elucidate the acute effect of insulin on its receptor, rat adipocytes were preincubated with insulin, washed with KCN to inhibit receptor cycling, and 125I-labeled insulin binding was measured. Preincubating cells from young insulin-sensitive rats with insulin increased cell surface binding up to approximately fourfold without changing apparent receptor affinity. This effect was rapid (t1/2 less than 5 min) and had a similar dose-response relationship as the effect on glucose transport. It was also energy dependent because preincubation with KCN completely abolished the effect of subsequent insulin exposure. The increased binding capacity was not recovered after cell solubilization or in partially purified receptors or isolated plasma membranes. Cells pretreated with insulin were less sensitive to the ability of trypsin to remove cell surface receptors, suggesting a conformational change of the receptors. This was also supported by the finding that the polyclonal binding in insulin-treated but not in control cells. Vanadate mimicked the effect of insulin to increase insulin binding, whereas concanavalin A, vasopressin, phorbol esters, or the adenosine analogue phenyl isopropyl adenosine was without effect. Insulin-resistant adipocytes from obese rats displayed no increase in cell surface binding after insulin treatment, despite normal tyrosine kinase activity in response to insulin. Thus, both insulin and vanadate elicit a rapid effect to markedly increase the number of cell surface insulin binding sites in intact rat adipocytes. This appears to occur independently of protein kinase C and the inhibitory GTP binding protein (Gi). Furthermore, the effect of insulin could not be demonstrated in insulin-resistant cells, suggesting that this mechanism may be of importance for the regulation of insulin sensitivity.
Diabetes 1992 Jun
PMID:Insulin can rapidly increase cell surface insulin binding capacity in rat adipocytes. A novel mechanism related to insulin sensitivity. 131 56

To investigate plasma renin and prorenin levels in non-insulin-dependent diabetes mellitus (NIDDM) and their relation with autonomic nervous function and renal impairment, we measured plasma renin and prorenin levels in 39 NIDDM patients. The patients included 21 males and 18 females, aged 56.3 +/- 6.2. Thirty-four normal age-matched subjects served as controls. Autonomic nervous function was evaluated in 23 patients by the performance of cardiovascular reflex tests. The plasma renin concentration was measured by angiotensin I generation after the addition of an exogenous substrate. Plasma prorenin was activated by trypsin. The results showed that the plasma renin concentration was similar between NIDDM patients and normal subjects, while plasma prorenin was higher in NIDDM patients. No correlation existed between the plasma renin or prorenin levels and autonomic nervous function. The patients with abnormally high levels of prorenin also had a similarly high plasma renin level but not a high creatinine clearance (Ccr) or daily proteinuria. The plasma renin level was correlated inversely with daily proteinuria but not with Ccr. These results suggest that the high plasma prorenin levels in some diabetic patients cannot be explained by renal impairment, poor prorenin conversion or autonomic dysfunction. The hyporeninemia in some patients may be related to microvascular involvement of the kidney.
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PMID:Plasma prorenin and renin levels in non-insulin-dependent diabetes mellitus. 136 16

In this series of studies, we have presented evidence for a novel, pancreatic islet-specific growth factor, which we call ilotropin. Ilotropin is acid stable, heat stable, ethanol-precipitable, and sensitive to trypsin digestion. It appears to have a molecular weight between 29 - 44,000, and preliminary data not presented here suggests that it has a relatively basic pI. Unlike many other growth factors, ilotropin does not bind to heparin. Ilotropin is distinguishable from most of the known growth factors on the basis of at least one of the characteristics established in these studies. The apparent molecular weight of 29 - 44,000 eliminates all but the larger growth factors such as PDGF and hepatic growth factor. The fact that ilotropin is acid stable rules out identity with hepatic growth factor, and its lack of binding to heparin and apparent basic pI rules out identity with PDGF. Thus, the combination of characteristics described in these studies eliminates most of the known growth factors as candidates for the role of ilotropin. Certain growth factor precursor molecules (e.g. TGF-a) and several interleukins and cytokines (e.g. pro-IL-1 and melanocyte growth factor) also fall into this molecular weight range. Whether these proteins might be related to ilotropin or play a role in its biological activity remains to be determined. Current studies of ilotropin include further purification to homogeneity, determination of the peptide sequence of ilotropin, and development of an in vitro bioassay using trophic responses of primary cultures of pancreatic duct cells as an indicator of ilotropin activity. With purified material we ought to be able to identify the cells of origin and the target cells for the action of ilotropin, and establish assays to determine the relationship to failure of beta-cell regeneration that accompanies diabetes. Ultimately we hope that ilotropin may lead to new ways of approaching aspects of the problems presented in pancreatic beta-cell failure.
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PMID:The partial isolation and characterization of ilotropin, a novel islet-specific growth factor. 144 77

Diabetes is accompanied by impaired platelet function and accelerated vascular disease. To find out whether a correlation exists between these two complications, and if modifications occurring in diabetic platelets influence their relationship with endothelium, we have studied the interaction between platelets isolated from plasma of diabetic patients and bovine valvular endothelial cells (VEC), in culture. For quantitative analysis, normal and diabetic [3H]-adenine-labeled platelets were incubated with confluent VEC grown in Dulbecco's modified Eagle medium, containing 4.5 g/l glucose, for 30 min at 37 degrees C. After extensive washing and solubilization of the monolayer, the calculated adhesion index showed a two-fold increased adherence of diabetic platelets to VEC as compared to normal platelets. Statistical analysis (by Pitman randomization test) indicated that the adhesion was significantly higher (p = 0.0003) than that of normal platelets to VEC. To partially identify the membrane components implicated in the adhesion process, either platelets or VEC were treated with neuraminidase, trypsin or heparinase prior to the adhesion assay. Trypsin or neuraminidase treatment of platelets significantly diminished their adherence to VEC, suggesting a role of platelets sialylated glycoproteins in the adhesion process. Neuraminidase or heparinase treatment of VEC increased the adhesion of both normal and diabetic platelets, indicating that the cell membrane sialyl residues and heparan sulfate participate in the normal thromboresistant properties of VEC. Transmission and scanning electron microscopy revealed a close apposition between platelets and VEC with the formation of an adhesion plaque, characterized by fine fibrillar bridges between the plasma membranes of the two cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased adhesion of human diabetic platelets to cultured valvular endothelial cells. 145 40

Qualitative disorders of an echopancreatogram are noted in half of patients with diabetes mellitus (both insulin dependent and noninsulin dependent). The most significant echopancreatographic quantitative and qualitative disorders were observed in diabetic patients with a maximal decrease in pancreatic enzyme excreting activity (on the basis of lipase and trypsin debit in a pancreozymin test, daily steatorrhea and chymotrypsin amount in daily feces). It has been assumed that a degree of ultrasound changes in the pancreas in diabetes depends on a degree of fibrosis of pancreatic exocrine tissue. Ultrasound investigations with quantitative and qualitative assessment of echopancreatograms is a valuable adjuvant diagnostic method in diabetes mellitus.
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PMID:[Echostructure of the pancreas. Comparison with exocrine secretory activity of the pancreas in patients with diabetes mellitus]. 151 83

Rat liver microsomes contain type-1 S6 phosphatase (acting on the serine residues phosphorylated by protein kinase A) and type-1 phosphorylase phosphatase activities. The main aim of this study has been to characterize the microsomal S6 phosphatase activity and to compare its properties with those of the phosphorylase phosphatase activity in the same microsomal preparation. The specific activities of both microsomal S6 phosphatase and phosphorylase phosphatase were 1.6- to 1.7-fold higher in the smooth endoplasmic reticulum than in the rough sarcoplasmic reticulum. Both phosphatase activities were inhibited to a similar extent by MgCl2 (10 mM) and NaF (22 mM), were completely suppressed by glycerophosphate (80 mM) and ZnCl2(10 mM), and were stimulated by MnCl2(1 mM). When analyzed by gel filtration on Sephadex G-100 superfine, both phosphatase activities eluted as broad peaks, stretching from the void volume to 45-60 kDa. The microsomal S6 phosphatase and phosphorylase phosphatase activities also displayed the following distinct characteristics: (a) Mn2+ stimulated the S6 phosphatase activity 2.9-fold more than the phosphorylase phosphatase activity, (b) limited trypsin digestion of microsomal preparations increased the phosphorylase phosphatase activity by 1.5- to 2-fold, but decreased the S6 phosphatase activity by 50%, (c) a synthetic peptide analog of S6 (S6229-239) (200 microM), which did not act as a substrate for the microsomal S6 phosphatase and did not affect its activity, inhibited the microsomal phosphorylase phosphatase activity by about 50%, and (d) the elution profile of the phosphorylase phosphatase activity was markedly broader than that of the S6 phosphatase activity. A series of in vivo studies showed that streptozotocin-diabetes and insulin replacement therapy as well as ip injection of insulin or vanadate, which modified the microsomal S6 phosphatase activity, had no statistically significant effects on the microsomal phosphorylase phosphatase activity. Taken together, these results suggest that the microsomal S6 phosphatase and phosphorylase phosphatase activities are due to two distinct enzyme populations.
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PMID:A comparative study of the microsomal S6 phosphatase and phosphorylase phosphatase activities in rat liver. 165 55


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