Figure 5.

Increased hepatic HKDC1 mRNA expression and serum HKDC1 levels in patients with AH are associated with higher incidence of AKI and decreased short-term survival. (A) Representative pictures of HKDC1 immunostaining (original magnification, ×200) in control livers and in livers from patients with AH, ALD cirrhosis, and non-ALD cirrhosis. (B) Gene expression of HKDC1 was analyzed in control (n = 13), AH (n = 69), HCV (n = 26), NASH (n = 37), and compensated AC liver tissue (n = 26). Data are shown as mean ± standard error of the mean. *P < .05 compared to control samples, #P < .05 compared to the other groups. (C) High HKDC1 mRNA expression (≥32-fold of control) is associated with the development of AKI during hospitalization in patients with AH. (D) Kaplan-Meier curve showing the 90-day survival in patients with AH with high (>32-fold of control) or low (<32-fold of control) hepatic HKDC1 expression. (E) Fasting serum levels of HKDC1 were evaluated in samples from healthy control individuals (n = 14), heavy drinkers (n = 10), and in patients with AH (n = 46), HCV (n = 17), NASH (n = 12), and compensated AC (n = 22). Data are shown as mean ± standard error of the mean; *P < .05 compared to all other groups. (F) High HKDC1 serum level (>2900 ng/mL) is associated with the development of AKI during hospitalization in patients with AH. (G) Kaplan-Meier curve showing the 90-day survival in patients with AH with high (>2900 ng/mL) or low (<2900 ng/mL) serum HKDC1 level. (H–J) Rat primary hepatocytes were treated with either AdCMV-HKDC1 or AdCMV-GFP as described in the Materials and Methods section. Cells were serum- and glucose-starved overnight followed by incubation with 30 mmol/L glucose for 4 hours. Hexokinase activity (H), G6P levels (I), and glycogen content (J) were determined as described in the Materials and Methods section. Data represent the mean for 3 independent experiments ± standard error; *P < .05 compared to the AdCMV-GFP–treated cells in medium plus glucose.