Consequences of limited exposure to elevated growth hormone in the mature oMt1a-oGH transgenic mouse

Citation
Am. Oberbauer et Jd. Murray, Consequences of limited exposure to elevated growth hormone in the mature oMt1a-oGH transgenic mouse, GROW DEV AG, 62(3), 1998, pp. 87-93
Citations number
31
Categorie Soggetti
Medical Research General Topics
Journal title
GROWTH DEVELOPMENT AND AGING
ISSN journal
10411232 → ACNP
Volume
62
Issue
3
Year of publication
1998
Pages
87 - 93
Database
ISI
SICI code
1041-1232(199823)62:3<87:COLETE>2.0.ZU;2-H
Abstract
Male and female transgenic mice carrying the regulatable ovine metallothion ein-ovine growth hormone (oMt1a-oGH) transgene were exogenously induced to express elevated GH at maturity. Male transgenics responded to continuously elevated GH with smaller white adipose tissue depots (WAT); cessation of t ransgene stimulation with restoration of basal circulating GH ablated the i mprovement in WAT. Transgenic males in which the transgene was never exogen ously activated expressed low levels of oGH (60.2 ng/ml) and this low, chro nic level resulted in 30-50% larger (p<0.05) gonadal, inguinal, and mesente ric WAT relative to all wildtype controls, transgenics actively expressing the transgene, or transgenics exposed to elevated GH for a limited time. Ma ture females continued to accrue body mass proportional to circulating CH. Similar to that observed in the males, transgenic females in which the tran sgene was never exogenously activated exhibited enlarged WAT that were 20-4 0% larger than the same depots in wildtype control females. However, in con trast to the data for the males, transgenic females that had experienced a four week exposure to elevated GH followed by a return to basal conditions tended to have the greatest WAT depots (p<0.10). This would indicate that f emale adipocytes are still capable of responding to elevated GH with prolif eration/differentiation at maturity. These data support the hypothesis that the generalized sexual dimorphic pattern of lipid deposition may be attrib uted to the sexually dimorphic pattern of GH experienced by the two sexes.