Pathogenesis and Management of Non- Alcoholic Fatty Liver Disease
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1 Barrett s Esophagus Pathogenesis and Management of Non- Alcoholic Fatty Liver Disease David E. Cohen, M.D., Ph.D. Director of Hepatology Brigham and Women s Hospital Director, Harvard-MIT Division of Health Sciences & Technology Robert H. Ebert Professor of Medicine Harvard Medical School
2 Disclosures Intercept, Merck, Genzyme, Catabasis, Synegeva, Esperion, Aegerion
3 Non-Alcoholic Fatty Liver Disease (NAFLD) Non-Alcoholic Fatty Liver Disease (NAFLD) Terminology Epidemiology Pathophysiology Diagnosis Treatment
4 Non-Alcoholic Fatty Liver Disease (NAFLD) Non-Alcoholic Fatty Liver Disease (NAFLD) Terminology
5 Non-Alcoholic Fatty Liver Disease (NAFLD) Non-Alcoholic Fatty Liver Disease (NAFLD) Alcohol-like liver disease in individuals who do not consume excessive alcohol Histologic spectrum of liver damage NAFL fatty liver (steatosis) NASH fatty liver + increased hepatocyte death (steatohepatitis)
6 NAFLD NAFLD: Spectrum of Hepatic Pathology Spectrum of Hepatic Pathology Steatohepatitis Steatosis Cirrhosis Hepatocellular carcinoma
7 Non-Alcoholic Fatty Liver (NAFL) Steatosis Non-Alcoholic Fatty Liver (NAFL) Steatosis Fatty hepatocytes Intracellular fat deposition
8 Non-Alcoholic SteatoHepatitis (NASH) Non-Alcoholic SteatoHepatitis (NASH) Intracellular fat deposition Necrosis Fibrosis Fat deposits Inflammation Fibrosis with necrosis
9 Cirrhosis Cirrhosis Regenerative nodule Fibrosis Nodules surrounded by fibrosis
10 Non-Alcoholic Fatty Liver Disease (NAFLD) Non-Alcoholic Fatty Liver Disease (NAFLD) Epidemiology
11 NAFLD NAFLD Prevalence Population-based data Data from selected populations Natural history
12 NAFLD Prevalence Population-based Data NAFLD Prevalence Population-based Data Dallas heart study National Health and Nutrition Examination Survey (NHANES) III
13 NAFLD Prevalence: Dallas Heart Study NAFLD Prevalence Dallas Heart Study Study cohort (~1100 African Americans, 700 Caucasians, 400 Hispanics) No risk factors (n = 375) H 1 -NMR spectroscopy Assess risk factors for fatty liver Define normal liver fat content Assess prevalence of increased liver fat (steatosis) in entire population & ethnic subgroups Browning, Hepatology 2004
14 Dallas Heart Study Results Liver fat <5.5% Liver fat > 5.5% Steatosis = 31% Liver enzymes NORMAL in most (79%) with steatosis Browning, Hepatology 2004
15 Hepatic Steatosis: Gender Disparities in Whites Hepatic Steatosis Gender Disparities in Whites Fatty liver 45% 42% M F M 24% 24% F M F Hispanics Whites Blacks Browning, Hepatology 2004
16 NHANES III NHANES III Study cohort 15,676 US adults AST, ALT HBsAg, HCV-Ab, Iron studies Alcohol intake AST, ALT Elevated (8%) AST, ALT Normal (92%) Explained (31%) Unexplained (69%) Clark, Am J Gastro 2003
17 NHANES III NHANES III Normal AST, ALT 5.5% Unexplained Hepatitis BMI Waist circumference Triglycerides Insulin HDL cholesterol Metabolic Syndrome Clark, Am J Gastro 2003
18 NAFLD Prevalence: General US Adult Population NAFLD Prevalence General US Adult Population Dallas Heart Study (2,200 adults) Assessed NAFLD with liver imaging General prevalence of fatty liver 31% (range 24% - 45%) Most individuals (79%) with fatty liver do not exhibit aminotransferase elevations NAFLD Prevalence % NHANES III (15, 700 adults) Assessed NAFLD with aminotransferases General prevalence of NAFLD 5.5% 3-10 x more prevalent than Hepatitis C
19 NAFLD in High-Risk Populations: Morbidly Obese Gastric Bypass Patients NAFLD in High-Risk Populations Morbidly Obese Gastric Bypass Patients Liver disease often unsuspected pre-operatively Intraoperative liver biopsy typically shows NAFLD Steatosis: 30-90% Steatohepatitis: 33-42% Fibrosis: idiopathic portal fibrosis: 33% advanced fibrosis: 12% cirrhosis: 1-2% Advanced fibrosis 13-14%
20 NAFLD in High-Risk Populations: Type 2 Diabetes Mellitus NAFLD in High-Risk Populations Type 2 Diabetes Mellitus Prevalence of NAFLD is high ultrasound detects fatty liver in 50% NASH unusually common NAFL: 12% NASH: 87% Fibrosis or cirrhosis documented in 20% Gupter, J Gastro Hepatol 2004 Tolman, Ann Intern Med 2004
21 NAFLD Prevalence - High-Risk Populations: Hyperlipidemia NAFLD Prevalence High-Risk Populations Hyperlipidemia Adult Lipid Clinic Patients (n= 95) Hypercholesterolemia Hypertriglyceridemia (55%) (30%) Mixed dyslipidemia (15%) Liver ultrasound Overall prevalence of fatty liver = 50% Hypertriglyceridemia, mixed dyslipidemia risk 5-fold Assy, Dig Dis Sci 2000
22 NAFLD Natural History NAFLD Natural History Liver-related morbidity and mortality NAFL NASH Cirrhosis
23 Prognostic Implications of NASH + Fibrosis Prognostic Implications of NASH + Fibrosis More consistent and rapid progression to cirrhosis than NAFL NAFL > 10 years Cirrhosis 3% NASH + fibrosis 5-10 years Cirrhosis 30% Matteoni, Gastroenterology 1999
24 Impact of NAFLD Cirrhosis complicates 1% of patients with steatosis, up to 33% of NASH NASH is associated with increased risk of HCC NASH cirrhosis will be the leading indication for OLT by 2020 Dam-Larsen, Gut 2007 Neuschwander-Tetri, Hepatology 2010
25 Implications of NAFLD Independent risk factor for type 2 diabetes Independent risk factor for CVD CVD is most common cause of death
26 Non-Alcoholic Fatty Liver Disease (NAFLD) Non-Alcoholic Fatty Liver Disease (NAFLD) Pathophysiology
27 Triglycerides are the Lipid Type that Accumulates in NAFLD - O O - C Fatty Acid CH - 2 CH - CH - 2 O O O - C O - C O O - C Triglyceride
28 Hepatic Triglyceride Balance Synthesis Oxidation Uptake Secretion
29 Triglycerides are the Lipid Type that Accumulates in NAFLD - O O - C Fatty Acid CH - 2 CH - CH - 2 O O O - C O - C O O - C Triglyceride
30 Space of Disse Plasma membrane Cytosol OMM IMM Mitochondria ER
31 Space of Disse NEFA Fatty acid uptake VLDL Plasma membrane Cytosol de novo Lipogenesis ACS Palmitic acid FAS Malonyl-CoA Pyruvate ACC Acetyl-CoA Citrate Glucose OMM FATP2 FATP5 CD36 ACS? ACS? ACS Acyl-CoA IMM Fatty acid oxidation CO TCA 2 Cycle Citrate OAA Acyl-CoA Acyl-CoA Acetyl-CoA Pyruvate CPT1 CPT2 Acyl-carnitine CACT Acyl-carnitine Ketone body Mitochondria Acyl-CoA VLDL Synthesis Palmitoyl-CoA (16:0) Stearoyl-CoA (18:0) Oleoyl-CoA (18:1) G-3-P LPA PA DAG TG + PL ELOVL6 SCD1 GPAT AGPAT Lipin1 DGAT MTP VLDL ER
32 NAFLD: Associated with Metabolic Syndrome NAFLD Associated with Metabolic Syndrome Obesity Diabetes Dyslipidemia Insulin Resistant State
33 Hepatic Triglyceride Balance in NAFLD Synthesis Oxidation Uptake Secretion
34 Non-Alcoholic Fatty Liver Disease (NAFLD) Fatty Acid Contributions in NAFLD Ferré and Foufelle, Diabetes Obes Metab 2010
35 Space of Disse NEFA Fatty acid uptake VLDL Plasma membrane Cytosol de novo Lipogenesis ACS Palmitic acid FAS Malonyl-CoA Pyruvate ACC Acetyl-CoA Citrate Glucose OMM FATP2 FATP5 CD36 ACS? ACS? ACS Acyl-CoA IMM Fatty acid oxidation CO TCA 2 Cycle Citrate OAA Acyl-CoA Acyl-CoA Acetyl-CoA Pyruvate CPT1 CPT2 Acyl-carnitine CACT Acyl-carnitine Ketone body Mitochondria Acyl-CoA VLDL Synthesis Palmitoyl-CoA (16:0) Stearoyl-CoA (18:0) Oleoyl-CoA (18:1) G-3-P LPA PA DAG TG + PL ELOVL6 SCD1 GPAT AGPAT Lipin1 DGAT MTP VLDL ER
36 Uptake Uptake
37 Non-Alcoholic Fatty Liver Disease (NAFLD) Hepatic Uptake of Plasma Fatty Acids Protein mediated Fatty acid transport proteins (FATP) Fatty acid translocate (CD36) Driven by plasma fatty acid concentrations Coupled to activation of fatty acids by esterification to Coenzyme A (CoA) by acyl-coa synthetasis
38 Space of Disse Plasma Fatty Acids Fatty acid uptake Plasma membrane Cytosol FATP2 FATP5 CD36 ACS? ACS? ACS Acyl-CoA OMM IMM Mitochondria ER
39 Non-Alcoholic Fatty Liver Disease (NAFLD) Fatty Acid Uptake in NAFLD Increased plasma fatty acid concentrations Insulin resistance Increased lipolysis in adipose tissue Increased transporter expression
40 Non-Alcoholic Fatty Liver Disease (NAFLD) Fatty Acid Contributions in NAFLD Insulin X Ferré and Foufelle, Diabetes Obes Metab 2010
41 Space of Disse Plasma Fatty Acids Plasma membrane Cytosol Fatty acid uptake FATP2 FATP5 CD36 ACS? ACS? ACS Acyl-CoA OMM IMM Mitochondria ER
42 Increased Uptake in NAFLD Uptake
43 Synthesis (de novo Lipogenesis) Synthesis
44 Space of Disse Plasma membrane Cytosol de novo Lipogenesis ACS Palmitic acid FAS Malonyl-CoA Pyruvate ACC Acetyl-CoA Citrate OMM IMM CO TCA 2 Cycle Citrate OAA Acyl-CoA Acetyl-CoA Pyruvate Mitochondria Acyl-CoA Palmitoyl-CoA (16:0) ELOVL6 Stearoyl-CoA (18:0) SCD1 Oleoyl-CoA (18:1) G-3-P GPAT LPA AGPAT PA Lipin1 DAG DGAT TG + PL Glucose ER
45 Non-Alcoholic Fatty Liver Disease (NAFLD) Controlled primarily at the transcriptional level Glucose Insulin Master transcription factors de novo Lipogenesis Carbohydrate response element binding protein (ChREBP) glucose activated lipogenic genes plus pyruvate kinase Sterol regulatory element binding protein (SREBP) 1c insulin activated lipogenic genes
46 Non-Alcoholic Fatty Liver Disease (NAFLD) de novo Lipogenesis: ChREBP Uyeda and Repa, Cell Metab 2006
47 Non-Alcoholic Fatty Liver Disease (NAFLD) de novo Lipogenesis: ChREBP Xu, Semin Liver Dis 2013
48 Non-Alcoholic Fatty Liver Disease (NAFLD) de novo Lipogenesis: SREBP1c Horton, Brown and Goldstein, J Clin Invest 2002
49 Non-Alcoholic Fatty Liver Disease (NAFLD) de novo Lipogenesis: SREBP1c Xu, Semin Liver Dis 2013
50 Non-Alcoholic Fatty Liver Disease (NAFLD) de novo Lipogenesis: SREBP1c Xu, Semin Liver Dis 2013
51 Space of Disse Plasma membrane Cytosol de novo Lipogenesis ACS Palmitic acid FAS Malonyl-CoA Pyruvate ACC Acetyl-CoA Citrate OMM IMM CO TCA 2 Cycle Citrate OAA Acyl-CoA Acetyl-CoA Pyruvate Mitochondria Acyl-CoA Palmitoyl-CoA (16:0) ELOVL6 Stearoyl-CoA (18:0) SCD1 Oleoyl-CoA (18:1) G-3-P GPAT LPA AGPAT PA Lipin1 DAG DGAT TG + PL Glucose ER
52 Consequences of insulin resistance Non-Alcoholic Fatty Liver Disease (NAFLD) Pathogenesis of Increased de novo Lipogenesis in NAFLD Hyperglycemia activates ChREBP Hyperinsulinemia activates SREBP Selective insulin resistance in the liver Gluconeogenesis is not suppressed by insulin de novo lipogenesis is continues to be responsive to insulin
53 Space of Disse Plasma membrane Cytosol de novo Lipogenesis ACS Palmitic acid FAS Malonyl-CoA Pyruvate ACC Acetyl-CoA Citrate OMM IMM CO TCA 2 Cycle Citrate OAA Acyl-CoA Acetyl-CoA Pyruvate Mitochondria Acyl-CoA Palmitoyl-CoA (16:0) ELOVL6 Stearoyl-CoA (18:0) SCD1 Oleoyl-CoA (18:1) G-3-P GPAT LPA AGPAT PA Lipin1 DAG DGAT TG + PL Glucose ER
54 Increased Synthesis in NAFLD Synthesis
55 Hepatic Triglyceride Balance Oxidation
56 Metabolic control Hepatic uptake of fatty acids Insulin and glucose limit entry of fatty acids into mitochondrial Malonyl-CoA inhibits CTP1 activity Glucagon activates AMPK, which inactivates ACC Transcriptional control Non-Alcoholic Fatty Liver Disease (NAFLD) Fatty Acid Oxidation Peroxisome proliferator-activated receptor (PPAR) α activated by fatty acids and promotes transcription of genes that mediate oxidation Sirtuin (SIRT) 1 and 3 histone deacetylases that activate genes that promote oxidation
57 Space of Disse Plasma membrane Cytosol OMM Acyl-CoA IMM Fatty acid oxidation CPT1 CPT2 Acyl-carnitine CACT CO TCA 2 Cycle Citrate OAA Acyl-CoA Acetyl-CoA Acyl-carnitine Ketone body Mitochondria ER
58 Non-Alcoholic Fatty Liver Disease (NAFLD) Fatty Acid Oxidation in NAFLD Evidence for decreased fatty acid oxidation Impaired mitochondrial ATP synthesis in livers of patients with NAFLD Evidence for increased fatty acid oxidation Increased rats of fatty acid oxidation in NAFLD patients
59 Space of Disse Plasma membrane Cytosol OMM Acyl-CoA IMM Fatty acid oxidation CPT1 CPT2 Acyl-carnitine CACT CO TCA 2 Cycle Citrate OAA Acyl-CoA Acetyl-CoA Acyl-carnitine Ketone body Mitochondria ER
60 Unchanged Oxidation in NAFLD Oxidation
61 Secretion Secretion
62 Non-Alcoholic Fatty Liver Disease (NAFLD) Hepatic triglycerides are secreted in VLDL particles Triglyceride-rich lipoprotein Formed in liver by cotranslational lipidation of apob-100 by microsomal triglyceride transfer protein (MTP) Regulation Hepatic Triglyceride Secretion Triglyceride synthesis/availability Insulin-mediated MTP transcription via FoxO1 ApoB-100 degradation
63 Space of Disse VLDL Plasma membrane Cytosol OMM IMM Mitochondria VLDL Synthesis TG + PL MTP VLDL ER
64 Assembly and Secretion of VLDL Presence of Triglycerides ApoB ApoB Endoplasmic MTP MTP Absence of Triglycerides Reticulum Degradation of apob
65 Non-Alcoholic Fatty Liver Disease (NAFLD) Control of VLDL Production by Insulin Kamagate, Cell Cyle 2008
66 Non-Alcoholic Fatty Liver Disease (NAFLD) Hepatic Triglyceride Secretion in NAFLD Increased triglyceride supply due to insulin resistance Hepatic uptake of fatty acids Increased de novo lipogenesis Reduced degradation of apob-100 Regulation Increased MTP transcription due to insulin resistance
67 Non-Alcoholic Fatty Liver Disease (NAFLD) Overproduction of VLDL in NAFLD Kamagate, Cell Cyle 2008
68 Space of Disse VLDL Plasma membrane Cytosol OMM IMM Mitochondria VLDL Synthesis TG + PL MTP VLDL ER
69 Increased Secretion in NAFLD, But not Sufficient to Compensate Secretion
70 Space of Disse Plasma Fatty Acids Fatty acid uptake VLDL Plasma membrane Cytosol de novo Lipogenesis ACS Palmitic acid FAS Malonyl-CoA Pyruvate ACC Acetyl-CoA Citrate Glucose OMM FATP2 FATP5 CD36 ACS? ACS? ACS Acyl-CoA IMM Fatty acid oxidation CO TCA 2 Cycle Citrate OAA Acyl-CoA Acyl-CoA Acetyl-CoA Pyruvate CPT1 CPT2 Acyl-carnitine CACT Acyl-carnitine Ketone body Mitochondria Acyl-CoA VLDL Synthesis Palmitoyl-CoA (16:0) Stearoyl-CoA (18:0) Oleoyl-CoA (18:1) G-3-P LPA PA DAG TG + PL ELOVL6 SCD1 GPAT AGPAT Lipin1 DGAT MTP VLDL ER
71 Hepatic Triglyceride Balance in NAFLD Synthesis Oxidation Uptake Secretion
72 Metabolic Syndrome Metabolic Syndrome and NASH Abnormal production of hormones & cytokines that regulate inflammatory responses PROinflammatory ANTIinflammatory
73 Fat-Derived Factors Regulate Hepatic Inflammatory Response Fat-Derived Factors Regulate Hepatic Inflammatory Response Fatty Acids Liver Fat Triglycerides Hormones Leptin Resistin Adiponectin Cytokines TNF alpha PAI-1 Neurotransmitters Norepinephrine Angiotensinogen
74 Adiponectin & TNF alpha Adiponectin & TNF alpha Adiponectin (Anti-inflammatory) Inhibits FA uptake Stimulates FA oxidation & lipid export Enhances insulin sensitivity TNF (Pro-inflammatory) Pro-apoptotic Recruits WBC s Promotes insulin resistance Mutually antagonistic
75 Metabolic Syndrome - Cytokine Imbalance Metabolic Syndrome Cytokine Imbalance TNF Pro-inflammatory Pro-apoptotic Recruits WBC s Promotes insulin resistance Adiponectin Anti-inflammatory Inhibits FA uptake Stimulates FA oxidation & lipid export Enhances insulin sensitivity Steatosis (NAFL) + cell death + inflammation (NASH) & insulin resistance
76 Genetics of NAFLD Macaluso, World J Gastroenterol 2015
77 Genetics of NAFLD: PNPLA3 Phospholipase domain containing patatin-like phospholipase 3 Expressed in adipocytes and hepatocytes Lipogenic and lipolytic activity May alter triglyceride lipase and DAG activity
78 Genetics of NAFLD: PNPLA3 G allele associated with hepatic steatosis Allele frequency Latino ancestry: 39% European ancestry: 23% African ancestry: 17% Mirrors population prevalence of NAFLD
79 Microbial Dysbiosis and NAFLD Weiland, Aliment Pharmacol Ther 2015
80 Microbial Dysbiosis and NAFLD: Altered Bile Acid Metabolism Weiland, Aliment Pharmacol Ther 2015
81 Non-Alcoholic Fatty Liver Disease (NAFLD) Non-Alcoholic Fatty Liver Disease (NAFLD) Diagnosis
82 Diagnosis Goals Diagnostic Goals Determine etiology of liver disease Distinguish specific type of fatty liver Establish clinical severity
83 Diagnostic Goal #1 Determine Etiology is FLD Determine Etiology Consider NAFLD in patients with The Metabolic Syndrome obese type 2 diabetic hypertensive dyslipidemic Fatty liver on an imaging study Elevated serum AST or ALT Cryptogenic cirrhosis
84 Diagnostic Goal #1 Determine Etiology is FLD Determine Etiology Laboratory findings AST, ALT < 10x uln and may be normal Negative tests for other liver diseases HBV, HCV, AIH, PBC, HH, Wilson s, 1-AT Markers of metabolic syndrome Hyperglycemia, elevated HgbA1C, hyperlipidemia No specific serologic marker for NAFLD
85 Diagnostic Goal #1 Determine Etiology is FLD Determine Etiology Test limitations Standard imaging tests may under- or overestimate liver fat content Fat on imaging test does not exclude other liver diseases Positive tests for other liver diseases do not exclude NAFLD
86 Diagnostic Goal #2 Specify Type of FLD Type of Fatty Liver: Alcoholic (AFLD) vs. NAFLD History distinguishes AFLD/NAFLD NAFLD implies no or safe * EtOH ingestion women < 1 drink/d, men < 2 drinks/d Safe levels of alcohol may vary May often coexist
87 Diagnostic Goal #3 Establish Severity Establish Severity General Themes Clinical prognosis depends on histology Steatosis generally benign Steatohepatitis increases risk for cirrhosis Signs of portal HTN identify high risk group
88 Diagnostic Goal #3 Establish Severity Establish Severity Liver Biopsy is gold standard Limitations Sampling error Risk Expense Impact on management
89 Diagnostic Goal #3 Establish Severity Establish Severity Blood Tests Aminotransferase level not useful Can be normal in advanced disease AST/ALT ratio may help High in cirrhotic NAFLD Thrombocytopenia suggests cirrhosis Hyperbilirubinemia, hypoalbuminemia and elevated PT are late findings
90 Diagnostic Goal #3 Establish Severity Establish Severity Imaging Tests Cannot distinguish NAFLD from NASH or early cirrhosis Stigmata of portal HTN suggest cirrhosis May detect unsuspected HCC
91 Diagnostic Goal #3 Establish Severity Composite Indices Establish Severity Clinical/laboratory parameters age >45-50, obesity or DM suggest bridging fibrosis Fibrosis markers Platelets Fibrotest Emerging markers Elastography (Fibroscan/ultrasound, MR)
92 Non-Alcoholic Fatty Liver Disease (NAFLD) Non-Alcoholic Fatty Liver Disease (NAFLD) Management
93 Weight Loss & Exercise are the Cornerstones of NASH Therapy Weight loss 3-5% weight loss improves steatosis 7-10 % weight loss has been associated with a significant reduction in NAS Weight loss surgery 69% had complete resolution of NASH 65% had partial or complete improvement in fibrosis Exercise in absence of weight loss decreases steatosis Ekstedt, J Hepatol 2007 Mummadi, Clin Gastroenterol Hepatol 2008 Pomrat, Hepatology 2010
94 Vitamin E Improves Steatosis & Inflammation RCT of 247 patients with biopsy proven NASH but without DM Vitamin E 800 units daily Vitamin E decreased lobular inflammation and steatosis No change in fibrosis Current recommendation: Consider use in nondiabetic NASH Sanyal, NEJM 2010
95 Pioglitazone Improves Inflammation in NASH Pioglitazone 30-45mg daily for weeks Necroinflammation and steatosis improved considerable in pioglitazone group No improvement in fibrosis Not recommended for NAFLD Belfort, NEJM, 2006 Sanyal, NEJM, 2010
96 Vitamin E and Prostate Cancer men randomized to selenium, vitamin E or both agents, or both matched placebos for 7-12 years. Compared with placebo, the absolute increase in risk of prostate cancer per 1000 personyears was 1.6 for vitamin E, 0.8 for selenium, and 0.4 for the combination. Use vitamin E with caution in men with NASH Klein, JAMA 2011
97 Diagnosis, Monitoring, and Management Considerations for NAFLD Rinella, JAMA 2015
98 Management Algorithm for Patients with NAFLD Ahmed, Clin Gastroenterol Hepatol 2015
99 Managing Metabolic Disease in NAFLD: Treatment Targets Corey, Clin Liver Dis 2012
100 Pharmacotherapy Under Investigation Anti-NAFLD Obetacholic Acid GFT-505 Aramchol Liragutide Anti-Fibrotic Emricasan Simtuzumab Cenicriviroc GR-MD-02
101 Non-Alcoholic Fatty Liver Disease (NAFLD) Non-Alcoholic Fatty Liver Disease (NAFLD) Terminology Epidemiology Pathophysiology Diagnosis Treatment
102 Non-Alcoholic Fatty Liver Disease (NAFLD): Take Home Messages Non-Alcoholic Fatty Liver Disease (NAFLD) NAFLD is an overarching term that encompasses NAFL and NASH. NAFLD affects approximately 20% of people; NAFL and NASH progress to cirrhosis at rates of ~3% and ~30% in 10 years, respectively. Insulin resistance is the underlying pathophysiological defect leading to NAFLD. NALFD is diagnosed by histopathology, with laboratory and imaging techniques providing much less definitive information. The treatment of NAFLD is largely oriented towards weight loss, with pharmacological approaches in development.
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