Insulin resistance (IR) is involved in the pathogenesis of endothelial dysfunction and is also present in patients with
cirrhosis. Intrahepatic endothelial dysfunction plays a major role, increasing hepatic vascular resistance and promoting
portal hypertension (PH). In addition, β-
adrenergic agonists and
insulin share several intracellular signaling pathways. Thus IR may influence the response to β-blockers. This study aimed at evaluating the relationship between IR and hepatic hemodynamics in patients with
cirrhosis and with the portal pressure response to acute β-blockade. Forty-nine patients with
cirrhosis and PH were included. Hepatic and systemic hemodynamics were measured, and IR was estimated by using the updated homeostasis model assessment (HOMA)-2 index. Patients with HOMA-2 > 2.4 were considered IR. In patients with hepatic venous pressure gradient (HVPG) ≥ 10 mmHg) [clinically significant PH (
CSPH)], hemodynamic measurements were performed again 20 min after intravenous
propranolol. Mean HOMA-2 index was 3 ± 1.4. Fifty-seven percent of patients had IR. A weak correlation between HOMA-2 index and HVPG was observed. Eighty-six percent of patients had
CSPH. HOMA-2 index was an independent predictor of
CSPH. However, in patients with
CSPH, the correlation between HOMA-2 index and HVPG was lost. HVPG, but not IR, predicted the presence of
esophageal varices. Response to
propranolol was not different between patients with or without IR. In nondiabetic patients with
cirrhosis, HOMA-2 index is directly associated with the presence of
CSPH and indirectly with
varices, but does not allow either grading HVPG or predicting its response to
propranolol.