Table 1.

The formulation of defatting multidrug combination.

Code	Drug name	Dose	Function	Mechanism of action
1	Visfatin	NA	Defatting drugs used in Yarmush et al's studies	Insulin mimetic
2	GW7647	1μM		PPAR-α agonist to promote β-oxidation
3	GW501516	1μM		PPAR-β/δ agonist
4	Forskolin	10μM or 1μM		Glucagon mimetic and cAMP activator that increases β-oxidation and Ketogenesis
5	Hypericin	10μM or 1μM		Activates pregnane X receptor (PXR), activates xenobiotic pathway
6	Scoparone	10μM or 1μM		Activates constitutive androstane receptor (CAR),activates xenobiotic pathway
7	L. Carnitine	10mM or 1μM	Defatting drugs used in our previsous and current studies based on literature reports	Increases fatty acid transportation to the mitochondria
8	All-trans Retinoic acid	20μM or 1μM		Activating etinoic acid, PPAR-β/δ receptors
9	Coenzyme A	5mM		β-oxidation substrate
10	Lipase	50u/mL		Catalyze lipoprotein/TG to into free fatty acid
11	Epigallocatechin gallate (EGCG or E)	0.1μM		Activating AMPK and anti-oxidation/inflammation
12	Resveratrol (R)	0.5μM		Activating AMPK and SIRT1

Dosages and mechanisms of action of the defatting drugs used in previous (No. 1-6) and current studies (No. 2-12) are listed. The perfusate of control group was supplemented with equal volume of DMSO to the defatting groups; the modified conventional defatting group (Yarmush eg al., Y defatting) was set up as reported (No. 2-10); the second defatting group included the drugs used in Y defatting study, Epigallocatechin gallate (EGCG), and Resveratrol (R) (No. 2-12, Y+E+R defatting). The third defatting group was treated without GW compounds and with dose-reduced defatting drugs (No. 4-12, Y’-GW+E+R defatting).