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Endocrinology. 2002 Nov;143(11):4203-9.
Time-dependent stimulation of insulin exocytosis by 3',5'-cyclic adenosine monophosphate in the rat islet beta-cell.

Yamada S, Komatsu M, Sato Y, Yamauchi K, Kojima I, Aizawa T, Hashizume K.

Department of Cell Biology, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, 371-8512, Japan.

Isolated rat islets were exposed to cAMP-elevating agents and/or nutrients. Insulin exocytosis subsequently triggered by a depolarizing concentration of K(+) or a stimulatory concentration of glucose was employed as an index of time-dependent potentiation (TDP). Stimulatory concentrations (>or=5.5 mM) of glucose caused TDP, and 6 micro M forskolin (an activator of adenylyl cyclase) significantly enhanced it (3.1-fold at most). Forskolin produced an 8.0-fold increase in islet cell cAMP; however, it returned to the baseline after washout by the time of stimulation of exocytosis. Two millimoles of dibutyryl cAMP (a cAMP analog), 0.1 mM isobutylmethylxanthine (a phosphodiesterase inhibitor), and 100 nM glucagon-like peptide-1 (an incretin hormone) also enhanced glucoseinduced TDP. The time-dependent effect of cAMP was not attenuated by protein kinase A inhibitors (200 micro M adenosine 3',5'-cyclic monophosphothioate, Rp isomer, and 10 micro M H89). Although glucose-induced TDP was attenuated by NaN(3) (a mitochondrial poison) and cerulenin (an inhibitor of protein acylation), cAMP enhancement of it was unaffected by these agents. In conclusion, cAMP time-dependently stimulates insulin exocytosis, provided the extracellular glucose concentration is equivalent to or higher than ambient plasma levels. Protein kinase A, mitochondrial metabolism, and protein acylation are not involved in this cAMP action. Incretin stimulation of insulin exocytosis may occur in part via this mechanism.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399413&dopt=Abstract

Endocrinology. 2002 Nov;143(11):4210-7.
3',5'-cyclic adenosine monophosphate augments intracellular Ca2+ concentration and gonadotropin-releasing hormone (GnRH) release in immortalized GnRH neurons in an Na+ -dependent manner.

Kaneishi K, Sakuma Y, Kobayashi H, Kato M.

Department of Physiology, Nippon Medical School, Tokyo 113-8602, Japan.

In GT1-7 cells, cAMP increases the intracellular Ca2+ concentration ([Ca2+](i)) through activation of the voltage-gated Ca2+ channels, thereby facilitating GnRH release. To activate these channels, the membrane potential must be depolarized. In the present study we hypothesize that cAMP depolarizes the cells by increasing the membrane Na+ permeability, as in the case of somatotrophs and pancreatic beta-cells. To examine this, we analyzed [Ca2+](i) and [Na+](i) in GT1-7 cells by an intracellular ion-imaging technique along with cAMP assay by RIA. Forskolin, a direct activator of adenylyl cyclase, increased [Ca2+](i) and [Na+](i) via cAMP formation. The forskolin-induced increase in [Ca2+](i) depended on the presence of Ca2+ and Na+ in the extracellular solution. This response was blocked by the voltage-gated Ca2+ channel blocker, nifedipine; the nonselective cation channel blocker, gadolinium (Gd3+); and the cyclic nucleotide-gated channel blocker, l-cis-diltiazem. In contrast, the forskolin-induced increase in [Na+](i) depended only on extracellular Na+, not on Ca2+. Gd3+ and l-cis-diltiazem also blocked the increase in [Na+](i). Furthermore, the forskolin-induced increase in GnRH release was blunted in both low Ca2+ and low Na+ media. The results indicate that cAMP increases the membrane Na+ permeability, probably through nonselective cation channels on GT1-7 cells, thereby promoting GnRH release.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399414&dopt=Abstract

Endocrinology. 2002 Nov;143(11):4243-8.
Prolonged retention after aggregation into secretory granules of human R183H-growth hormone (GH), a mutant that causes autosomal dominant GH deficiency type II.

Zhu YL, Conway-Campbell B, Waters MJ, Dannies PS.

Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.

Human R183H-GH causes autosomal dominant GH deficiency type II. Because we show here that the mutant hormone is fully bioactive, we have sought to locate an impairment in its progress through the secretory pathway as assessed by pulse chase experiments. Newly synthesized wild-type and R183H-GH were stable when expressed transiently in AtT20 cells, and both formed equivalent amounts of Lubrol-insoluble aggregates within 40 min after synthesis. There was no evidence for intermolecular disulfide bond formation in aggregates of wild-type hormone or the R183H mutant. Both wild-type and R183H-GH were packaged into secretory granules, assessed by the ability of 1 mM BaCl2 to stimulate release and by immunocytochemistry. The mutant differed from wild-type hormone in its retention in the cells after packaging into secretory granules; 50% more R183H-GH than wild-type aggregates were retained in AtT20 cells 120 min after synthesis, and stimulated release of R183H-GH or a mixture of R183H-GH and wild-type that had been retained in the cell was reduced. The longer retention of R183H-GH aggregates indicates that a single point mutation in a protein contained in secretory granules affects the rate of secretory granule release.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399418&dopt=Abstract

Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1999 Jan;122(1):115-20.
Effects of exposure to diethyl phthalate, 4-(tert)-octylphenol, and 2,4,5-trichlorobiphenyl on activity of chitobiase in the epidermis and hepatopancreas of the fiddler crab, Uca pugilator.

Zou E, Fingerman M.

Department of Ecology, Evolution, and Organismal Biology, Tulane University, New Orleans, LA 70118, USA.

Seven-day exposure of fiddler crabs, Uca pugilator, to diethyl phthalate at 50.0 mg l-1 significantly inhibited the activity of chitobiase (also known as N-acetyl-beta-glucosaminidase) in the epidermis and hepatopancreas. Epidermal chitobiase activity of crabs exposed to 10.0 mg l-1 4-(tert)-octylphenol for 7 days significantly decreased. PCB29 at 0.5 and 2.0 mg l-1 significantly inhibited chitobiase activity in the epidermis and hepatopancreas of crabs exposed for 3 days. The inhibitory effects rendered by diethyl phthalate and PCB29 can at least partly account for the delayed molting they cause because chitobiase is needed to break down the old exoskeleton of crustaceans prior to ecdysis. Since chitinolytic enzymes are apparently the products of ecdysteroid regulated genes in arthropods, the decline in chitobiase activity after exposure to diethyl phthalate, 4-(tert)-octylphenol, and PCB29 along with the delayed molting they cause strongly suggests that these xenobiotics disturb the Y-organ-ecdysteroid receptor axis. Such disturbance may involve an interaction between ecdysteroid receptors and steroid mimics where the steroid mimics act as antagonists of endogenous steroid molting hormones, and/or arise from the interference with synthesis and excretion of ecdysteroids by these compounds.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10190035&dopt=Abstract

Endocrinology. 2002 Nov;143(11):4281-6.
Two placental hormones are agonists in stimulating megakaryocyte growth and differentiation.

Zhou B, Lum HE, Lin J, Linzer DI.

Department of Biochemistry, Molecular Biology, and Cell Biology, Northwestern University, Evanston, Illinois 60208, USA.

Previously, we demonstrated that a placental hormone, PRL-like protein E, stimulates megakaryocyte growth and differentiation. We now find that PRL-like protein E and a second placental hormone, PRL-like protein F (PLP-F), bind the same receptor. PLP-F, which is produced later in pregnancy, might therefore act as either an agonist or antagonist of PRL-like protein E. To resolve this question, we produced recombinant PLP-F in mammalian cell cultures, purified the secreted glycoprotein hormone, and determined its activity in primary mouse bone marrow cultures. PLP-F induces megakaryocyte differentiation and megakaryocyte progenitor growth in a dose-dependent manner, with significant activity detected at a concentration as low as 50 ng/ml. PLP-F in maternal serum reaches at least 1 micro g/ml on gestational d 14.5, and thus the biological activity of PLP-F is detected at physiological concentrations. These results show that PRL-like proteins E and F have the same stimulatory effects on megakaryocyte growth and differentiation, and therefore represent gestation stage-specific agonists.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12399423&dopt=Abstract

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