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. 2023 Jul 6;75:101773. doi: 10.1016/j.molmet.2023.101773

Figure 1.

Figure 1

External fatty acids induce HILPDA expression in adipocytes partly via FFAR4. A). HILPDA protein level and B) mRNA expression of Hilpda in 3T3-L1 adipocytes treated with a 2:1 mixture of oleate and palmitate (OA:PA, concentrations are indicated in μM) for 12 h. N = 3. C) Lipid-sensitive gene expression in 3T3-L1 adipocytes treated with 1 mM oleate for 24 h. SLR, signal log ratio. D) HILPDA protein level and E) mRNA expression of Hilpda in SVF-derived adipocytes treated with OA:PA (600 μM) for 12 h. N = 3. F) HILPDA protein level in SVF-derived adipocytes treated with OA:PA (600 μM) in the presence or absence of 10 μM actinomycin D for 6 h. HILPDA protein level in SVF-derived adipocytes treated with G) 10 μM rosiglitazone, H) 600 μM OA:PA in the presence or absence of 5 nM PPARγ antagonist GW9662, or I) 10 μM FFAR4 antagonist AH7614 for 12 h. J) HILPDA protein level in SVF-derived adipocytes treated with TUG-891 for 24 h. HILPDA protein level in 3T3-L1 adipocytes treated with 600 μM OA:PA in the presence or absence of K) 20 μM CPT1 inhibitor etomoxir or 1 μM ACOX1 inhibitor 10,12-Tricosadiynoic acid, or L) 10 μM lysosomal protease inhibitor e64d or proteasomal protease inhibitor MG132 for 12 h. The cells were preincubated with inhibitors for 30 min before treatment with OA:PA. Western blots were probed with antibodies against HILPDA and HSP90.