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Biomedical subjects

N G Baranetsky

Publications and source records attributed to N G Baranetsky.

14 recordsLinked to original sources
PubMed1988

The effects of human insulin on antibody formation in pregnant diabetics and their newborns.

We studied the immunogenicity of human insulin in 11 diabetic mothers and their newborns. Serum antibody formation was assayed by two different methods. Upon switching four patients from beef/pork insulin to human insulin, we found that elevated baseline antibody levels in three women decreased, in two to undetectable levels at term. The fourth patient had undetectable antibody levels at baseline and borderline levels at term. Only one of their four newborns had antibodies. Upon initiation of insulin treatment in another five diabetics without detectable antibodies at baseline, only two developed antibodies, and only one of their newborns developed antibodies. Two other patients, initially not on insulin, had baseline elevations of antibody that decreased with administration of human insulin; both of their newborns had antibodies. Overt diabetes evolved subsequently in both mothers after pregnancy. We conclude the following: 1) Upon transfer from beef/pork insulin to human insulin, mothers and their newborns show a decrease in insulin antibodies; 2) new patients initiated on insulin develop low levels of antibodies, if any, and their newborns also have low levels of antibodies if any; and 3) the decreased or absent immunogenicity of human insulin supports its use in pregnant diabetics.

Adolescent↗
PubMed1987

Effects of vitamin A deficiency and repletion on rat insulin secretion in vivo and in vitro from isolated islets.

We studied the effects of vitamin A deficiency and repletion on rat insulin release and islet cellular retinol binding protein (CRBP) and cellular retinoic acid binding protein (CRABP). Biphasic insulin release from vitamin A-deficient perifused islets was markedly impaired. Release remained impaired with retinoic acid (RA) repletion, 2 micrograms/g diet compared to release from islets of rats repleted with retinol in the form of retinyl palmitate, 4 micrograms/g diet. Release normalized with RA, 8 micrograms/g diet. Vitamin A deficiency did not affect islet insulin content, cell size, number or structure. In vivo, vitamin A-deficient rats had impaired glucose-induced acute insulin release and glucose intolerance, which improved with repletion. Normal islets had greater concentrations of CRBP than CRABP; vitamin A deficiency reduced CRBP but not CRABP levels. We conclude retinol is required for normal insulin secretion. Retinoic acid may substitute for retinol in this function.

Animals↗
PubMed1986

Renal hypophosphatemic osteomalacia unmasked by hyperthyroidism.

A case of renal hypophosphatemic osteomalacia (RHO) that was unmasked by hyperthyroidism is presented. The patient presented at age 64 with pathologic leg fractures. There was no family history of osteomalacia or rickets. Initial evaluation revealed hyperthyroidism, which was treated with radioactive iodine. Despite control of thyroid function, the patient had recurrent pathologic fractures. Further evaluation revealed histologically proven osteomalacia and the biochemical findings of RHO: elevated serum alkaline phosphatase, decreased serum phosphate and tubular resorption of phosphate, and normal serum calcium, parathyroid hormone, and vitamin D levels. Other causes of osteomalacia were excluded. Treatment with phosphate and calcitriol reversed the osteomalacia. This case demonstrates that hyperthyroidism, and possibly other illnesses that affect vitamin D or bone metabolism, may unmask metabolic bone disease and that physicians should be alert for the subtle clinical and biochemical indicators of unrecognized metabolic bone disease in adults.

Bone and Bones↗
PubMed1986

Islet insulin release and net calcium retention in vitro in vitamin D-deficient rats.

In our previous studies, perifused islets from vitamin D-deficient (D-def) rats showed marked impairment of glucose-induced biphasic release, accounted for at least in part by a decrease in food intake. In studies reported here, we test whether D-def rat islets have an impaired response to 5.6 mM glucose or tolbutamide, (T), and if so, whether this impairment is related to a decrease in food intake or a defect in islet calcium metabolism. We isolated islets of normal rats, D-def rats, and rats pair fed (PF) to D-def rats. Biphasic insulin release from perifused islets and net 45Ca retention in lot-incubated islets were measured in response to 5.6 mM glucose, 0.37 mM T, or both. Compared with secretion from normal islets, biphasic insulin release from islets of both D-def rats and PF rats was diminished by greater than 50% in response to 5.6 mM glucose alone or 5.6 mM glucose plus T. Insulin secretion was not significantly different between islets of D-def rats and islets of PF rats. In contrast, net calcium retention in islets of D-def rats was decreased to 68% of retention in islets of PF rats. However, net calcium retention in islets of both PF and D-def rats increased in response to T. The pair-feeding experiments suggest that the decrease in insulin release from islets of D-def rats is due to the decrease in food intake associated with the D-def state.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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↗
PubMed1980

Persistence of spermatogenesis in hypogonadotropic hypogonadism treated with testosterone.

The case histories are reported of two patients who had persistent spermatogenesis as evidenced by normal semen analyses and fertility in the face of hypogonadotropic hypogonadism and testosterone administration. When not receiving testosterone, both men consistently had normal or low serum gonadotropin levels. Since pooled serum testosterone levels were low simultaneously, these "normal" gonadotropin values are still consistent with hypogonadotropic hypogonadism. Standard testosterone replacement therapy maintained secondary sex characteristics and, surprisingly, spermatogenesis in both men. A review of the literature revealed conflicting evidence concerning the roles of gonadotropins and testosterone in affecting spermatogenesis. In applying this evidence to our patients, it appears that gonadotropins may have only a minimal role in maintaining fertility in patients with established spermatogenesis and "adequate" testosterone levels; it also appears that relatively low doses of exogenous testosterone may maintain or enhance spermatogenesis in certain individuals. We conclude that men with acquired hypogonadotropic hypogonadism should not be presumed to be sterile and that a larger study of fertility in these patients is necessary. Until then, we recommend that the semen of these patients be analyzed at the time of diagnosis and during treatment with testosterone.

Adult↗
PubMed1979

Adrenocorticotropin-dependent virilizing paraovarian tumors in Nelson's syndrome.

A 35-yr-old woman with Nelson's syndrome presented with amenorrhea and virilization. Serum testosterone (T) concentration was 605 ng/dl and fell to 33 ng/dl when dexamethasone was administered. The MCR of T fell from 1383 to 991 liters/day and the T production rate decreased by 96%. With administration of synthetic ACTH, T concentration rose to 338 ng/dl. Plasma ACTH concentration paralleled T during repeated suppression testing, suggesting that T secretion was dependent on ACTH hypersecretion. Preoperative and intraoperative ovarian vein catheterization suggested that the predominant source of androgen production was from the right ovarian vein. Laporatomy revealed multiple paraovarian tumors in the right mesosalpinyx and mesovarium. Incubation of tumor slices and ovarian tissue with [3H]pregnenolone and [14C]17-hydroxyprogesterone demonstrated conversion of both precursors to T by the tumor and confirmed that the tumors were the source of androgen excess. The microscopic appearance of the tumors closely resembled the morphology of testicular and paratesticular tumors of men with congenital adrenal hyperplasia and Nelson's syndrome. The analogous dependency of the tumors on ACTH hypersecretion in men with paratesticular tumors and in this woman with paraovarian tumors suggests that the tumors may arise in both males and females from a common steroid-secreting cell of adrenogenital origin.

Adrenocorticotropic Hormone↗