Enhanced Effects of 1,25(OH)2D3 Plus Genistein on Adipogenesis and Apoptosis in 3T3‐L1 Adipocytes

Obesity - Tập 16 Số 3 - Trang 539-546 - 2008
Srujana Rayalam1, Mary Anne Della‐Fera1, Suresh Ambati1, Jeong‐Yeh Yang1, Hea Jin Park1, Clifton A. Baile1,2
1Department of Animal and Dairy Science, University of Georgia, Athens, Georgia, USA
2Department of Foods and Nutrition, University of Georgia, Athens, Georgia, USA

Tóm tắt

Objective: To investigate the ability of 1,25(OH)2D3 (D) and genistein (G), alone and in combination, to inhibit adipogenesis and induce apoptosis in 3T3‐L1 adipocytes.Methods and Procedures: 3T3‐L1 preadipocytes and mature adipocytes were incubated with various concentrations of D and G, alone and in combination, for 48 h. Viability was determined using the Cell Titer 96 Aqueous One Solution Cell Proliferation Assay. Post‐confluent preadipocytes were incubated with D and G for up to 6 days during adipogenesis and lipid content was quantified by Nile Red dye; apoptosis was quantified by measurement of single‐stranded DNA. Expression of adipocyte‐specific proteins and VDR was analyzed by western blotting.Results: Combining D and G did not cause an enhanced effect on cell viability in either preadipocytes or mature adipocytes. In maturing preadipocytes, D at 0.5 nmol/l (D0.5) increased apoptosis by 47 ± 10.25% (P < 0.05) and inhibited lipid accumulation by 28 ± 10% (P < 0.001), while G at 25 μmol/l (G25) had no significant effect. However, D+G caused an enhanced apoptosis by 136 ± 12.6% (P < 0.001) and enhanced inhibition of lipid accumulation by 82.46 ± 2.95% (P < 0.001). Similarly, D0.5 alone decreased adipose‐specific gene 422 (aP2) expression to 34.2 ± 2.3% and increased VDR expression levels by 41.8 ± 11% (P < 0.001), but G25 showed no effect. However, D0.5+G25 decreased aP2 expression to 52 ± 4.2% (P < 0.05) and increased VDR expression levels by 131 ± 14.5% (P < 0.0001).Discussion: These findings suggest that combining 1,25(OH)2D3 with genistein results in an enhanced inhibition of lipid accumulation and induction of apoptosis in maturing 3T3‐L1 preadipocytes.

Từ khóa


Tài liệu tham khảo

10.1016/0300-2977(95)00008-B

10.1210/endo-125-4-1870

10.1289/ehp.95103346

10.1210/en.138.5.1777

10.1016/j.mehy.2004.11.046

10.1210/endo.140.4.6663

10.1093/jn/136.2.409

10.1210/en.2003-0076

10.1051/rnd:19990408

Messina MJ, 2001, Soy for breast cancer survivors: a critical review of the literature, J Nutr, 131, S3095, 10.1093/jn/131.11.3095S

10.1097/00029330-200608010-00008

10.1152/ajpendo.00410.2005

Sun X., 2004, Role of uncoupling protein 2 (UCP2) expression and 1alpha, 25‐dihydroxyvitamin D3 in modulating adipocyte apoptosis, Faseb J, 18, 1430, 10.1096/fj.04-1971fje

10.1007/BF00265373

10.1016/0168-8227(95)01040-K

10.2337/diacare.24.8.1496

10.2337/diacare.27.12.2813

10.1007/BF00422375

10.1677/joe.0.1500275

10.1210/en.133.2.553

Hedlund TE, 1996, Stable expression of the nuclear vitamin D receptor in the human prostatic carcinoma cell line JCA‐1: evidence that the antiproliferative effects of 1 alpha, 25‐dihydroxyvitamin D3 are mediated exclusively through the genomic signaling pathway, Endocrinology, 137, 1554, 10.1210/endo.137.5.8612485

10.1016/j.mce.2005.05.001

10.1101/gad.13.17.2231

10.1146/annurev.nu.14.070194.000531

10.1101/gad.948702

10.1152/ajpcell.2001.280.4.C807

10.1042/BJ20020300

10.1074/jbc.M510343200

10.1074/jbc.272.41.25913

10.1016/0300-9629(93)90424-3

Frankfurt OS, 2004, Immunoassay for single‐stranded DNA in apoptotic cells, Methods Mol Biol, 282, 85

10.1111/j.1462-5822.2007.00901.x

10.1042/cs0920003

10.1002/jcp.1041350326

Kawada T., 1996, The possibility of active form of vitamins A and D as suppressors on adipocyte development via ligand‐dependent transcriptional regulators, Int J Obes Relat Metab Disord, 20, S52

10.1016/S0024-3205(98)00059-9

10.1210/endo.139.5.5970

10.1002/jcb.10507

10.1093/jn/133.5.1238

10.1159/000012756

10.1128/MCB.16.8.4128

10.1152/physrev.1998.78.3.783

10.1016/S1570-0232(02)00081-8

Thông tin
Thông tin xuất bản

Obesity

Tập 16 Số 3

539-546

Thông tin tác giả