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Biomedical subjects

W I Sivitz

Publications and source records attributed to W I Sivitz.

43 records · Page 3Linked to original sources
PubMed1986

Combined phenytoin and salicylate effects on thyroid function tests.

To evaluate the effects of salicylates (ASA) on thyroid function tests (TFT's) in patients already taking phenytoin (DPH), 6 adults received a daily dose of DPH to achieve a steady state serum DPH. ASA was then added stepwise (325, 650, 975 mg q 4hr) at 2-day intervals. TFTs, total serum and free salivary DPH were measured. Therapeutic steady state phenytoin levels caused a significant decrease in serum free thyroxine (FT4), total T4, total T3 (TT3) and a significant but slight increase in T3RU. The TSH remained normal. When ASA was co-administered with DPH, the serum free DPH increased, the total T4, TT3, FT4 significantly decreased further, and the T3RU significantly declined toward pre-treatment levels. The decrease of FT4 was in contrast to the increase in FT4 known to occur with ASA alone. Despite the decline in total T4, TT3, and FT4, the TSH remained normal. In conclusion, when ASA is co-administered with DPH, further alterations in TFTs occur which require cautious interpretation. Our in vivo and in vitro data show that these changes are consistent with ASA-induced displacement of T4 from its binding proteins and DPH-induced clearance of FT4.

Aspirin↗
PubMed1983

Cellular mechanisms of insulin release: the effects of vitamin D deficiency and repletion on rat insulin secretion.

To determine whether impaired insulin release from perifused rat islets of vitamin D-deficient (D-def) rats is a result of vitamin D-deficiency specifically or an associated decrease in food intake, we: 1) compared insulin release from islets of vitamin D-def rats with insulin release from islets of pair fed (pf) normal rats, and 2) measured the effects of 1,25(OH)2D3 treatment on food intake and insulin secretion from islets of D-def rats. Both vitamin D-def and pf normal rat islets showed significantly diminished insulin release in comparison with normal controls but were not different from each other. When D-def rats were repleted with 1,25(OH)2D3, food intake increased and insulin secretion improved during perifusion of rat islets. When D-def rats treated with 1,25(OH)2D3 were prevented from increasing their food intake in response to 1,25(OH)2D3 by pair feeding to a group of untreated D-def rats, insulin release from islets of treated rats was not significantly different from untreated D-def rats. To separate the effects of vitamin D deficiency from hypocalcemia, a group of vitamin D-def hypocalcemic rats was compared with a group of D-def normocalcemic rats. Normocalcemia did not reverse the defect in insulin release. In studies of cellular calcium uptake, both pf and D-def rat islets took up less calcium than normal islets but calcium uptake was not different between pf and D-def rat islets. Our studies suggest that vitamin D deficiency is associated with marked impairment of biphasic insulin release and that the decrease in food intake may account for this impairment at least in part.

Animals↗
PubMed1983

Cellular mechanisms of insulin release. Effects of retinoids on rat islet cell-to-cell adhesion, reaggregation, and insulin release.

We studied the effects of retinoids on islet cell-to-cell adhesiveness and glucose-induced insulin release from rat islets. For adhesion studies, islets were dispersed using low concentrations of trypsin. Thirteen cis-retinoic acid (13 cis-RA) was added to a suspension of 15 X 10(5) islet cells and adhesion of cells was quantitated using a hemocytometer. For functional studies, we measured biphasic insulin release from collagenase-isolated perifused islets, dispersed cells, and single large aggregates (clumps) of islet cells. Thirteen cis-RA (10(-4) M) stimulated insulin secretion at 9.7, 12.5, 16.7, and 27.7 mM glucose. Maximal effects of 13 cis-RA (174% of control) were evident during second phase release at 9.7 mM glucose. Thirteen cis-RA (10(-7) and 10(-6) M) caused cells to adhere to each other, and at higher concentrations, 13 cis-RA caused dispersed cells to reaggregate into a single clump. These retinoid-induced clumps were perifused in a Bio-Gel P-2 gel column. Secretion from the clump was twofold greater than from an equal number of perifused dispersed cells. Electron microscopic and freeze-fracture examination of the clump showed reaggregated cells to be intact and the presence of gap junctions between cells. In conclusion, 13 cis-RA has marked effects on islet cell-to-cell adhesiveness. Trypsin-dispersed cells reaggregated by 13 cis-RA have anatomical contacts and secrete more insulin as an aggregate than as dispersed cells. Thirteen cis-RA increases insulin release possibly by increasing adhesion or interactions between beta-cells.

Animals↗
PubMed1982

Theophylline interferes with ligand binding in radioimmunoassays for somatostatin.

Theophylline is often utilized as a secretagogue in studies on the in vitro release of somatostatin and other hormones. We report here on the effect of theophylline on ligand binding in somatostatin radioimmunoassays performed with three different antisera. For all three radioimmunoassays, tracer binding both in the presence and absence of unlabelled somatostatin was inhibited by the addition of theophylline to the RIA reaction mixture. This effect occurred at final assay concentrations of theophylline which may likely be encountered when assaying samples obtained in studies of theophylline-induced hormone release in vitro. The possible interfering effect of theophylline in radioimmunoassays should be considered whenever theophylline is used as a tool to study hormone release.

Animals↗
PubMed1982

Vitamin A palmitate decreases intravenous glucose tolerance in man.

We tested retinyl palmitate for in vivo effects in man and in vitro effects on the IM-9 lymphocyte insulin receptor. Intravenous glucose tolerance tests (IVGTT) with 25 g glucose were performed on 10 healthy subjects before and after two intramuscular injections of retinyl palmitate (25,000 IU) 18 hours apart. In 9 of 10 subjects, glucose disposition was impaired after treatment with retinyl palmitate. In vitro, retinyl palmitate 10(-4) - 10(-6) M did not affect the binding or displacement of insulin 125I from lymphocyte receptors. We conclude that retinyl palmitate decreases glucose tolerance without demonstrable effects on insulin release or insulin binding to receptors.

Adult↗