Obesity linked to increased MASLD and liver fibrosis risk in patients with type 2 diabetes
By Dr Sasha Ellery BM BCh
Six in 10 primary care patients with type 2 diabetes (T2DM) have metabolic dysfunction-associated steatotic liver disease (MASLD), with a small proportion showing early signs of liver fibrosis, finds a new Swedish study. Notably, the risk of advanced liver disease was significantly higher in patients with coexisting T2DM and obesity, researchers reported in The Journal of Internal Medicine.
MASLD, formerly known as nonalcoholic fatty liver disease, refers to excess fat accumulation in the liver due to metabolic dysfunction and, the researchers wrote, is now the most common cause of chronic liver disease globally.
The researchers prospectively studied 308 primary care patients with T2DM (mean age 64 years; 37% female) and found that 59% had MASLD, 14% had suspected significant fibrosis and 7% had suspected advanced fibrosis. Among those with MASLD, body mass index (BMI) was higher and obesity more prevalent compared with patients without the condition.
Professor Simone Strasser, Director of the Liver Foundation and Head of Department of the AW Morrow Gastroenterology and Liver Centre at the Royal Prince Alfred Hospital, Sydney, said the findings reflected what was being seen locally.
In Australia, she said the condition was referred to by consensus as metabolic dysfunction-associated fatty liver disease (MAFLD), which differed slightly from the MASLD definition used in the study. Under the MAFLD definition, a person with hepatic steatosis met the diagnostic criteria if they also had T2DM, were living with overweight or obesity or had two metabolic risk factors. In contrast, the MASLD definition excluded individuals with secondary causes of liver disease, such as significant alcohol use.
‘In a patient with T2DM, they have a significant risk of having MASLD or MAFLD. And if they also have severe obesity, the risk is over 90% – you can assume they have MASLD or MAFLD,’ she told Medicine Today.
The researchers also identified obesity as a key risk factor for advanced liver disease, with participants living with obesity having an eightfold increased risk of fibrotic MASLD. Among those with a BMI of 30kg/m2 or greater, 13% had suspected advanced fibrosis, compared with 2% in patients with normal weight and overweight.
Professor Strasser noted that the Gastroenterological Society of Australia and the Australian Diabetes Society both recommended that patients with diabetes and obesity were assessed for MAFLD, and if they had MAFLD, were risk assessed for fibrosis using the fibrosis-4 score.
Transient elastography was used to assess for liver fibrosis in the study, but access across Australia was varied, she said.
‘FibroScan is available through public hospital liver clinics. Some machines are [available] in the community and there are portable versions,’ Professor Strasser explained. She said most ultrasound practices likely used shear wave elastography, a less validated technology that was more widely available but considered less reliable.
Notably, in the study, cardiac MRI revealed left ventricular changes, such as reduced stroke volume and increased concentricity, in the MASLD group, despite no differences in overt cardiovascular disease.
‘A finding of MAFLD can predate the structural changes in the heart – so [it is] potentially an early marker of other cardiometabolic complications,’ Professor Strasser said. ‘The most common cause of death in patients with MAFLD is cardiovascular disease... increasingly heart failure and arrhythmias such as atrial fibrillation.’
The researchers said their findings supported a targeted screening approach. In the absence of obesity, MASLD was rarely associated with fibrosis, but among patients with obesity, early liver damage was not uncommon.
For GPs, Professor Strasser said, ‘[It is] important to be aware of the need to screen for [MAFLD] in patients with risk factors, or the presence of hepatic steatosis.’ Early identification was critical, as timely lifestyle and metabolic interventions might help prevent progression and potentially reverse liver damage.