PubMed Health⌕ Search

Biomedical subjects

S Baba

Publications and source records attributed to S Baba.

At least 919 records · Page 51Linked to original sources
PubMed1984

Plasma levels of proinsulin, insulin and C-peptide in chronic renal, hepatic and muscular disorders.

Proinsulin, insulin and C-peptide levels were investigated in chronic renal, hepatic and muscular disorders. The proinsulin levels in human plasma were determined by radioimmunoassay using insulin-degrading enzyme (IDE). The fasting levels of proinsulin in 29 patients with chronic renal failure (0.95 +/- 0.05) were significantly higher than those in 10 patients with liver cirrhosis (0.46 +/- 0.04), six with muscular dystrophy (0.37 +/- 0.02) and 52 normal subjects (0.24 +/- 0.02 ng/ml, mean +/- S.E.). The fasting levels of insulin and C-peptide in chronic renal failure were also the highest among these groups. The insulin levels in liver cirrhosis and muscular dystrophy were significantly greater than those in normal subjects and increased molar ratios of proinsulin to total insulin immunoreactivity in chronic renal failure were observed. These results suggest that the kidney, liver and muscle are related to circulating insulin levels and that the kidney plays a particularly important role in circulating proinsulin levels. It can be concluded that increases in these peptides are due to a hypersecretion of B-cells, a decreased degradation or excretion.

C-Peptide↗
PubMed1984

Degradation of insulin by isolated mouse pancreatic acini. Evidence for cell surface protease activity.

In the present study, we have used isolated mouse pancreatic acini to investigate the relationship between 125I-insulin binding and its degradation in order to probe the nature and cellular localization of the degradative process. In these cells, the proteolysis of 125I-insulin was dependent on time and cell concentration, and was saturated by unlabeled insulin with a Km of 290 nM. Since this value was much higher than the Kd for insulin binding to its receptor (1.1 nM), the data indicated that 125I-insulin degradation by acini occurred primarily via nonreceptor mechanisms. Several lines of evidence suggested that insulin was being degraded by the neutral thiol protease, insulin degrading enzyme (IDE). First, insulin degradation was inhibited by thiolreacting agents such as N-ethylmaleimide and p-chloromercuribenzoate. Second, the Km for degradation in acini was similar to the reported Km for IDE in other tissues. Third, the enzyme activity had a relative mol wt of approximately 130,000 by gel filtration, a value similar to that reported for purified IDE. Fourth, the degrading activity was removed with a specific antibody to IDE. Other lines of evidence suggested that enzymes located on the cell surface played a role in insulin degradation by acini. First, the nonpenetrating sulfhydryl reacting agent 5,5' dithiobis-2-nitrobenzoic acid blocked 125I-insulin degradation. Second, a specific antibody to IDE identified the presence of the enzyme on the cell surface. Third, chloroquine, leupeptin and antipain, agents that inhibit lysosomal function, did not influence 125I-insulin degradation. Fourth, highly purified pancreatic plasma membranes degraded 125I-insulin.

Animals↗
PubMed1984

Degradation of insulin-like growth factors I and II by a human insulin degrading enzyme.

A human insulin degrading enzyme purified from IM-9 lymphocytes was tested for its ability to degrade insulin-like growth factor I (IGF-I) and insulin-like growth factor II (IGF-II). Degradation of these molecules was assessed by trichloroacetic acid precipitation, binding to specific receptors and chromatography on Sephadex G-50. All three techniques indicated that the enzyme readily degraded IGF-II and slightly degraded IGF-I. The IGF-II degrading activity chromatofocused with the insulin degrading activity and was absorbed by specific antibodies to the insulin degrading enzyme. These studies indicate, therefore, that a human insulin degrading enzyme can degrade IGF-II and, to a lesser extent, IGF-I.

Chemical Phenomena↗
PubMed1984

Disposition of suprofen in rats following intravenous injection.

Distribution and excretion of DL-2-(4-(2-thienylcarbonyl)phenyl)propionic acid (suprofen) were evaluated in male and female rats following intravenous (i.v.) injection of labeled suprofen. The radiometric findings following i.v. administration of 2 mg/kg of 3H-suprofen to male and female rats showed similar patterns of blood level and excretion of the radioactivity. Elimination of 3H-suprofen from the blood was rapid; most of the radioactivity was excreted in the urine and a portion in the feces within 24 h after injection. After rats with biliary fistulas were given an i.v. dose of 2 mg/kg of 3H-suprofen, approximately half of the dose was excreted in the bile during 48 h. The only tissues with concentrations higher than that in the plasma were those involved in metabolism and excretion (liver and kidney); other tissue levels were all very low and there was no evidence of accumulation of drug-related material in any tissue.

Animals↗
PubMed1984

Autoradiographic study on the distribution of suprofen in rats of both sexes.

The tissue distribution of 14C-labeled DL-2-(4-(2-thienylcarbonyl) phenyl) propionic acid (suprofen) after po administration was studied in male, female, and pregnant rats by whole-body autoradiography. 14C localized rapidly in such highly vascularized tissues as liver, kidney, and lung as well as heart in rats of both sexes, but no significant uptake was found in the central nervous system. About half of the 14C in the liver and kidney was found to be unchanged suprofen; smaller amounts of 2-(4-(2-thienylhydroxymethyl)phenyl)propionic acid and 2-(4-carboxyphenyl)propionic acid were also detected. In pregnant rats, a low level was found in the uterus and placenta; the drug penetrated the fetuses to only a limited degree. No appreciable radioactivity was found in rat tissues 24 h after dosing.

Administration, Oral↗
PubMed1984

Distribution of suprofen in rats of both sexes.

The tissue distribution of 3H-labeled DL-2-(4-(2-thienylcarbonyl) phenyl) propionic acid (suprofen) after po administration was studied in male, female, and pregnant rats by radiometry. The only tissues with concentrations comparable to plasma levels were those involved in metabolism and excretion (liver and kidney), except for the gastrointestinal tract, and all other tissue levels were very low. In pregnant rats, radioactivity crossed the blood-placenta barrier to a moderate extent and low concentrations were found in fetuses. Radioactivity disappeared from most tissues of male, female, and pregnant rats at rates similar to that from plasma and no appreciable radioactivity was found in rat tissues 24 h after dosing.

Administration, Oral↗
PubMed1984

A clinical evaluation of N-5' with perennial-type allergic rhinitis--a test by the multi-clinic, intergroup, double-blind comparative method.

N-(3,4-dimethoxycinnamoyl) anthranilic acid (N-5'), a new orally useable mast cell stabilizer, was investigated for its efficacy, safety and usefulness in the treatment of 302 patients with perennial nasal allergy by an intergroup, double-blind comparative test using disodium cromoglycate (DSCG) and an inactive placebo as control. The results indicated that N-5', as a mild mast cell stabilizer, was comparable to DSCG in efficacy and minimum in side effect.

Clinical Trials as Topic↗