22-02-2017, 12:33 AM
(21-02-2017, 10:24 PM)Lotus Wrote:(30-06-2015, 07:15 AM)Lotus Wrote: The bottom line is that vitamin D is a potent aromatase, this is most likely why you feel fullness.
(08-06-2015, 10:01 PM)Lotus Wrote: Vitamin D3 may indirectly affect cAMP production from PGE1 by 5x, in other words, this (D3) will help upregulate aromatase.
1,25DIHYDROXYCHOLECALCIFEROL INDUCES AN INCREASE IN PGE 1 - AND FORSKOLIN-STIMULATED CYCLICAMP PRODUCTION IN T47D HUMAN BREAST CANCER CELL LINE
ABSTRACT — The effect of 1, 25-dihydroxycholecalciferol [1, 25(OH)2 D3], the active form of vitamin D3, on cell growth, clonogenicity, and cyclic adenosine monophosphate (cAMP) production was examined in human breast cancer cell line T47D. 1,25(OH)2 D3 markedly inhibited proliferation of T47D cells in a time- and concentration-dependent manner. 1,25(OH)2 D3 5 times 10−7 reduced to 70% [3H]thymidine incorporation into DNA. Specific high affinity nuclear receptors for 1,25(OH)2 D3 were present in this cell line. The cAMP produced by T47D cells was measured during 10 min stimulation by effectors (prostaglandin E1 or forskolin). Without effector, T47D cells produced similar amounts of cAMP in control and 1,25(OH)2 D3-treated cells. After 3 days in the presence of 1,25(OH)2 D3, cAMP production was significantly increased compared to control cells when stimulated by 10−4 M prostaglandin E1 or 5 times 10−7 M forskolin (3.2- and 2.4-fold increase, respectively). This cAMP increase was concentration dependent within the same range that inhibited cell growth and clonogenicity. These results suggest that 1,25(OH)2 D3 may indirectly affect cAMP production by modulating the target cell response to stimulatory agents of cAMP production.
http://www.researchgate.net/publication/..._CELL_LINE
vitamin D analogs significantly upregulated E2- and DHT-induced CK response. These analogs upregulated the CK response to selective estrogen receptor modulators (SERMs). An estrogenic response (from vitamin D) is seen in the intestinal tract. Vitamin D also helps with hair growth.
http://www.howtomakeyourhairgrowfast.net...rowth.html
Interaction Between Estrogen and Vitamin D–Endocrine System: A Potential Addition to the Unitary Model of Osteoporosis
http://onlinelibrary.wiley.com/doi/10.13....1954/full
Vitamin D modulation of the activity of estrogenic compounds in bone cells in vitro and in vivo.
Somjen D1.
Author information
Abstract
Vitamin D analogs modulate different organs, including modulation of energy metabolism, through the induction of creatine kinase (CK) activity. Skeletal organs from vitamin D-depleted rats showed lower constituent CK than those from vitamin D-replete rats. Moreover, estradiol-17beta (E2) or dihydrotestosterone (DHT), which increased CK in organs from intact female or male rats, respectively, stimulated much less CK in vitamin D-depleted rats. Treatment of intact female rats with noncalcemic vitamin D analogs significantly upregulated E2- and DHT-induced CKresponse. These analogs upregulated the CK response to selective estrogen receptor modulators (SERMs) in organs from intact or ovariectomized (Ovx) female rats but abolished SERMs' inhibitory effect on E2-induced CK. These analogs significantly increased estradiol receptor alpha (ERalpha) protein in skeletal organs as well as histomorphological and biochemical changes due to this treatment followed by E2 or DHT. The analogs alone markedly altered the growth plate and the trabeculae and increased trabecular bone volume (%TB V) and trabecular width. The addition of E2 or DHT to this treatment restored all parameters as well as increased %TBV and cell proliferation. Treatment of Ovx female rats with JK 1624 F2-2 (JKF) decreased growth-plate width and increased %TB V, whereas QW1624 F2-2 (QW) restored growth-plate width and %TB V. Treatment of E2 with JKF restored %TBV and growth-plate width, whereas E2 with QW restored all parameters, including cortical width. There was also upregulation of the response of CK to E2 in both combined treatments. Our human-derived osteoblast (hObs)-like cell cultures respond to estrogenic compounds, and pretreating them with JKF upregulated the CK response to E2, raloxifene (Ral), and some phytoestrogens. ERalpha and ERbeta proteins, as well as mRNA, were modulated by CB 1093 (CB) and JKF. JKF increased specific nuclear E2 binding in female hObs but inhibited specific membranal E2 binding. hObs express 25 hydroxyvitamin D3-1alpha hydroxylase (1-OHase)-mRNA and its biological activity, which are both modulated by parathyroid hormone (PTH) and estrogenic compounds. Our results demonstrate mutual interaction between vitamin D and estrogenic compounds. We therefore conclude that combined treatment with less-calcemic analogs of vitamin D and estrogenic compounds might be superior for treatment of bone damage caused by ovariectomy in female rats, with possible application for postmenopausal osteoporosis.
PMID: 17725484 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/17725484
In addition:
Vitamin A modulates glucocorticoid synthesis, which has potential to lower visceral fat.....a good thing in my opinion (negates DHT). . Vitamin D potentiates lipogenesis....in other words (pro-aromatase)...especially in Pre-adipocytes.
Induction of fatty acid synthetase synthesis in differentiating 3T3-L1 preadipocytes.
Student AK, Hsu RY, Lane MD.
Abstract
3T3-L1 preadipocytes, cloned from 3T3 mouse embryo fibroblasts, differentiate in monolayer culture into cells with morphological and biochemical characteristics of adipocytes. Deposition of cytoplasmic triglyceride is associated with an increased lipogenic rate and a coordinate rise in the activities of many lipogenic enzymes (Mackall, J.C., Student, A.K., Polakis, S.E., and Lane, M.D. (1976) J. Biol. Chem. 251, 6462-6464). During differentiation induced by a 48-h treatment of postconfluent cells with methylisobutylxanthine, dexamethasone, and insulin, fatty acid synthetase activity increased to a level 19.5-fold higher than that of undifferentiated 3T3-L1 cells or nondifferentiating 3T3-C2 cells. The rate of [3H]leucine incorporation into immunoadsorbable fatty acid synthetase rose to a maximum and then declined to a new level 12.5-fold higher in differentiated than in undifferentiated 3T3-L1 cells. The kinetics of the changing [3H]leucine incorporation rate was reflected in the kinetics of the rise in fatty acid synthetase activity. The rate of degradation of fatty acid synthetase, determined by pulse-chase experiments, was unaffected by differentiation, the t1/2 remaining constant at 1.4 days. It is concluded that the higher level of fatty acid synthetase activity in differentiated 3T3-L1 cells can be attributed entirely to an increased rate of enzyme synthesis. The rate of total cellular protein synthesis also increases early early in differentiation, lending support to a model in which the synthesis of a large number of "differentiated proteins" is coordinately induced.
Complex Role of the Vitamin D Receptor and Its Ligand in Adipogenesis in 3T3-L1 Cells*
Abstract
The vitamin D receptor (VDR) and its ligand 1,25-OH2-VD3 (calcitriol) play an essential role in mineral homeostasis in mammals. Interestingly, the VDR is expressed very early in adipogenesis in 3T3-L1 cells, suggesting that the VDR signaling pathway may play a role in adipocyte biology and function. Indeed, it has been known for a number of years that calcitriol is a potent inhibitor of adipogenesis in this model but with no clear mechanism identified. In this study, we have further defined the molecular mechanism by which the unliganded VDR and calcitriol-liganded VDR regulate adipogenesis. In the presence of calcitriol, the VDR blocks adipogenesis by down-regulating both C/EBPβ mRNA expression and C/EBPβ nuclear protein levels at a critical stage of differentiation. In addition, calcitriol allows for the up-regulation of the recently described C/EBPβ corerepressor, ETO, which would further inhibit the action of any remaining C/EBPβ, whose action is required for adipogenesis. In contrast, in the absence of calcitriol, the unliganded VDR appears necessary for lipid accumulation, since knock-down of the VDR using siRNA both delays and prevents this process. Taken together, these data support the notion that the intracellular concentrations of calcitriol can play an important role in either promoting or inhibiting adipogenesis via the VDR and the transcriptional pathways that it targets. Further examination of this hypothesis in vivo may shed new light on the biology of adipogenesis.
