Table 1.
Clinical and biological characteristics of the subjects.
Fig 1.
Calorie intake (Panel A) and diet composition (Panel B) were determined by self-administered questionnaire and analysis using GENI software. Data are expressed as mean ± SEM. Calorie, * POIS vs. CT = 0.0007; $ POIR vs. CT = 0.0003. Proteins, * POIS vs. CT = 0.0007; $ POIR vs. CT = 0.009. Fats, $ POIR vs. CT = 0.0003. Carbohydrates, * POIS vs. CT = 0.04.
Table 2.
Levels of adipokines and markers of systemic inflammation.
Fig 2.
Inflammation and fibrosis in SAT.
Panel A: Total macrophages (CD68+), pro-inflammatory (CD68+/CD86+), and anti-inflammatory (CD68+/CD206+) macrophages were counted after staining in SAT. For CD68, and CD86 or CD206 markers, four and two non-consecutive entire sections per subject were analyzed for 7 CT, 5 OIS and 6 OIR subjects. Data are expressed as mean ± SEM. $: POIR vs. CT = 0.008. Panel B: Adipocyte average size (μm2) in SAT; 10–15 sections per subject were respectively analyzed for 4 subjects per group. Data are expressed as mean ± SEM. Panel C: Relative quantification of Col5A, Col6A, TNFα, IL-1β, IL-6 and MCP-1 mRNA expression in SAT (nCT = 10, nOIS = 11, nOIR = 9). Data are expressed as mean ± SEM and relatively to CT values, which were set at 1.0. $ POIR vs. CT = 0.004. Panel D: Western blot analysis of IκBα expression in SAT (nCT = 9, nOIS = 8, nOIR = 8). The graph represents IκBα protein quantification after correction by α/β tubulin protein levels, used as an indicator of protein loading. Data are expressed as mean ± SEM and relatively to CT values, which were set at 1.0.
Fig 3.
Panel A: Western blot analysis of P-Akt/Akt ratio in SAT with and without incubation with insulin (nCT = 9, nOIS = 10, nOIR = 9). The graph represents P-Akt protein quantification after correction by total Akt protein levels, used as an indicator of protein loading. Data are expressed as mean ± SEM and relatively to CT values, which were set at 1.0. § PCT±insulin = 0.008; POIS±insulin = 0.002; POIR±insulin = 0.004. Panel B: Fold induction of P-Akt/Akt level in SAT after insulin stimulation. Data are expressed as mean ± SEM. Panels C and D: Correlations (Spearman analysis) between insulin-stimulated P-Akt/Akt fold induction in SAT and HOMAIR (C) or GIR (D).
Fig 4.
Inflammation and fibrosis in skeletal muscle.
Panel A: Total macrophages (CD68+), and pro-inflammatory (CD68+/CD86+) and anti-inflammatory (CD68+/CD206+) macrophages were counted after staining in skeletal muscle. For CD68, and CD86 or CD206 markers, four and two non-consecutive entire sections per subject were respectively analyzed for 6 CT, 6 OIS and 5 OIR subjects. Data are expressed as mean ± SEM. Panel B: Relative quantification of Col5A, Col6A, TNFα, IL-1β, IL-6 and MCP-1, mRNA expression in skeletal muscle (nCT = 10, nOIS = 11, nOIR = 9). Data are expressed as mean ± SEM and relatively to CT values, which were set at 1.0. Panel C: Western blot analysis of IκBα expression in skeletal muscle (nCT = 10, nOIS = 9, nOIR = 9). The graph represents IκBα protein quantification after correction by α/β tubulin protein levels, used as an indicator of protein loading. Data are expressed as mean ± SEM and relatively to CT values, which were set at 1.0. $ POIR vs. CT = 0.04.
Fig 5.
Insulin response in skeletal muscle.
Panel A: Western blot analysis of P-Akt/Akt ratio in skeletal muscle with and without incubation with insulin (nCT = 10, nOIS = 11, nOIR = 8). The graph represents P-Akt protein quantification after correction by total Akt protein levels, used as an indicator of protein loading. Data are expressed as mean ± SEM and relatively to CT values, which were set at 1.0. § PCT±insulin = 0.002; POIS±insulin = 0.002. POIR±insulin = 0.129. Panel B: Fold induction of P-Akt/Akt in skeletal muscle after insulin stimulation. Data are mean ± SEM. $ POIR vs. CT = 0.008 and # POIR vs. OIS = 0.0005. Panels C and D: Correlations (Spearman analysis) between insulin-stimulated P-Akt/Akt fold induction in skeletal muscle and HOMAIR (C) or GIR (D).