In the present study, we examined the effect of epigallocatechin gallate (EGCG) on the growth and differentiation of human preadipocyte cells, AML-I. EGCG exhibited cytotoxic activity on AML-I cells, accompanied by the appearance of characteristics of apoptosis by Annexin V-FITC staining method. Among apoptosis-related proteins examined, loss of NF-kappaB and p-Akt, and accumulation of Bad were displayed in EGCG-treated cells by Western blot analysis. Among 6 structure-related catechins including catechin (C), epicatechin (EC), catechin gallate (CG), epigallocatechin (EGC), epicatechin gallate (ECG) and EGCG, the catechins containing galloyl moiety exhibited apoptotic capacity. Interestingly, exposure of AML-I to EGCG increased the amounts of cytoplasmic lipid droplets as well as the expression of fatty acid synthase and peroxisome proliferator activated receptor-gamma proteins. Our results suggest that EGCG induces growth arrest and apoptosis, but does not affect adipocyte conversion of preadipocytes.
Adipose tissue is a potential site of retinoic acid (RA) action, but its physiological significance remains to be clarified. We have examined the effect of all‐trans retinoic acid (ATRA) on growth and differentiation of preadipocytes, and on adipokine gene expression in mature adipocytes using human preadipocyte cell model, AML‐I. Both ATRA and 9‐cis RA induced growth arrest in AML‐I preadipocyte at between 50 and 100 µM, which was accompanied by apoptosis. Western blotting showed a loss of NF‐κB, Bcl‐2 and p‐Akt, and the accumulation of Bad and Akt in cytoplasm of ATRA‐treated AML‐I preadipocytes. Exposure of AML‐I to ATRA or 9‐cis RA increased intracellular lipid accumulation in a time‐dependent manner compared to vehicle‐treated cells. Expression of fatty acid synthase (FAS) and peroxisome proliferator‐activated receptor‐γ (PPAR‐γ) proteins was increased in ATRA‐treated cells. Thus, both ATRA and 9‐cis RA promoted differentiation, inhibited proliferation and induced apoptosis in AML‐I preadipocytes. ATRA also modulated adipokine expression by increasing the mRNA level of adipocytokines (adiponectin, leptin and LPL), and by inhibiting PAI‐1 mRNA expression in mature AML‐I adipocytes. The data suggest that ATRA exerts a wide range of effects—growth arrest, apoptosis, lipogenesis and modulation of adipokine gene expression—during the maturation of preadipocytes into adipocytes.
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