Fig. 4: Effects of native HSP70/GRP78 inhibition with mAbs on insulin sensitivity. | Nature Communications

Fig. 4: Effects of native HSP70/GRP78 inhibition with mAbs on insulin sensitivity.

From: Upper gut heat shock proteins HSP70 and GRP78 promote insulin resistance, hyperglycemia, and non-alcoholic steatohepatitis

Fig. 4

a Glucose disposition index (DI) metrics showing experimental data and fitting curves. Total β-cell responsivity to glucose (Φ) is a function of whole-body insulin sensitivity (SI). b, c Time courses of blood glucose and plasma insulin concentrations during an oral glucose tolerance test. d–f Hepatic phosphorylation of Akt on Ser473 (d), FoxO1 on Thr24 (e), and GSK3ab on Ser21/9 (f). g Gene expression of key enzymes involved in hepatic gluconeogenesis and glycolysis. h Representative images showing periodic acid Schiff (PAS) staining of liver section from rats fed HFD and infused with monoclonal antibodies against HSP70 or GRP78 or antibody isotype. i–k Western blot analysis of Akt Ser473 (i) and GSK3αβ Ser21/9 (j) phosphorylation and GLUT4 (k) expression in skeletal muscle. l, m Representative images showing PAS (l) and Oil red O (ORO) (m) staining of skeletal muscle sections from rats fed HFD and infused with monoclonal antibodies against HSP70 or GRP78 or antibody isotype. Magnification ×20. Scale bar: 0.10 mm. Data are presented as mean value ± SEM of n = 10 biologically independent animals. Statistical significances were calculated by Kruskal–Wallis test with Dunnett’s correction for multiple comparisons. Source data are provided as a Source Data file.

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