High Triglycerides in Obesity: Dual Metabolic Defects
July 27, 2011 — Results from a study of 38 men provide new insights into the mechanisms that trigger hypertriglyceridemia in obese men.
"Our results show for the first time that the 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 [very-low-density lipoprotein] VLDL1 particles (associated with increased plasma levels of apolipoprotein C-III)," write senior author Jan Borén, MD, PhD, from the Department of Molecular and Clinical Medicine, University of Gothenburg, and director of the Wallenberg Laboratory for Cardiovascular Research, in Gothenburg, Sweden, and colleagues.
"These results," published online July 21 and in print September 2011 in Arteriosclerosis, Thrombosis and Vascular Biology: Journal of the American Heart Association, "provide new insights into the pathophysiology of dyslipidemia in obesity."
Dr. Borén and his team used isotope kinetic studies to determine the rate of secretion and turnover of triglycerides and apoprotein B-100 in triglyceride-rich VLDL1 and smaller VLDL2 lipoproteins to find out why some, but not all, obese people develop dyslipidemia.
"Specifically, we tested whether hypertriglyceridemia in obese men with similar [body mass index] (BMI) and waist circumference is caused solely by increased hepatic secretion of VLDL induced by increased liver fat," they write.
The researchers studied 38 men: 14 obese men who were hypertriglyceridemic; 14 obese men who were normotriglyceridemic, but with comparable BMI and visceral fat volume; and 10 normotriglyceridemic men who were of normal weight.
They found that serum triglyceride levels in the obese men were elevated by dual mechanisms: increased secretion and severely impaired clearance of triglyceride-rich VLDL1. They also found that elevated levels of liver and subcutaneous abdominal fat were associated with increased secretion of VLDL1 particles, but increased plasma levels of apolipoprotein C-III were linked with impaired clearance in obese hypertriglyceridemic men.
"[I]t 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 write. "[A]n increased liver fat content represents a dietary- and lifestyle-modifiable 'metabolic' component of hypertriglyceridemia," the authors note, adding, "The results emphasize the clinical importance of assessing [hypertriglyceridemic] waist to identify obese subjects at high cardiometabolic risk."
The study was supported by grants from the Swedish Research Council, the Swedish Heart-Lung Foundation, the Swedish Foundation for Strategic Research, Sigrid Juselius Foundation, Clinical Research institute HUCH Ltd, Novo-Nordisk Foundation, and the European Union-funded projects HEPADIP and ETHERPATHS. The authors have disclosed no relevant financial relationships.
Arterioscler Thromb Vasc Biol. Published online July 21, 2011.
"Our results show for the first time that the 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 [very-low-density lipoprotein] VLDL1 particles (associated with increased plasma levels of apolipoprotein C-III)," write senior author Jan Borén, MD, PhD, from the Department of Molecular and Clinical Medicine, University of Gothenburg, and director of the Wallenberg Laboratory for Cardiovascular Research, in Gothenburg, Sweden, and colleagues.
"These results," published online July 21 and in print September 2011 in Arteriosclerosis, Thrombosis and Vascular Biology: Journal of the American Heart Association, "provide new insights into the pathophysiology of dyslipidemia in obesity."
Dr. Borén and his team used isotope kinetic studies to determine the rate of secretion and turnover of triglycerides and apoprotein B-100 in triglyceride-rich VLDL1 and smaller VLDL2 lipoproteins to find out why some, but not all, obese people develop dyslipidemia.
"Specifically, we tested whether hypertriglyceridemia in obese men with similar [body mass index] (BMI) and waist circumference is caused solely by increased hepatic secretion of VLDL induced by increased liver fat," they write.
The researchers studied 38 men: 14 obese men who were hypertriglyceridemic; 14 obese men who were normotriglyceridemic, but with comparable BMI and visceral fat volume; and 10 normotriglyceridemic men who were of normal weight.
They found that serum triglyceride levels in the obese men were elevated by dual mechanisms: increased secretion and severely impaired clearance of triglyceride-rich VLDL1. They also found that elevated levels of liver and subcutaneous abdominal fat were associated with increased secretion of VLDL1 particles, but increased plasma levels of apolipoprotein C-III were linked with impaired clearance in obese hypertriglyceridemic men.
"[I]t 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 write. "[A]n increased liver fat content represents a dietary- and lifestyle-modifiable 'metabolic' component of hypertriglyceridemia," the authors note, adding, "The results emphasize the clinical importance of assessing [hypertriglyceridemic] waist to identify obese subjects at high cardiometabolic risk."
The study was supported by grants from the Swedish Research Council, the Swedish Heart-Lung Foundation, the Swedish Foundation for Strategic Research, Sigrid Juselius Foundation, Clinical Research institute HUCH Ltd, Novo-Nordisk Foundation, and the European Union-funded projects HEPADIP and ETHERPATHS. The authors have disclosed no relevant financial relationships.
Arterioscler Thromb Vasc Biol. Published online July 21, 2011.
posted by vanwash at 11:27 AM
0 Comments:
Post a Comment
<< Home