Low liver fat may be bad for the heart

The distribution of body fat contributes to the risk of coronary heart disease (CHD), with the risk of cardiovascular events further increasing among individuals with low liver fat (LF) and high visceral adipose tissue (VAT) or abdominal fat, results of a recent study have shown.

Such finding indicates that liver triglyceride regulation has a significant impact on cardiovascular health in individuals with frictional VAT and LF.

“Recent studies have shown different fat deposits have variable impact on the development of cardiometabolic disease, said co-author Jennifer Linge, lead scientist at AMRA Medical AB in Linköping, Sweden, who presented the study at The Liver Meeting Digital Experience by the American Association for the Study of Liver Diseases (AASLD 2020).

“Understanding patients’ individual way of storing fat can be valuable in developing targeted prevention and treatment strategies,” she added.

Linge and her team used magnetic resonance images scanned from 12,276 individuals in the UK Biobank imaging study to measure VAT and liver proton density fat fraction. Then, they divided participants into four phenotype groups defined by sex-specific median values of VAT and LF: low VAT-low LF, low VAT-high LF, high VAT-low AF, and high VAT-high LF.

The associations of VAT-LF groups with incident CHD (ischaemic heart disease or presence of aortocoronary bypass graft) were assessed using logistic regression. The researchers also calculated odds ratios (ORs) and 95 percent confidence intervals (CIs) with low VAT-low LF as reference, with an additional analysis adjusting for age and body mass index (BMI).

Participants (mean age, 62.6 years; 51 percent females; BMI, 26.6 kg/m²) were followed for a mean of 1.3 years, with a total of 176 CHD events recorded following imaging. Sex-specific median values for females and males were 2.3 and 4.7 L for VAT and 2.2 percent and 3.1 percent for LF, respectively.

The combination of high VAT and low LF showed the most robust association with an increased risk of incident CHD (OR, 2.33, 95 percent CI, 1.50–3.58; p<0.001). On the other hand, the combination of low VAT and high LF did not correlate with higher CHD risk (OR, 0.81, 95 percent CI, 0.42–1.45; p=0.495). [AASLD 2020, abstract 89]

After adjusting for confounding factors, the strong association between high VAT-low LF and increased CHD risk persisted (adjusted OR, 1.65, 95 percent CI, 1.03–2.63), but the relation of high VAT-high LF with CHD was reduced (adjusted OR, 1.00, 95 percent CI, 0.64–1.58; p=0.983).

“These results indicate the importance of proper liver triglyceride regulation in the context of visceral adiposity,” Linge said, noting that a decrease in liver fat alone might be insufficient to reduce the cardiometabolic risk of patients with nonalcoholic fatty liver disease.

“In fact, it seems that a decrease in liver fat without a resolution of visceral obesity may put the patient at a greater risk of developing heart disease. This is what we want to investigate further,” she added.

Further research is warranted to determine if a discordant VAT-LF phenotype is an expression of an inability to handle ectopic fat deposition via the liver associated with incident CHD, and if decreased LF due to liver dysfunction heightens CHD risk, according to the researchers.