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Biomedical subjects

D B Goodman

Publications and source records attributed to D B Goodman.

At least 91 records · Page 5Linked to original sources
PubMed1981

Effect of 25-hydroxyvitamin D3 on vitamin D metabolites in primary biliary cirrhosis.

The osteopenic bone disease associated with primary biliary cirrhosis is thought to be de to a deficiency in vitamin D or its metabolites. However, this has never been proven. Therefore, we measured serum levels of 25-hydroxyvitamin D3 (25-OHD3), 1,25-dihydroxyvitamin D (1,25(OD)2D), and 24,25-dihydroxyvitamin D3 (24,25(OH)2D3), before and after a 1 yr treatment with oral 25,OHD3, in 10 patients with primary biliary cirrhosis selected because of documented osteopenic bone disease. Only in 1 patient was the pretreatment serum 25-OHD3 level below normal, less than 4.4 ng/ml. In 8 patients the serum 25,OHD3 level was in the low normal range and in one, was above normal. Serum levels of 1,25(OH)2D, the vitamin D metabolite with the greatest stimulatory effect on intestinal calcium absorption, were normal in 9 patients and elevated in 1. In contrast, serum levels of 24,25-(OH)2D3, a metabolite whose function is not known with certainty, were undetectable in 8 patients, low normal in a ninth, and normal in 1 patient who had been on large amounts of vitamin D2 (50,000 U b.i.w.,) before the start of the study. After 1 yr of treatment with oral 25-OHD3, serum 25-OHD3 rose to above normal in 9 patients. Serum 1,25-(OH)2D levels did not change significantly, while 24,25-(OH)2D3 rose to normal levels or higher in 9 of 10 patients. The bone disease of primary biliary cirrhosis is not due to 25-hydroxyvitamin D deficiency alone and is certainly not due to a deficiency of 1,25-(OH)2D as has been postulated. It may be related to low blood levels of 24,25-(OH)2D3 or to other as yet undefined factors.

24,25-Dihydroxyvitamin D 3↗
PubMed1980

Somatostatin: occurrence in urinary bladder epithelium and renal tubules of the toad, Bufo marinus.

Immunohistochemical techniques were used to detect immunoreactive somatostatin-like material in toad urinary bladder epithelium and in kidney distal tubules and collecting ducts. This material has immunological and chromatographic properties identical to those of synthetic cyclic somatostatin. The occurrence of somatostatin-like material in antidiuretic hormone-sensitive portions of the renal urinary system suggests a local regulatory or paracrine role for somatostatin.

Animals↗
PubMed1980

Selective stimulation of erythrocyte membrane phospholipid fatty acid turnover associated with decreased cell volume.

Treatment of erythrocytes with the divalent cation ionophore A23187 results in net uptake of calcium and a calcium-dependent decrease in cellular potassium content and cell volume. These changes in membrane properties are associated with a selective stimulation of fatty acid incorporation into membrane phosphatidylethanolamine (PE). In this study the relationship between this selective stimulation of phospholipid fatty acid turnover and changes in calcium uptake, cellular potassium content, and cell volume has been examined by 1) preventing the calcium-dependent loss of potassium without abolishing calcium uptake and 2) altering cellular potassium content and cell volume without increasing net uptake of calcium by utilizing the monovalent cation inonophore nigericin or increasing the osmolarity of the buffer. It has been shown that treatment of erythrocytes with A23187, nigericin, or hypertonic buffer results in a selective stimulation of fatty acid incorporation into PE. These results suggest that a mechanical or conformational change in the membrane is associated with a selective stimulation of fatty acid turnover in phosphatidylethanolamine.

Biological Transport, Active↗
PubMed1980

Glyoxylate cycle in toad urinary bladder: possible stimulation by aldosterone.

A homogenate of the toad urinary bladder epithelial cell layer has the two enzymatic activities unique to the glyoxylate cycle--isocitrate lyase (threo-Ds-isocitrate glyoxylate-lyase, EC 4.1.3.1) and malate synthase [L-malate glyoxylate-lyase (CA-acetylating), EC 4.1.3.2]--as well as the capacity to carry out CN-insensitive palmitoyl-CoA oxidation. When tissue is incubated in the presence of a fatty acid substrate, tissue glycogen levels increase. Additionally, in the presence of aldosterone, glycogen levels are higher. These data demonstrate the presence of glyoxylate cycle enzymes in tissue of a higher animal and raise the possibility that such tissue can convert lipid to carbohydrate.

Aldosterone↗
PubMed1980

Somatostatin: an endogenous peptide in the toad urinary bladder inhibits vasopressin-stimulated water flow.

Somatostatin (somatotropin release-inhibiting factor; SRIF) is a tetradecapeptide present in brain, pancreas, gastrointestinal tract, and thyroid that inhibits the secretion or action of several hormones in these tissues. We observed that the toad urinary bladder contains concentrations of endogenous somatostatin (8.0 pg/micrograms of protein) comparable to those found in the mammalian pancreas and gastrointestinal tract. To determine if somatostatin directly alter the action of vasopressinn we studied the effects of this polypeptide on vasopressin-stimulated transport processes in the toad urinary bladder in vitro. Somatostatin produced a dose-dependent, reversible inhibition of vasopressin-stimulated osmotic water flow; it inhibited theophylline-stimulated osmotic water flow but not the water flow stimulated by 8-p-chlorophenylthioadenosine 3',5'-cyclic monophosphate. These data are consistent with an inhibition of both basal and hormone-stimulated adenylate cyclase. Vasopressin-stimulated short circuit current was not inhibited by somatostatin. These studies provide direct evidence for an effect of somatostatin on hormone-modulated epithelial transport in tissues other than the gastrointestinal tract. We propose that endogenous somatostatin may function as a local regulator of the cellular action of vasopressin on osmotic water flow.

Animals↗
PubMed1980

Definition of the pathway for membrane phospholipid fatty acid turnover in human erythrocytes.

Techniques have been developed to permit detection of acyl thioesters derived from exogenous fatty acids in erythrocytes. These acyl thioesters have been shown to act as intermediates in the acylation of endogenous lysophospholipid. Release of fatty acids from erythrocyte phospholipids has also been detected. Such release reflect the activity of an endogenous phospholipase that utilizes endogenous phospholipid as substrate. These observations permit further definition of the biochemical pathway for erythrocyte phospholipid fatty acid turnover.

Chemical Phenomena↗
PubMed1979

Inhibition of fatty acid synthesis prevents the incorporation of aldosterone-induced proteins into membranes.

2-Methyl-2-[p-(1,2,3,4-tetrahydro-1-naphthyl)phenoxy]propionic acid (TPIA), an acetyl coenzyme A carboxylase inhibitor, blocks the aldosterone-induced increase in transepithelial sodium transport. To examine the requirement for ongoing fatty acid synthesis and/or elongation in the aldosterone-induced alteration of cellular protein metabolism in the toad's urinary bladder, the effect of TPIA has been examined in double-labeled amino acid incorporation experiments. TPIA itself has no effect on the pattern of protein labeling in either the "soluble" or a plasma membrane-enriched fraction. However, inhibition of fatty acid synthesis selectively inhibits the aldosterone-induced incorporation of membrane proteins without altering the labeling of soluble cell protein. These results indicate that ongoing fatty acid synthesis is required for the hormone-induced changes in plasma membrane protein metabolism.

Aldosterone↗
PubMed1979

Skeletal muscle calcium metabolism and contractile force in vitamin D-deficient chicks.

The myopathy associated with vitamin D deficiency has not been well characterized, and it is not known if weakness is a result of a specific effect of vitamin D deficiency on skeletal muscle. Chicks were raised from hatching on a vitamin D-deficient diet, and by 3 wk of age were hypocalcemic and appeared weak. Tension generated by triceps surae during repetitive stimulation of posterior tibial nerve was significantly less than that developed by chicks given vitamin D(3) supplements (309 g tension/g wet weight of triceps surae, SD 60, for vitamin D-deficient chicks; 470, SD 77, for vitamin D(3)-treated chicks, P < 0.01). Histochemical and electron microscopic examination of skeletal muscles of these chicks showed no abnormalities, and there were no electrophysiologic evidences of motor nerve or neuromuscular junction dysfunction. The concentration of ATP in skeletal muscle of the vitamin D-deficient chicks (5.75 mumol/g wet weight, SD 0.17) was not significantly different from that in vitamin D-treated chicks (5.60, SD 0.50). There was no correlation between strength and serum calcium, serum inorganic phosphate, or skeletal muscle inorganic phosphate. Relaxation of tension after tetanic stimulation was slowed in the vitamin D-deficient chicks (20.6 ms, SD 1.7, vs. 15.4, SD 1.3, in vitamin D-treated chicks and 15.3, SD 1.0, in normal control chicks), and in vitro (45)Ca(++) transport by sarcoplasmic reticulum from the vitamin D-deficient chicks was reduced. Calcium content of mitochondria prepared from leg muscles of vitamin D-deficient chicks (24 nmol/mg mitochondrial protein, SD 6) was considerably lower than that of mitochondria from normal control chicks (45, SD 8) or from chicks treated with vitamin D for 2 wk or more (66-100, depending upon level and duration of therapy). Treatment of the vitamin D-deficient chicks from hatching with sufficient dietary calcium to produce hypercalcemia did not significantly raise skeletal muscle mitochondrial calcium content (31 nmol/mg mitochondrial protein, SD 7) and did not prevent weakness. These studies demonstrate objective weakness as a result of myopathy in vitamin D-deficient chicks, and provide evidence that vitamin D deficiency has effects on skeletal muscle calcium metabolism not secondary to altered plasma concentrations of calcium and phosphate.

Animals↗
PubMed1978

Purification and characterization of chick intestine brush border membrane. Effects of 1alpha(OH) vitamin D3 treatment.

A new technique has been developed for the isolation of membrane vesicles from the vitamin D-deficient and vitamin D-treated chick intestinal brush border membrane. The technique involves removal of nuclei from a low speed pellet by discontinuous sucrose gradient centrifugation. The resulting intact brush borders are then homogenized in 0.5 M Tris and the membrane fragments purified on a glycerol gradient. This preparation represents a 20-fold purification of the brush border marker sucrase. After 1alpha-hydroxyvitamin D3 treatment there is a significant increase in membrane phospholipid phosphorous, an alteration in the fatty acid composition of the phosphatidylcholine fraction of membrane phospholipid, and a decrease in sucrase specific activity.

Animals↗
PubMed1978

Ionic and metabolic requirements for the hydroosmotic response to antidiuretic hormone in toad urinary bladder.

A study has been conducted to determine the ionic and metabolic requirements for full expression of the hydroosmotic response to antidiuretic hormone in the toad urinary bladder. By appropriate manipulation of incubation conditions it can be shown that there is a pool of serosal sodium necessary for a full hormone response. This serosal sodium pool is not related to the transepithelial sodium transport pool A full hydroosmotic response also requires serosal potassium; however, no specific anion requirement was demonstrated. Additionally, anaerobic or aerobic metabolism support a full hydroosmotic response equally well.

Animals↗
PubMed1978

Synthesis and characterization of 2-nitro-5-aziodobenzoylglycyloxytocin, an oxytocin photoaffinity label.

The oxytocin analogue, 2-nitro-5-azidobenzoylglycyloxytocin (NAB-Gly-oxytocin), has been synthesized and purified. The analogue is a full agonist for the stimulation of osmotic water flow in the toad urinary bladder (one-half maximal activity at 3.2 X 10(-6)M). It also enhances [14C]urea permeability in this tissue. Repetitive photolysis in the presence of NAB-Gly-oxytocin (8 X 10(-6)M) results in a progressive permanent inhibition of oxytocin stimulated urea permeability but does not alter hormone induced 3H2O movement. The inhibition is dependent on the photogeneration of the aryl nitrene intermediate and is relieved by protecting the hormone receptor with excess oxytocin (10(-6)M) during the photolysis. These results suggest that the photodependent permanent inhibition of the response to oxytocin in the toad bladder is due to covalent incorporation of the photoaffinity label, NAB-Gly-oxytocin, into the hormone receptor.

Affinity Labels↗
PubMed1978

Photoaffinity labeling of the antidiuretic hormone receptor.

A study to determine the feasibility of photoaffinity labeling the antidiuretic hormone receptor in the toad urinary bladder has been carried out. Two photoactivated derivatives of oxytocin have been synthesized, purified, and characterized chemically and biologically. Photolysis of the toad bladder in the presence of one of these derivatives, 2-nitro-5-azidobenzoylglycyloxytocin, produces a permanent inhibition of the response to native oxytocin. This inhibition can be relieved by protecting the hormone receptor with excess oxytocin during the photolysis. These results suggest that the photolysis-dependent inhibition of the response to native hormone is due to covalent incorporation of the photoaffinity label into the hormone receptor.

Affinity Labels↗
PubMed1978

The effects cytochalasin B on the surface morphology of the toad urinary bladder epithelium: a scanning electron microscopic study.

Cytochalasin B depresses the hydroosmotic response of the toad urinary bladder to vasopressin without affecting basal (bulk flow) permeability, diffusional permeability, or the hormone induced increase in short circuit current. Fine structural studies demonstrated that this macrolide fungal metabolite, in the presence of both an osmotic gradient and vasopressin, induces the formation of large intracellular vacuoles or 'lakes' in epitelial cells lining the bladder mucosa. Some surface changes (shortening and irregularity of microvilli, clumping of the glycocalyx, etc.) were reported by transmission electron microscopy. Scanning electron microscopy demonstrates that cytochalasin B drastically alters the mucosal surface morphology of the hormone stimulated bladder. Lesser changes were seen in the absence of vasopressin. In the presence of arginine vasopressin, excessive cellular swelling and possible rupturing, as well as surface membrane infolding and rippling, were seen in the cytochalasin treated tissues, The specific entity most affected by this treatment is the granular cell.

Animals↗