Show simple item record

dc.contributor.authorSchwartz, Yael
dc.contributor.authorYamaguchi, Hiroshi
dc.contributor.authorGoodman, H. Maurice
dc.date2022-08-11T08:10:02.000
dc.date.accessioned2022-08-23T16:52:59Z
dc.date.available2022-08-23T16:52:59Z
dc.date.issued1992-08-01
dc.date.submitted2008-07-09
dc.identifier.citation<p>Endocrinology. 1992 Aug;131(2):772-8.</p>
dc.identifier.issn0013-7227 (Print)
dc.identifier.pmid1639023
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42172
dc.description.abstractAdipocytes that have been preincubated for 3 h or more in hormone-free medium respond to GH with a transient insulin-like increase in glucose metabolism, followed by a period of refractoriness to further insulin-like stimulation. Adipocytes freshly isolated from normal rats and adipocytes that were exposed to GH in the first hour of a 4-h incubation period are refractory to this insulin-like effect. Because earlier studies revealed a relationship between refractoriness and cellular calcium, we examined the effects of GH on the intracellular calcium concentration ([Ca2+]i) under a variety of conditions in which sensitivity to insulin-like stimulation or refractoriness is known to be affected. A dual nitrogen laser imaging microscope with computer-assisted image processing to measure fluorescence changes in individual adipocytes loaded with fura-2 AM was used to measure [Ca2+]i. After prolonged incubation in vitro, resting [Ca+2]i was 120 +/- 6 nM and remained unchanged for more than 1 h after the addition of 100 ng/ml human GH (hGH), which doubled the rate of incorporation of [3-3H] glucose into triglycerides in this interval. Lipogenesis declined in the second hour, and [Ca+2]i slowly increased, reaching 324 +/- 49 nM by the end of the third hour (P less than 0.05). When added with GH, actinomycin-D, an inhibitor of RNA synthesis, caused the accelerated rate of lipogenesis to persist for at least 5 h and blocked the delayed increase in resting [Ca+2]i. Resting [Ca2+]i in freshly isolated, and hence refractory, adipocytes was 342 +/- 34 nM and declined to 112 +/- 11 nM concomitant with acquisition of insulin-like sensitivity to GH. The addition of 100 ng/ml hGH to these cells at the beginning of incubation, under conditions known to sustain refractoriness prevented the decline in resting [Ca2+]i and enabled them to exhibit a further acute increase in [Ca2+]i in response to a second exposure to hGH in the fourth hour. When added 60 min after GH, actinomycin-D blocked the ability to raise [Ca2+]i acutely in response to GH, but did not interfere with GH's action to sustain resting [Ca2+]i, which remained at about 300 nM. The concentration of GH needed to increase [Ca2+]i acutely in refractory cells is about 6-fold higher than that needed to maintain resting [Ca+2]i. Differences in the time of sensitivity to actinomycin-D and dose dependency suggest that sustaining resting [Ca2+]i and production of the acute increase in [Ca2+]i are separate phenomena.(ABSTRACT TRUNCATED AT 400 WORDS)
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=1639023&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1210/endo.131.2.1639023
dc.subjectAdipose Tissue
dc.subjectAnimals
dc.subjectCalcium
dc.subject*Carbohydrate Metabolism
dc.subjectDactinomycin
dc.subjectEpididymis
dc.subjectFluorescent Dyes
dc.subjectFura-2
dc.subjectGrowth Hormone
dc.subjectImage Processing, Computer-Assisted
dc.subjectKinetics
dc.subjectMale
dc.subjectRats
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleGrowth hormone increases intracellular free calcium in rat adipocytes: correlation with actions on carbohydrate metabolism
dc.typeArticle
dc.source.journaltitleEndocrinology
dc.source.volume131
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/543
dc.identifier.contextkey545025
html.description.abstract<p>Adipocytes that have been preincubated for 3 h or more in hormone-free medium respond to GH with a transient insulin-like increase in glucose metabolism, followed by a period of refractoriness to further insulin-like stimulation. Adipocytes freshly isolated from normal rats and adipocytes that were exposed to GH in the first hour of a 4-h incubation period are refractory to this insulin-like effect. Because earlier studies revealed a relationship between refractoriness and cellular calcium, we examined the effects of GH on the intracellular calcium concentration ([Ca2+]i) under a variety of conditions in which sensitivity to insulin-like stimulation or refractoriness is known to be affected. A dual nitrogen laser imaging microscope with computer-assisted image processing to measure fluorescence changes in individual adipocytes loaded with fura-2 AM was used to measure [Ca2+]i. After prolonged incubation in vitro, resting [Ca+2]i was 120 +/- 6 nM and remained unchanged for more than 1 h after the addition of 100 ng/ml human GH (hGH), which doubled the rate of incorporation of [3-3H] glucose into triglycerides in this interval. Lipogenesis declined in the second hour, and [Ca+2]i slowly increased, reaching 324 +/- 49 nM by the end of the third hour (P less than 0.05). When added with GH, actinomycin-D, an inhibitor of RNA synthesis, caused the accelerated rate of lipogenesis to persist for at least 5 h and blocked the delayed increase in resting [Ca+2]i. Resting [Ca2+]i in freshly isolated, and hence refractory, adipocytes was 342 +/- 34 nM and declined to 112 +/- 11 nM concomitant with acquisition of insulin-like sensitivity to GH. The addition of 100 ng/ml hGH to these cells at the beginning of incubation, under conditions known to sustain refractoriness prevented the decline in resting [Ca2+]i and enabled them to exhibit a further acute increase in [Ca2+]i in response to a second exposure to hGH in the fourth hour. When added 60 min after GH, actinomycin-D blocked the ability to raise [Ca2+]i acutely in response to GH, but did not interfere with GH's action to sustain resting [Ca2+]i, which remained at about 300 nM. The concentration of GH needed to increase [Ca2+]i acutely in refractory cells is about 6-fold higher than that needed to maintain resting [Ca+2]i. Differences in the time of sensitivity to actinomycin-D and dose dependency suggest that sustaining resting [Ca2+]i and production of the acute increase in [Ca2+]i are separate phenomena.(ABSTRACT TRUNCATED AT 400 WORDS)</p>
dc.identifier.submissionpathoapubs/543
dc.contributor.departmentDepartment of Physiology
dc.source.pages772-8


This item appears in the following Collection(s)

Show simple item record