Cholesterol-Induced Hepatic Inflammation Does Not Underlie the Predisposition to Insulin Resistance in Dyslipidemic Female LDL Receptor Knockout Mice

Figure 4

Hepatic inflammation does not induce hepatic insulin resistance in lean Ldlr^−/− mice. To assess systemic insulin resistance, we performed an oral glucose tolerance test (a) and an insulin tolerance test (b) in WT and Ldlr^−/− mice fed a chow, high-fat (HF), or high-fat cholesterol (HFC) diet ( = 5-6). To distinguish between hepatic and peripheral insulin resistance, a hyperinsulinemic-euglycemic clamp was performed during which glucose infusion rate (GIR) (c), metabolic clearance rate (MCR) (d), and hepatic glucose production (HGP) (e) were determined ( = 5–7). (f) Phosphorylation status of AKT in liver tissues obtained from WT and Ldlr^−/− mice fed a chow, HF, or HFC diet sacrificed 15 min after saline () or insulin injection () and determined by Western Blot analysis. Data are expressed as means ± SEM for WT mice (white bars) and Ldlr^−/− mice (black bars). WT versus KO; ^# HF, HFC versus chow; HF versus HFC.

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