Author information
1
Centre for Obesity Research and Education, Central Clinical School, Monash University, Level 6, 99 Commercial Road, Melbourne, 3181, Australia. geraldineooi@gmail.com.
2
Department of General Surgery, The Alfred Hospital, Melbourne, Australia. geraldineooi@gmail.com.
3
Centre for Obesity Research and Education, Central Clinical School, Monash University, Level 6, 99 Commercial Road, Melbourne, 3181, Australia.
4
Department of General Surgery, The Alfred Hospital, Melbourne, Australia.
5
Department of Physiology, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Australia.
6
Department of Physiology, School of Biomedical Sciences, Melbourne University, Parkville, Australia.
7
Biostatistics, School of Public Health and Preventative Medicine, Monash University, Melbourne, Australia.
8
Department of Gastroenterology, The Alfred Hospital, Melbourne, Australia.
9
Department of Anatomical Pathology, The Alfred Hospital, Melbourne, Australia.
Abstract
BACKGROUND:
Non-alcoholic fatty liver disease (NAFLD), driven by the obesity epidemic, has become the most common form of liver disease. Despite this, there is controversy regarding the prevalence and severity of NAFLD in obesity. Obesity-related factors, such as increasing adiposity, metabolic disease and inflammation, may influence prevalence. We therefore prospectively measured NAFLD prevalence in obesity and studied factors associated with NAFLD.
MATERIALS AND METHODS:
We recruited consecutive bariatric patients. Intraoperative liver biopsies were taken. The liver, adipose tissue and serum were collected to measure inflammation. Adipocyte cell size was measured. NAFLD severity was correlated to body mass index (BMI), metabolic health and adipose characteristics.
RESULTS:
There were 216 participants; BMI 45.9 ± 8.9 kg/m2, age 44.4 ± 12.1 years, 75.5% female. Overall NAFLD prevalence was 74.1%, with 17.1% having non-alcoholic steatohepatitis (NASH) and/or steatofibrosis. Odds of NASH/steatofibrosis increased independently with BMI category (odds ratio (OR) 2.28-3.46, all p < 0.05) and metabolic disease (OR 3.79, p = 0.003). These odds markedly increased when both super obesity (BMI > 50) and metabolic disease were present (OR 9.71, p < 0.001). NASH/steatofibrosis prevalence was significantly greater with diabetes, hypertension and dyslipidemia. Although greater visceral adipocyte hypertrophy was evident in NASH/steatofibrosis, there was no significant association between adipose inflammation and NASH/steatofibrosis.
CONCLUSION:
NAFLD remains endemic in obesity; however, NASH/steatofibrosis are less common than previously reported. Worsening obesity and metabolic disease increase odds of NAFLD independently, with substantially compounded effect with both. These observations may help with risk stratification in obese populations. We were unable to delineate clear associations between adipose inflammation and NASH/steatofibrosis in this obese population.
TRIAL REGISTRATION:
Australian Clinical Trials Registry ( ACTRN12615000875505 ).