3T3-L1

The 3T3-L1 Swiss subclone line has been widely utilized, since its development, due to its affinity for lipid droplet deposition in vitro.

[1][2][3] 3T3-L1 cells can be utilized to study a number of cellular and molecular mechanisms related to insulin-resistance, obesity, and diabetes in vitro.

[2] Aside from its usages, this cell line is widely developed and can be purchased for continuous propagation for numerous research studies.

[2][3] In 1962, the original 3T3 cell line that it was established by George Todaro and Howard Green of the New York University School of Medicine.

In 1971, Green and Kehinde established a subline of 3T3 cells, called 3T3-L1, which demonstrated a greater propensity for differentiation into adipocytes and a higher affinity for lipid deposition.

The process of adipogenesis, and the start of differentiation can be induced in 3T3-L1 cells through the addition of compounds such as a synthetic glucocorticoid, a phosphodiesterase inhibitor, and insulin.

[3][10][11][12][13] 3T3-L1 cells are commonly utilized as an effective model for white adipocytes because of their similar fibroblast-like morphology, lipid accumulation, gene expression, and basal energy exchanges and transformations.

While a majority of in vitro experiments utilize the common insulin, dexamethasone, and IBMX combinations, others have found other methods of differentiating and inducing the process of adipogenesis.

In 3T3-L1 adipocytes, oleanolic acid (5umol/L) down regulated the expression of PPARy and cytidine-cytidine-adenosine-adenosine-thymidine (CCAAT) enhancer binding protein a (C/EBPa) during differentiation.

[16] Long term treatment of flavonoid, luteolin, affected PPARy activation and suppressed adipogenesis 3T3-L1 adipocytes.

[17] Isopanduratin A also inhibited adipogenesis in 3T3-L1 adipocytes by impacting multiple targets in the adipogenic growth cycle such as PPARy, C/EBPa, sterol regulatory binding protein- 1c (SREB-1c), adiponectin, and lipoprotein lipase(LPL).