Pathophysiology of Non Alcoholic Fatty Liver Disease

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Abstract

The physiopathology of fatty liver and metabolic syndrome are influenced by diet, life style and inflammation, which have a major impact on the severity of the clinicopathologic outcome of non-alcoholic fatty liver disease. A short comprehensive review is provided on current knowledge of the pathophysiological interplay among major circulating effectors/mediators of fatty liver, such as circulating lipids, mediators released by adipose, muscle and liver tissues and pancreatic and gut hormones in relation to diet, exercise and inflammation.

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Skeletal muscle metabolism is a major determinant of resting energy expenditure.

F Zurlo, K. Larson, C Bogardus … (1990)

Energy expenditure varies among people, independent of body size and composition, and persons with a "low" metabolic rate seem to be at higher risk of gaining weight. To assess the importance of skeletal muscle metabolism as a determinant of metabolic rate, 24-h energy expenditure, basal metabolic rate (BMR), and sleeping metabolic rate (SMR) were measured by indirect calorimetry in 14 subjects (7 males, 7 females; 30 +/- 6 yr [mean +/- SD]; 79.1 +/- 17.3 kg; 22 +/- 7% body fat), and compared to forearm oxygen uptake. Values of energy expenditure were adjusted for individual differences in fat-free mass, fat mass, age, and sex. Adjusted BMR and SMR, expressed as deviations from predicted values, correlated with forearm resting oxygen uptake (ml O2/liter forearm) (r = 0.72, P less than 0.005 and r = 0.53, P = 0.05, respectively). These findings suggest that differences in resting muscle metabolism account for part of the variance in metabolic rate among individuals and may play a role in the pathogenesis of obesity.

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Increased hepatic synthesis and dysregulation of cholesterol metabolism is associated with the severity of nonalcoholic fatty liver disease.

Hae-Ki Min, Ashwani Kapoor, Michael Fuchs … (2012)

Nonalcoholic fatty liver disease (NAFLD) is associated with increased cardiovascular and liver-related mortality. NAFLD is characterized by both triglyceride and free cholesterol (FC) accumulation without a corresponding increment in cholesterol esters. The aim of this study was to evaluate the expression of cholesterol metabolic genes in NAFLD and relate these to disease phenotype. NAFLD was associated with increased SREBP-2 maturation, HMG CoA reductase (HMGCR) expression and decreased phosphorylation of HMGCR. Cholesterol synthesis was increased as measured by the circulating desmosterol:cholesterol ratio. miR-34a, a microRNA increased in NAFLD, inhibited sirtuin-1 with downstream dephosphorylation of AMP kinase and HMGCR. Cholesterol ester hydrolase was increased while ACAT-2 remained unchanged. LDL receptor expression was significantly decreased and similar in NAFLD subjects on or off statins. HMGCR expression was correlated with FC, histologic severity of NAFLD and LDL-cholesterol. These data demonstrate dysregulated cholesterol metabolism in NAFLD which may contribute to disease severity and cardiovascular risks. Copyright © 2012 Elsevier Inc. All rights reserved.

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The weight of leptin in immunity.

Antonio La Cava, Giuseppe Matarese (2004)

Leptin is an adipocyte-derived hormone/cytokine that links nutritional status with neuroendocrine and immune functions. As a hormone, leptin regulates food intake and basal metabolism, and is sexually dimorphic - that is, its serum concentration is higher in females than in males with a similar body fat mass. As a cytokine, leptin can affect thymic homeostasis and the secretion of acute-phase reactants such as interleukin-1 and tumour-necrosis factor. Similar to other pro-inflammatory cytokines, leptin promotes T helper 1 (TH1)-cell differentiation and can modulate the onset and progression of autoimmune responses in several animal models of disease. Here, we review the advances and controversy for a role of leptin in the pathophysiology of immune responses.

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Author and article information

Contributors

Amedeo Lonardo: Role: Academic Editor

Giovanni Targher: Role: Academic Editor

Journal

Journal ID (nlm-ta): Int J Mol Sci

Journal ID (iso-abbrev): Int J Mol Sci

Journal ID (publisher-id): ijms

Title: International Journal of Molecular Sciences

Publisher: MDPI

ISSN (Electronic): 1422-0067

Publication date (Electronic): 11 December 2016

Publication date Collection: December 2016

Volume: 17

Issue: 12

Electronic Location Identifier: 2082

Affiliations

[1 ]Gastroenterology, Di.Bi.M.I.S Policlinic Paolo Giaccone Hospital, University of Palermo, PC 90127 Palermo, Italy; petsa@ 123456inwind.it

[2 ]Cardiometabolic Risk Unit—Institute of Clinical Physiology, CNR, PC 56124 Pisa, Italy; amalia@ 123456ifc.cnr.it

[3 ]Department of Clinical and Experimental Medicine, University of Pisa, PC 56122 Pisa, Italy; elenirebelos@ 123456gmail.com

[4 ]Gastroenterology and Hepatology, Department of Medical Sciences, Città della, Salute e della Scienza di Torino Hospital, University of Turin, PC 10122 Turin, Italy; ebugianesi@ 123456yahoo.it

[5 ]Department of Nephrology, Urology and Renal Transplant—Fondazione IRCCS Ca’, Granda, PC 20122 Milano, Italy; pmessa@ 123456policlinico.mi.it

[6 ]Institute of Internal Medicine, Gastroenterology and Liver Diseases Unit, Fondazione Policlinico Gemelli, Catholic University of Rome, PC 00168 Rome, Italy; luca.miele@ 123456policlinicogemelli.it

[7 ]Department of Gastroenterology 1 and Obesity 2, Polytechnic University of Marche, PC 60121 Ancona, Italy; gsvegliati@ 123456gmail.com

[8 ]Metabolic Liver Diseases—Università degli Studi Milano-Fondazione IRCCS Ca’, Granda via F Sforza 35, PC 20122 Milano, Italy; luca.valenti@ 123456unimi.it

[9 ]Institute for Health, PC 53042 Chianciano Terme, Italy

Author notes

[* ]Correspondence: ferruccio.bonino@ 123456unipi.it ; Tel.: +39-337-221-762

Article

Publisher ID: ijms-17-02082

DOI: 10.3390/ijms17122082

PMC ID: 5187882

PubMed ID: 27973438

SO-VID: 52bf9d94-6d9e-49f3-8e4a-cff0b8af637f

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This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

Pathophysiology of Non Alcoholic Fatty Liver Disease

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Abstract

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Karger: Nutrition and Dietetics

Most cited references 157

Skeletal muscle metabolism is a major determinant of resting energy expenditure.

Increased hepatic synthesis and dysregulation of cholesterol metabolism is associated with the severity of nonalcoholic fatty liver disease.

The weight of leptin in immunity.

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