Fig. 3: The mRNA expression of biomarkers related with gut signaling and inflammation in the brown adipose tissue (BAT), liver and small intestine after intermittent treatments.

a Toll-like receptor 4 (TLR4), fibroblast growth factor 21 (FGF21), proliferator-activated receptor γ coactivator 1α (PGC-1α), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), tumor necrosis factor-α (TNF-α) in brown adipose tissue (BAT). b Expression of TLR4, FGF21, PGC-1α, NF-κB, and TNF-α in the liver. c Free fatty acid receptors 2 and 3 (FFAR2 and FFAR3), G-protein-coupled bile acid receptor 5 (TGR5), farnesoid X receptor (FXR), toll-like receptor 4 (TLR4), nod-like receptors 2 (Nod2), peptidoglycan recognition proteins 1 and 2 (Pglyrp1 and Pglyrp2) in the small intestine. d Cyclic adenosine monophosphate (cAMP), protein kinase A (PKA), cAMP response element binding protein (CREB), phosphoinositide-3-kinase (PI3K), protein kinase B (AKT or PKB), inhibitor of nuclear factor kappa B kinase subunit alpha (IKKα), mammalian target of rapamycin (mTOR) in the small intestine. e Inflammatory markers, such as nuclear NF-κB, TNF-α, interleukin 6, 10, and 15 (IL-6, IL-10, and IL-15), proliferating cell nuclear antigen (PCNA) and cysteine-aspartic acid protease 3 (Caspase-3) in the small intestine. f Transient receptor potential channel of vanilloid types 3 and 4 (Trpv3, Trpv4), type 1 iodothyronine deiodinase (Dio1), tryptophan hydroxylase 2 (Tph2), and 5-hydroxytryptamine receptor 1 F (HTR1F). The data are presented as the means ± SEM (n = 6–7 per group). *P < 0.05, **P < 0.01. Con, control group that received only saline; PTU, the rats that received 10 mg/kg propylthiouracil (PTU) during the experiment; GS, the rats that were administered 10 mg/kg PTU and underwent a regimen of alternating two-week treatment periods with 0.6 g/kg ginseng (dash area) and two-week periods without treatment; LT, the rats that were treated with 10 mg/kg PTU and received 0.5 mg/kg L-thyroxine (LT) with the same regimen as the GS group.