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Hypertriglyceridemia in the Obese is Due to Two Defects

Obesity is a recognized risk factor for heart disease, but it is the location of fat — in the belly or in the liver — that combines to drive metabolic defects that produce hypertriglyceridemia, researchers found.

Between two groups of obese patients with similar BMI and visceral fat volume, patients with higher liver and subcutaneous abdominal fat were found to have increased very low density lipoprotein1 (VLDL1) levels, Jan Borén, MD, of the University of Gothenburg in Sweden, and colleagues reported. 

In addition, those with increased plasma levels of apolipoprotein C-III (apoC-III) were more likely to have impaired triglyceride clearance, the authors wrote. “Our results show for the first time that serum concentration of triglycerides in obese subjects is increased by dual metabolic defects, namely the combination of increased secretion (linked to increased liver and subcutaneous abdominal fat) and severely impaired clearance of triglyceride-rich VLDL1 particles (associated increased plasma levels of apoC- III),” Borén wrote. 

“It should be recognized that serum triglyceride levels are dependent not only on the secretion capacity but also on the removal capacity of triglyceride-rich lipoproteins,” the authors added.

The study measured liver, subcutaneous abdominal, and visceral fat of 38 middle-aged, white, Finnish men, including 14 obese patients with high triglycerides, 14 obese patients with normal triglycerides, and 10 nonobese patients with normal triglycerides as a control. The average age of each group was 52, 55, and 48, respectively. Liver fat was measured with proton MR spectroscopy, and subcutaneous abdominal and visceral fat were measured with MRI. None of the patients were taking any lipid lowering or modifying drugs, the authors wrote. 

Liver and subcutaneous fat correlated with serum triglycerides both overall and in obese patients (P<0.05 for all). Moreover, obese patients with elevated triglycerides had a "significantly increased secretion of VLDL1-triglycerides” and apolipoprotein B100 (apoB100) compared with the two normal triglyceride groups. Removal of the VLDL1 and apoB100 triglycerides was roughly 50% lower in the high triglyceride group compared with the two normal triglyceride groups. Levels of apoC-III did not correlate with VLDL1 secretion rates, but they did correlate with the fractional catabolic rate of VLDL1-triglycerides and apoB100. 

Borén and colleagues concluded that management of liver fat is a metabolic component of hypertriglyceridemia that is modifiable by patients through diet and lifestyle.

Furthermore, “the results emphasize the clinical importance of assessing hypertriglyceridemic waist to identify obese subjects at high cardiometabolic risk,” they said. 

Practice Pearls:  

  • Note that hypertriglyceridemia and cardiovascular risk are not uniformly observed in obese patients. 
  • Note that this study suggests that hypertriglyceridemia in the obese is due to two defects: increased secretion (associated with increased liver and subcutaneous abdominal fat) and reduced clearance of VLD1 due to increased plasma levels of apolipoprotein C-III.
Borén J, et al “Dual metabolic defects are required to produce hypertriglyceridemia in obese subjects” Arterioscler Thromb Vasc Biol 2011; DOI:10.1161/ATVBAHA.111.224808.