AI Article Synopsis
- The PNPLA3-148M variant is linked to higher liver fat but its effect on triglyceride-rich lipoprotein metabolism is unclear.
- In a study comparing homozygous PNPLA3-148M subjects to controls, researchers found liver fat levels were over three times higher in the PNPLA3-148M group.
- Despite the increased liver fat, the production rates of triglycerides and apoB100 in VLDL were similar between the two groups, indicating that VLDL production was not affected by the PNPLA3 variant.
Article Abstract
Background: The phospholipase domain-containing 3 gene (PNPLA3)-148M variant is associated with liver steatosis but its influence on the metabolism of triglyceride-rich lipoproteins remains unclear. Here, we investigated the kinetics of large, triglyceride-rich very-low-density lipoprotein (VLDL), (VLDL ), and smaller VLDL in homozygotes for the PNPLA3-148M variant.
Methods And Results: The kinetics of apolipoprotein (apo) B100 (apoB100) and triglyceride in VLDL subfractions were analysed in nine subjects homozygous for PNPLA3-148M and nine subjects homozygous for PNPLA3-148I (controls). Liver fat was >3-fold higher in the 148M subjects. Production rates for apoB100 and triglyceride in VLDL did not differ significantly between the two groups. Likewise, production rates for VLDL -apoB100 and -triglyceride, and fractional clearance rates for both apoB100 and triglyceride in VLDL and VLDL , were not significantly different.
Conclusions: Despite the higher liver fat content in PNPLA3 148M homozygotes, there was no increase in VLDL production. Equally, VLDL production was maintained at normal levels despite the putative impairment in cytosolic lipid hydrolysis in these subjects.
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| http://dx.doi.org/10.1111/joim.13375 | DOI Listing |
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