Fig 1.
Chemical structure of aspalathin (A), dose dependent effect of aspalathin on improving glucose uptake (B), and the effect of insulin and metformin in palmitate-exposed C3A cells (C). Results are expressed as mean ± SEM of three independent experiments. ** p < 0.01, *** p < 0.001 versus normal control.
Fig 2.
The effect of aspalathin on glucose uptake (A), glucose 2 protein expression (B), and palmitate uptake (C) in insulin resistant C3A liver cells. Results are expressed as mean ± SEM of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 versus normal control (no insulin); # p < 0.05, ## p < 0.01, ### p < 0.001 versus palmitate control (no insulin).
Fig 3.
The effect of aspalathin on protein kinase B (AKT) protein expression (A), and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) protein expression (B) in insulin resistant C3A liver cells. Results are expressed as mean ± SEM of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 versus normal control (no insulin); # p < 0.05, ### p < 0.001 versus palmitate control (no insulin).
Fig 4.
The effect of aspalathin on carnitine palmitoyltransferase 1 (CPT1) protein expression (A), and AMP-activated protein kinase (AMPK) protein expression (B) in palmitate exposed C3A cells. Results are expressed as mean ± SEM of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 versus normal control (no insulin); # p < 0.05, ## p < 0.01, ### p < 0.001 versus palmitate control (no insulin).
Fig 5.
The effect of aspalathin on metabolic activity in insulin-resistant C3A liver cells, as measured by assessing MTT activity (A) and ATP production (B), respectively. Results are expressed as mean ± SEM of three independent experiments. * p < 0.05, ** p < 0.01 versus vehicle normal control (no insulin); # p < 0.05, ### p < 0.001 versus palmitate control (no insulin).
Fig 6.
The effects of aspalathin on mitochondrial respiration in insulin-resistant C3A liver cells.
The graph shows oxygen consumption rate of all treatments (OCR) (A), individual parameters for basal respiration (B), ATP production (C), maximal respiration (D), and spare respiratory capacity (E), and extracellular acidification rates (F). Oxygen consumption rate was measured under basal conditions followed by the sequential injection of oligomycin (1 μM), FCCP (0.75 μM), as well as rotenone (0.5 μM) & antimycin A (0.5 μM), as indicated. Each data point represents an OCR measurement. Data are expressed as means ± SEM, n = 2 independent experiments. **** p < 0.0001 versus normal (no insulin) control, #### p < 0.0001 versus palmitate control.
Fig 7.
Extracellular acidification rates (ECAR) response of C3A liver cells to aspalathin (10 μM), glucose (10 mM), oligomycin (1 μM) and 2-deoxyglucose (2-DG) (100 mM), respectively (A). Individual parameters for glycolysis, glycolytic capacity, glycolytic reserve of C3A liver cells after aspalathin treatment (B and C), and the effect of palmitate and aspalathin on OCAR/ECAR (D). ECAR was measured under basal conditions followed by the sequential addition of aspalathin (10 μM), glucose (10 mM), oligomycin (1 μM), and 2-deoxyglucose (2-DG) (100 mM) the order was as follows (aspalathin>Glu > Oli > 2-DG). Data are expressed as means ± SEM, n = 3 independent experiments. **** p < 0.0001 versus normal (no insulin) control, #### p < 0.0001 versus palmitate control.