Streptozotocin-induced diabetes increases?-glutamyltranspeptidase activity but not expression in rat liver

Significant Correlation Between Insulin Resistance and Serum Gamma‐Glutamyl Transpeptidase (γ‐GTP) Activity in Non‐Drinkers

“…Another explanation for the correlation between the ␥-GTP level and the insulin resistance level in nondrinkers is that an increase in insulin resistance, namely a decrease in insulin utility, may affect ␥-GTP activity in the tissues. Since insulin intrinsically decreases ␥-GTP activity in the liver (Shoukry, 1988;Watkins et al, 1998) and small intestine (el Maraghi-Ater et al, 1986), an insufficient supply of insulin to the tissues may also lead to an elevation in ␥-GTP activity in various tissues, resulting in the increased ␥-GTP level observed in sera. However, we must also consider the fact that insulin is essential for the survival of various cells, including hepatocytes.…”

“…Indeed, insulin suppresses ␥-GTP activity in the small intestine (el Maraghi-Ater et al, 1986), and microsomal induction in the liver (Ishida et al, 2000). In addition, a recent study has demonstrated that serum ␥-GTP activity increases in rats treated with streptozotocin to damage insulin secretion (Shoukry, 1988;Watkins et al, 1998) and that the elevated level returned to normal after insulin administration (Shoukry, 1988). These findings suggest that a decrease in insulin utility in tissues may induce ␥-GTP activity.…”

Diabetes and hypertriglyceridemia modify the mode of acetaminophen-induced hepatotoxicity and nephrotoxicity in rats and mice

“…34 No. 1 (Watkins et al, 1998). Shankar et al (2003a) reported that the resistance of STZ-induced diabetic mice against APAP hepatotoxicity appears to be mediated by a combination of enhanced APAP clearance and robust compensatory tissue repair.…”

“…Type 1 diabetic mice exhibit early onset of liver tissue repair as well as lower bioactivation of thioacetamide (TA) and are resistant to TAinduced hepatotoxicity (Shanker et al, 2003b), while type 1 diabetic rats are sensitive to TA-induced hepatotoxicity due to induced CYP2E1 (Wang et al, 2000) and inhibited compensatory tissue repair (Sawant et al, 2006). It was also reported that modulation of carbon tetrachloride-induced hepatotoxicity was different between diabetic rats and diabetic mice (Gaynes and Watkins, 1989;Watkins et al, 1998). Moreover, unlike type 2 diabetic rats, type 2 diabetic mice are resistant to carbon tetrachloride and bromobenzene (Sawant et al, 2006).…”

“…Diabetes is also associated with increased blood glucose which leads to systemic oxidative stress in diabetes (Hunt and Wolff, 1991). In addition, changes in the antioxidant enzymatic systems activity occur in various tissues including the kidney (Kedziora-Kornatowska et al, 2003) togethkidney (Hoshiyama et al, 2003) and with unchanged or decreased GSH levels (Mukherjee et al, 1994;Watkins et al, 1998). The diabetic state also enhances the clearance of APAP from plasma irrespective of the level of liver injury (Shankar et al, 2003a), perhaps due to diabetes-related changes in renal morphology and function Vol.…”