Fig. 4: High glucose induces a metabolic switch from mitochondrial oxidative phosphorylation (OXPHOS) to glycolysis, which facilitates mtROS production in HK-2 cells. | Cell Death & Disease

Fig. 4: High glucose induces a metabolic switch from mitochondrial oxidative phosphorylation (OXPHOS) to glycolysis, which facilitates mtROS production in HK-2 cells.

From: CD36 promotes NLRP3 inflammasome activation via the mtROS pathway in renal tubular epithelial cells of diabetic kidneys

Fig. 4

A−E The metabolic status of the HK-2 cells was determined by evaluating the oxygen consumption rates (OCR) (A, C–E), and the extracellular acidification rate of the media (ECAR) (B–D and E) using Agilent Seahorse XF technology. A, B The left panels show the representative OCR (A) and ECAR (B) curves from HK-2 cells treated with NG, HG, PA, and HG + PA for 72 h. Right panels show the quantified data from replicate studies (n = 4 per group). C−E The levels of OCR and ECAR were quantified from HK-2 cells treated with HG, PA, HG + PA at various time points (n = 4 per group). F Levels of p-AMPK, p-ACC, and CPT1 expression from HK-2 cells treated with culture medium or 30 mM d-glucose for 72 h. G, H OCR curve and OCR, ECAR quantified data from HK-2 cells under NG, HG, and HG + AICAR conditions. I The level of mtROS expression was detected by FACS using MitoNeoD reagent. NG: 5.6 mM d-glucose; HG: 30 mM d-glucose; PA: NG + 300 μM palmitic acid; HG + PA: HG + 300 μM palmitic acid; HG + AICAR: HG + AICAR (AMPK activator; 1 mM). Values are expressed as the mean ± SD. **P < 0.01 versus the NG group by an ANOVA.

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