{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T12:20:30Z","timestamp":1792412430312,"version":"4.4.0"},"reference-count":0,"publisher":"Oxford University Press (OUP)","issue":"2","content-domain":{"domain":["eje.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2010,2]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>GH replacement lowers total cholesterol and low-density lipoprotein cholesterol (LDL-C) in GH-deficient adults, but effects on high-density lipoprotein (HDL) cholesterol (HDL-C) are variable. Both GH and glucocorticoids decrease cholesteryl ester transfer protein (CETP) activity, which is important in HDL metabolism. We determined the extent to which the changes in HDL-C in response to GH replacement are predicted by the \u2212629C&gt;A <jats:italic>CETP<\/jats:italic> promoter polymorphism, and questioned whether this association is modified by concomitant glucocorticoid treatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Design and methods<\/jats:title><jats:p>A total of 91 GH-deficient adults (63 receiving glucocorticoids) were genotyped for the \u2212629 <jats:italic>CETP<\/jats:italic> C&gt;A polymorphism. Fasting serum lipids were measured before and after 1.2\u00b10.4 years of GH treatment (Genotropin, Pfizer Inc., Stockholm, Sweden).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In the whole group, total cholesterol and LDL-C decreased (<jats:italic>P<\/jats:italic>&lt;0.05) after GH treatment, but the changes in HDL-C were not significant. In CC carriers receiving glucocorticoids (<jats:italic>n<\/jats:italic>=19), HDL-C rose by 0.15\u00b10.25\u200ammol\/l (<jats:italic>P<\/jats:italic>=0.02; <jats:italic>P<\/jats:italic>&lt;0.03 from unchanged HDL-C in \u2212629 AA+CA carriers on glucocorticoids and from CC homozygotes not receiving glucocorticoids). Multivariate regression analysis showed that individual changes in HDL-C were predicted by the <jats:italic>CETP<\/jats:italic> polymorphism (CC versus AA+CC, <jats:italic>P<\/jats:italic>=0.006) in glucocorticoid users, independently of baseline HDL-C and other variables including <jats:italic>apolipoprotein E4<\/jats:italic> carrier status; an opposite association with the <jats:italic>CETP<\/jats:italic> polymorphism was found in patients not receiving glucocorticoids (<jats:italic>P<\/jats:italic>=0.053).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>We suggest a common <jats:italic>CETP<\/jats:italic> variant-glucocorticoid treatment interaction concerning the effect of GH replacement on HDL-C. This may explain some of the reported variation in the HDL-C response to GH.<\/jats:p><\/jats:sec>","DOI":"10.1530\/eje-09-0742","type":"journal-article","created":{"date-parts":[[2009,11,20]],"date-time":"2009-11-20T03:05:53Z","timestamp":1258686353000},"page":"227-234","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":3,"title":["HDL cholesterol response to GH replacement is associated with common cholesteryl ester transfer protein gene variation (\u2212629C&gt;A) and modified by glucocorticoid treatment"],"prefix":"10.1093","volume":"162","author":[{"given":"Robin P F","family":"Dullaart","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerrit","family":"van den Berg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aafke M","family":"van der Knaap","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janneke","family":"Dijck-Brouwer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Geesje M","family":"Dallinga-Thie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter M J","family":"Zelissen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wim J","family":"Sluiter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andr\u00e9 P","family":"van Beek","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","container-title":["European Journal of Endocrinology"],"original-title":[],"link":[{"URL":"https:\/\/eje.bioscientifica.com\/view\/journals\/eje\/162\/2\/227.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/eje.bioscientifica.com\/view\/journals\/eje\/162\/2\/227.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,2,14]],"date-time":"2023-02-14T16:24:11Z","timestamp":1676391851000},"score":1,"resource":{"primary":{"URL":"https:\/\/academic.oup.com\/ejendo\/article\/162\/2\/227\/6676699"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2010,2]]},"references-count":0,"journal-issue":{"issue":"2"},"URL":"https:\/\/doi.org\/10.1530\/eje-09-0742","relation":{},"ISSN":["0804-4643","1479-683X"],"issn-type":[{"value":"0804-4643","type":"print"},{"value":"1479-683X","type":"electronic"}],"subject":[],"published":{"date-parts":[[2010,2]]}}}