Fig. 4. Adipocyte mitochondrial function and fatty acid flux genes decrease in subjects with obesity and relate to AT Treg abundance and IFNγ-enhanced MHCII expression.

VAT adipocyte (VAd) and SAT adipocyte (SAd) gene expression in lean (N = 15) and obese (N = 83) subjects of markers of mitochondrial function (a, c) and fatty acid oxidation/synthesis (b, d); ***p < 0.001; **p < 0.01; *p < 0.05 analyzed by two-sided, independent T test. e Maximal and basal oxygen consumption rate (OCR) in lean (N = 2) and obese (N = 3) human SAd and VAd by Seahorse; ^aP < 0.05, ^aaP < 0.01, and ^aaaP < 0.001 vs. lean SAd; ^bP < 0.05, ^bbP < 0.01, and ^bbbP < 0.001 vs. lean VAd. f VAd gene expession of STAT1 in lean (N = 11) and obese (N = 15) subjects (*P < 0.05) analyzed by two-sided, independent T test without correction for multiple variables. Protein levels of (g) STAT1 and (h) MHCII-related genes in mature SAd treated with a JAK inhibitor (JAK I, 10 µM) with or without recombinant IFNγ (20 ng/ml) for 48 hr; ^†P < 0.01 vs. Vehicle; ^#P < 0.01 vs. IFNγ (N = 3). Data was analyzed by two-sided, independent T tests without correction for multiple variables. i Gene expression of MHCII-related genes in mature SAd treated with a JAK inhibitor (JAK I, 10 µM) with or without IFNγ (20 ng/ml) for 48 hr; ***P < 0.001 vs. IFNγ (N = 3). j Gene Expression of fatty acid oxidation/synthesis and adipokines/cytokines in adipocytes treated with a JAK inhibitor (JAK I, 10 µM) with or without IFNγ (20 ng/ml) for 48 hr. *P < 0.05 and ^†P < 0.01 vs. Vehicle (Its mean is 1 and bars not shown); ^§P < 0.05 and ^#P < 0.01 vs. IFNγ (N = 3). k In differentiated SAd, STAT1 siRNA decreased STAT1 protein and attenuated the IFNγ (20 ng/ml) effect to stimulate MHCII proteins, while scrambled siRNA had no effect. *P < 0.05 and **P < 0.01, and ^†P < 0.10 vs. scramble siRNA+IFNγ (N = 3). l Maximal and basal OCR from human SAd + /- IFNγ (N = 3). All data presented as mean ± SEM. Source data are provided as a Source Data file.