Fig. 4: Insulin-induced glucose uptake in human adipocytes and skeletal myocytes. | Nature Communications

Fig. 4: Insulin-induced glucose uptake in human adipocytes and skeletal myocytes.

From: Repurposing anti-inflammasome NRTIs for improving insulin sensitivity and reducing type 2 diabetes development

Fig. 4

The results of glucose uptake assays in human adipocytes a and in human skeletal myocytes b are shown. Cells from nondiabetic (Non-DM) persons were treated with either tumor necrosis factor (TNF; 2.5 nM) or with high glucose (25 mM) and high insulin (100 nM) (HG) to induce insulin resistance. Cells from diabetic (DM) and nondiabetic persons were treated with lamivudine (Lam; 100 μM) or phosphate-buffered saline (PBS; vehicle). Glucose uptake measurements were performed by exposing cells to insulin (20 nM) using a fluorescent derivative of glucose, and quantified as relative fluorescence units (RFU) and normalized to baseline (prior to insulin treatment) levels of fluorescence. Data are reported as mean ± s.e.m.* In Non-DM adipocytes, P = 0.02 (HG versus PBS), P = 0.01 (HG + 3TC versus HG), P = 0.01 (TNF versus PBS), P = 0.02 (TNF + 3TC versus TNF), two-tailed unpaired Student t test. In DM adipocytes, P = 0.02 (3TC versus PBS), two-tailed paired Student t test. n = 5 samples per group (a). In Non-DM myocytes, P < 0.001 (HG versus PBS), P = 0.001 (HG + 3TC versus HG), P < 0.001 (TNF versus PBS), P = 0.01 (TNF + 3TC versus TNF), two-tailed unpaired Student t test. In DM myocytes, P = 0.03 (3TC versus PBS), two-tailed paired Student t test. n = 6 (nondiabetic) or 5 (diabetic) samples per group (b). Source data are provided as a Source Data file.

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