SOCS2 Inhibits Mitochondrial Fatty Acid Oxidation via Suppressing LepR/JAK2/AMPK Signaling Pathway in Mouse Adipocytes

Figure 6

SOCS2 aggravated oligomycin-induced mitochondrial dysfunction. Preadipocytes from mice iWAT were transfected with control vector, Ad-SOCS2, and sh-SOCS2 induced differentiation for 8 days, incubated with 1 μM oligomycin for 1 h before harvested. (a) Cell viability was detected by CCK-8 kit after 1 μM oligomycin treatment 1 h (). (b) ATP level with 1 μM oligomycin treatment for 1 h (). (c) ATP level after transfection and oligomycin incubation (). (d) Fatty acid oxidation. Palmitate oxidation to CO₂ was measured for 3 h after transfection and oligomycin incubation (). (e–g) SCOS2 mRNA level, leptin, and its receptor mRNA level after transfection and treatment with oligomycin. (h) p-JAK level after transfection and treatment with oligomycin. (i, j) Protein expression levels of CPT-1b and p-ACC after transfection and treatment with 1 μM oligomycin for 1 h (). All the protein levels (h–j) were detected by the ELISA test. Values are the . , .

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)

(i)

(j)