Fig 2: Adipose-specific ATGL deletion suppresses mitochondrial activity and prevents browning in WAT post-burn injury: Twelve-week-old ATGL floxed and knockout mice were treated with 30%TBSA injury and monitored daily for 7 days. (A) Mitochondria respiration profiles of isolated WAT mitochondria from control (black), control AKO (white), burn (light grey), and burn AKO (dark grey). (B) Coupling efficiency (%) measured by the Seahorse stress test report generator. Respiration paramateres (C) Basal, (D) state 3, (E) state 3u in isolated mitochondria as measured via Seahorse assay. (F-J) Isolated mitochondrial protein was run and assessed in a gradient gel via BN-PAGE, and activity assays were performed for complexes such as I, II, IV, and ATP synthase. (K) Citrate synthase activity. (L) Immunohistochemistry for UCP1 expression. (M) Quantitative PCR analysis of browning markers (Ucp1, Pgc1a, and Prdm16) and (N) Western blot analysis of UCP1 expression normalized to Ponceau S as loading control in WAT. The results displayed are the average and SEM analyzed in the specified number of mice samples. Statistical significance was assessed using two-way ANOVA tests as appropriate

Fig 3: JPTGY treatment alters the protein expression levels of biomarkers of BAT and WAT in mice after treatment with JPTGY. (A) Protein levels of the BAT biomarkers PGC-1α and UCP-1; (B) protein levels of WAT biomarkers, including AGT, PSTA, and EDNRA, in abdominal adipose tissue. The relative protein levels were calculated and are presented in histograms. *P<0.05 vs. control; #P<0.05 vs. obesity. JPTGY, Jian Pi Tiao Gan Yin; WAT, white adipose tissue; BAT, brown adipose tissue; PGC-1α, peroxisome proliferator-activated receptor gamma coactivator-1-alpha; UCP-1, uncoupling protein-1; AGT, angiotensinogen; PSTA, primary subtalar arthrodesis; EDNRA, endothelin receptor type A.

Fig 4: Effects of GD intake on ICR mice on a high-fat diet (HFD). Change in plasma TG (A), plasma TCHO (B), and VAT volume (C) after 2 weeks of GD administration. (D) Represents micro-CT images of the four groups. The red dotted lines demarcate the area for which VAT volume was measured (from the xiphoid process of the sternum to the hip joint). Yellow indicates the visceral adipose tissue, and orange indicates the subcutaneous adipose tissue. (E) GD-induced Ucp1 expression in mice eWAT. (F) Fluorescent immunohistochemical staining (FIHC) with anti-mouse Ucp1 antibody in eWAT sections. PD, phrase difference images; Scale bar = 50 μm. (G) Average adipocyte size (n = 30) of the four mouse groups in (F). *p < 0.05, **p < 0.01 vs. HFD, n = 10, error bars indicate SD.

Fig 5: IL-1β expression is increased in UCP1-deficient PVAT.WT and Ucp1 KO mice were fed with STC or HFD for 12 weeks before isolation of aorta and surrounding PVAT. (A and B) Expression levels of mRNA encoding several adipokines (A) and inflammatory cytokines (B) in PVAT, determined by real-time PCR analysis, n = 6 to 8. (C) Comparison of mRNA expression of Il-1β in aortas and PVAT, n = 8 to 10. (D) IL-1β protein levels in the conditional medium from ex vivo culture of aorta and PVAT, measured by enzyme-linked immunosorbent assay (ELISA), n = 6 to 8. (E) IL-1β protein in PVAT lysates and (F) in serum determined by ELISA, n = 6 to 8. *P < 0.05.