Page 49 - EASL POSTGRADUATE COURSE
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by the adipocytes or by the inflammatory cells that infiltrate the adipose tissue in IR states. Expanded
visceral adipose tissue common in IR states represents a preferential source of adipokines and cytokines
potentially acting on the liver tissue [14, 15]. In conclusion, IR can act both as the first and second hit in
the development of NASH. The varying outcome of the disease might be related to the relative impact
of metabolic derangements, environmental conditions and host factors (e.g. the genetic and hormonal
milieu), as in other conditions associated with IR, such as diabetes, hypertension, and CVD.
References
[1] Kahn CR. Insulin resistance, insulin insensitivity, and insulin unresponsiveness: a necessary distinction.
Metabolism 1978;27:1893-1902.
[2] Bugianesi E, McCullough AJ, Marchesini G. Insulin resistance: a metabolic pathway to chronic liver
disease. Hepatology 2005;42:987-1000.
[3] Muniyappa R, Lee S, Chen H, et al. Current approaches for assessing insulin sensitivity and resistance in
vivo: advantages, limitations, and appropriate The usage. Am J Physiol Endocrinol Metab 2008;294:E15-
26.
[4] Pacini G, Mari A. Methods for clinical assessment of insulin sensitivity and beta-cell function. Best Pract
Res Clin Endocrinol Metab 2003;17:305-322.
[5] DeFronzo RA, Tobin JD, Andres R. Glucose clamp technique: a method for quantifying insulin secretion
and resistance. Am J Physiol 1979;237:E214-223.
[6] Bugianesi E, Gastaldelli A, Vanni E, et al. Insulin resistance in non-diabetic patients with non-alcoholic
fatty liver disease: sites and mechanisms. Diabetologia 2005;48:634-642.
[7] Marchesini G, Brizi M, Bianchi G, et al. Nonalcoholic fatty liver disease: a feature of the metabolic
syndrome. Diabetes 2001;50:1844-1850.
[8] Lomonaco R, Ortiz-Lopez C, Orsak B, et al. Effect of adipose tissue insulin resistance on metabolic
parameters and liver histology in obese patients with nonalcoholic fatty liver disease. Hepatology
2012;55:1389-1397.
[9] Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assessment: insulin resistance and beta-
cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28:412-
419.
[10] Marchesini G, Bugianesi E, Forlani G, et al. Nonalcoholic fatty liver, steatohepatitis, and the metabolic
syndrome. Hepatology 2003;37:917-923.
[11] Mari A, Pacini G, Murphy E, et al. A model-based method for assessing insulin sensitivity from the oral
glucose tolerance test. Diabetes Care 2001;24:539-548.
[12] Bugianesi E, Manzini P, D’Antico S, et al. Relative contribution of iron burden, HFE mutations, and
insulin resistance to fibrosis in nonalcoholic fatty liver. Hepatology 2004;39:179-187.
[13] Svegliati-Baroni G, Bugianesi E, Bouserhal T, et al. Post-load insulin resistance is an independent
predictor of hepatic fibrosis in virus C chronic hepatitis and in non-alcoholic fatty liver disease. Gut
2007;56:1296-1301.
[14] Bugianesi E, Moscatiello S, Ciaravella MF, et al. Insulin resistance in nonalcoholic fatty liver disease.
Curr Pharm Des 2010;16:1941-1951.
[15] Vanni E, Bugianesi E, Kotronen A, et al. From the metabolic syndrome to NAFLD or vice versa? Dig
Liver Dis 2010;42:320-330.
The International Liver Congress™ 2015 • Vienna, Austria • April 22–23, 2015 49
visceral adipose tissue common in IR states represents a preferential source of adipokines and cytokines
potentially acting on the liver tissue [14, 15]. In conclusion, IR can act both as the first and second hit in
the development of NASH. The varying outcome of the disease might be related to the relative impact
of metabolic derangements, environmental conditions and host factors (e.g. the genetic and hormonal
milieu), as in other conditions associated with IR, such as diabetes, hypertension, and CVD.
References
[1] Kahn CR. Insulin resistance, insulin insensitivity, and insulin unresponsiveness: a necessary distinction.
Metabolism 1978;27:1893-1902.
[2] Bugianesi E, McCullough AJ, Marchesini G. Insulin resistance: a metabolic pathway to chronic liver
disease. Hepatology 2005;42:987-1000.
[3] Muniyappa R, Lee S, Chen H, et al. Current approaches for assessing insulin sensitivity and resistance in
vivo: advantages, limitations, and appropriate The usage. Am J Physiol Endocrinol Metab 2008;294:E15-
26.
[4] Pacini G, Mari A. Methods for clinical assessment of insulin sensitivity and beta-cell function. Best Pract
Res Clin Endocrinol Metab 2003;17:305-322.
[5] DeFronzo RA, Tobin JD, Andres R. Glucose clamp technique: a method for quantifying insulin secretion
and resistance. Am J Physiol 1979;237:E214-223.
[6] Bugianesi E, Gastaldelli A, Vanni E, et al. Insulin resistance in non-diabetic patients with non-alcoholic
fatty liver disease: sites and mechanisms. Diabetologia 2005;48:634-642.
[7] Marchesini G, Brizi M, Bianchi G, et al. Nonalcoholic fatty liver disease: a feature of the metabolic
syndrome. Diabetes 2001;50:1844-1850.
[8] Lomonaco R, Ortiz-Lopez C, Orsak B, et al. Effect of adipose tissue insulin resistance on metabolic
parameters and liver histology in obese patients with nonalcoholic fatty liver disease. Hepatology
2012;55:1389-1397.
[9] Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assessment: insulin resistance and beta-
cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28:412-
419.
[10] Marchesini G, Bugianesi E, Forlani G, et al. Nonalcoholic fatty liver, steatohepatitis, and the metabolic
syndrome. Hepatology 2003;37:917-923.
[11] Mari A, Pacini G, Murphy E, et al. A model-based method for assessing insulin sensitivity from the oral
glucose tolerance test. Diabetes Care 2001;24:539-548.
[12] Bugianesi E, Manzini P, D’Antico S, et al. Relative contribution of iron burden, HFE mutations, and
insulin resistance to fibrosis in nonalcoholic fatty liver. Hepatology 2004;39:179-187.
[13] Svegliati-Baroni G, Bugianesi E, Bouserhal T, et al. Post-load insulin resistance is an independent
predictor of hepatic fibrosis in virus C chronic hepatitis and in non-alcoholic fatty liver disease. Gut
2007;56:1296-1301.
[14] Bugianesi E, Moscatiello S, Ciaravella MF, et al. Insulin resistance in nonalcoholic fatty liver disease.
Curr Pharm Des 2010;16:1941-1951.
[15] Vanni E, Bugianesi E, Kotronen A, et al. From the metabolic syndrome to NAFLD or vice versa? Dig
Liver Dis 2010;42:320-330.
The International Liver Congress™ 2015 • Vienna, Austria • April 22–23, 2015 49
