P Mu1, Z Tan, Y Cui, H Liu, X Xu, Q Huang, L Zeng, T Wang. 1. Department of Endocrinology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, China.
Abstract
BACKGROUND: Although estrogen contributes to glucose homeostasis, its mechanisms remain unclear. AIMS: To investigate the role of caveolin-3 in estrogen's effects on glucose metabolism. METHODS: Ovariectomized (OVX) and sham-operated rats, fed with normal chow diet (NCD) or high-calorie diet (HCD), received 17β-estradiol (E(2)) or placebo. Fasting plasma glucose (FPG) was detected and HOMA-IR was calculated. Primary cultured skeletal muscle cells were treated with E(2), in the presence or absence of β-methyl-cyclodextrin and tamoxifen. Glucose consumption and transportation and expression of caveolin-3 were examined. RESULTS: In NCD-fed rats, OVX or E(2) had no effects on FPG or HOMA-IR. In HCD-fed rats, OVX led to the increase of FPG and HOMA-IR, which was attenuated by E(2). In cultured cells, E(2) improved glucose consumption and transportation and enhanced caveolin-3 expression, which were blocked by β-methyl-cyclodextrin and tamoxifen. CONCLUSION: Caveolin-3 plays an important role in the mechanism by which E(2) attenuates diet-induced glucose intolerance.
BACKGROUND: Although estrogen contributes to glucose homeostasis, its mechanisms remain unclear. AIMS: To investigate the role of caveolin-3 in estrogen's effects on glucose metabolism. METHODS: Ovariectomized (OVX) and sham-operated rats, fed with normal chow diet (NCD) or high-calorie diet (HCD), received 17β-estradiol (E(2)) or placebo. Fasting plasma glucose (FPG) was detected and HOMA-IR was calculated. Primary cultured skeletal muscle cells were treated with E(2), in the presence or absence of β-methyl-cyclodextrin and tamoxifen. Glucose consumption and transportation and expression of caveolin-3 were examined. RESULTS: In NCD-fed rats, OVX or E(2) had no effects on FPG or HOMA-IR. In HCD-fed rats, OVX led to the increase of FPG and HOMA-IR, which was attenuated by E(2). In cultured cells, E(2) improved glucose consumption and transportation and enhanced caveolin-3 expression, which were blocked by β-methyl-cyclodextrin and tamoxifen. CONCLUSION:Caveolin-3 plays an important role in the mechanism by which E(2) attenuates diet-induced glucose intolerance.
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