Session: FP15-Adipocyte Biology
Bench to Bedside
Room 303 (Moscone Center)
Poster Board SUN-672
Methods: To mimic adipose tissue fibrosis we incubated SGBS adipocytes with increasing doses of THP-1 macrophage conditioned medium in the presence or absence of 100 µM resveratrol. Fibronectin (FN) and collagen 1A1 (col1A1) were studied as markers of fibrosis.
Results: Treatment with 10% MacCM resulted in upregulation of FN (~3.5 fold) and col1A1 (~2.1 fold) mRNA in adipocytes. The same effect was detected on the protein level. This was completely inhibited by coincubation with resveratrol. In order to elicudate the molecular pathway involved, we took advantage of small molecule inhibitors targeting either Sirt1 or PI3K. Interestingly, inhibition of Sirt1 with sirtinol (10 µM) didn't interfere with the effects of resveratrol, indicating that Sirt1 is not involved in mediating the effects of resveratrol on adipocyte fibrosis. Inhibition of PI3K with Ly294002 (20 µM) however, prevented the MacCM-induced upregulation of FN and Col1A1 mRNA expression. Western blot analysis revealed that MacCM induced phosphorylation of Akt and its downstream targets GSK3β, FOXO1 and mTOR, which was again inhibited by resveratrol.
Summary & conclusion: We show that resveratrol inhibits the inflammation-induced development of fibrosis in adipocytes, mediating its anti-fibrotic effect by involving the PI3K/Akt pathway. Taken together, our results demonstrate that resveratrol has health beneficial effects on human adipocytes. Preventing proinflammatory conditions and fibrosis in adipose tissue might be a useful strategy to prevent the development of insulin resistance in the obese state.
Nothing to Disclose: IZ, DT, HH, SZ, KMD, MW, PF
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