FIG. 6.

Acetylated mutant of STAT3 suppresses glucose intolerance in db/db mice. db/db mice (db) or control mice (lean) were manipulated to express wild-type STAT3 or K685Q mutant in their livers via infection with adenovirus vector and then examined for hepatic phosphorylation of STAT3 induced by glucose administration (A), blood glucose levels in a randomly fed state (B and C), and a GTT (D–G). A: Tyrosine phosphorylation of hepatic STAT3 in the fasting state and after glucose administration (left). Quantitation of STAT3 phosphorylation levels is normalized to β-actin and is represented as mean ± SE (right). *P < 0.05 (n = 4 in each group); open bar, fasting mice; closed bar, glucose-administered mice. B and C: Blood glucose levels in mice in a randomly fed state are represented as mean ± SE (n = 6 in each group) in lean mice (B) and db/db mice (C). Blood glucose level (D and E) and plasma insulin levels (F and G) during the GTT in lean mice (D and F) or in db/db mice (E and G) are represented as mean ± SE (n = 6 in each group). *P < 0.05 vs. β-galactosidase overexpression; †P < 0.05 vs. wild-type STAT3 overexpression; ○, β-galactosidase overexpression; □, wild-type STAT3 overexpression; ■, K685Q mutant overexpression.