Search Results

You are looking at 1 - 3 of 3 items for

  • Author: G Andersson x
  • Refine by Access: All content x
Clear All Modify Search
Restricted access

L. van Neste, B. Husman, C. Möller, G. Andersson, and G. Norstedt


Parenchymal and non-parenchymal cell fractions isolated from rat liver were analysed for the distribution of somatogenic receptors and for insulin-like growth factor-I (IGF-I) mRNA. The effect of hypophysectomy either alone or in combination with a single injection of human GH (hGH) on the levels of IGF-I mRNA was also studied in the two cell fractions.

The contamination of parenchymal cells in the non-parenchymal cell fraction was in the range of 2– 3%. Somatogenic receptors were found only in the parenchymal cell fraction. IGF-I mRNA was detected in both cell fractions, although the level of this mRNA was about fivefold higher in parenchymal cells. When RNA was studied by Northern gel analysis no major differences were observed in the size distribution of IGF-I transcripts in the two cell fractions.

In hypophysectomized animals, the IGF-I mRNA level was decreased to 10 and 30% of control values in the parenchymal and non-parenchymal cell fractions respectively. Treatment of hypophysectomized animals with a single dose of hGH restored IGF-I mRNA in parenchymal and in non-parenchymal cells to the extent found in intact animals.

In conclusion, our data indicate that somatogenic receptors are exclusively, and IGF-I mRNA predominantly, expressed in liver parenchymal cells compared with a total non-parenchymal cell fraction. The most marked effect of GH, correlating with the presence of somatogenic receptors, was seen in the parenchymal cells. The minor non-GH dependent expression of IGF-I mRNA suggests that this peptide may elicit effects in addition to the well-established GH-dependent activity.

J. Endocr. (1988) 119, 69–74

Free access

MK Lindberg, Z Weihua, N Andersson, S Moverare, H Gao, O Vidal, M Erlandsson, S Windahl, G Andersson, DB Lubahn, H Carlsten, K Dahlman-Wright, JA Gustafsson, and C Ohlsson

Estrogen exerts a variety of important physiological effects, which have been suggested to be mediated via the two known estrogen receptors (ERs), alpha and beta. Three-month-old ovariectomized mice, lacking one or both of the two estrogen receptors, were given estrogen subcutaneously (2.3 micro g/mouse per day) and the effects on different estrogen-responsive parameters, including skeletal effects, were studied. We found that estrogen increased the cortical bone dimensions in both wild-type (WT) and double ER knockout (DERKO) mice. DNA microarray analysis was performed to characterize this effect on cortical bone and it identified four genes that were regulated by estrogen in both WT and DERKO mice. The effect of estrogen on cortical bone in DERKO mice might either be due to remaining ERalpha activity or represent an ERalpha/ERbeta-independent effect. Other effects of estrogen, such as increased trabecular bone mineral density, thymic atrophy, fat reduction and increased uterine weight, were mainly ERalpha mediated.

Free access

MK Lindberg, M Erlandsson, SL Alatalo, S Windahl, G Andersson, JM Halleen, H Carlsten, JA Gustafsson, and C Ohlsson

Estrogens are important for the male skeleton. Osteoprotegerin (OPG), receptor activator of NF-kappa B ligand (RANKL), interleukin-6 (IL-6), IL-1 and tumor necrosis factor alpha (TNFalpha) have been suggested to be involved in the skeletal effects of estrogen. We treated orchidectomized mice with estradiol for 2 weeks and observed a 143% increase in the trabecular bone mineral density of the distal metaphysis of femur that was associated with a decreased OPG/RANKL mRNA ratio in vertebral bone. A similar decreased OPG/RANKL ratio was also seen after estrogen treatment of ovariectomized female mice. The effect of estrogen receptor (ER) inactivation on the OPG/RANKL ratio was dissected by using intact male mice lacking ER alpha (ERKO), ER beta (BERKO) or both receptors (DERKO). The expression of OPG was increased in ERKO and DERKO but not in BERKO male mice, resulting in an increased OPG/RANKL ratio. Furthermore, serum levels of IL-6 and tartrate-resistant acid phosphatase 5b (TRAP 5b) were decreased in ERKO and DERKO, but not in BERKO male mice. These results demonstrate that ER alpha, but not ER beta, is involved in the regulation of the vertebral OPG/RANKL ratio, serum levels of IL-6 and TRAP 5b in male mice.