A study by Elisa Fabbrini and colleagues found that intrahepatic triglyceride (IHTG) content, not visceral adipose tissue (VAT), is a better marker of metabolic complications associated with obesity. The research compared groups of obese individuals with varying IHTG levels but similar VAT volumes, and vice versa. Using stable isotope tracer techniques and euglycemic-hyperinsulinemic clamps, they assessed insulin sensitivity and very-low-density lipoprotein-triglyceride (VLDL-TG) secretion rates. They also evaluated tissue biopsies to examine factors involved in ectopic triglyceride accumulation. The study found that individuals with higher IHTG had significantly lower insulin sensitivity in the liver, adipose tissue, and skeletal muscle, and a much higher VLDL-TG secretion rate compared to those with normal IHTG. Additionally, adipose tissue CD36 expression was lower, while skeletal muscle CD36 expression was higher in those with higher IHTG. These findings suggest that IHTG, not VAT, is a better marker of metabolic dysfunction in obesity. The study also indicates that alterations in tissue fatty acid transport may contribute to ectopic triglyceride accumulation by redirecting plasma fatty acid uptake from adipose tissue to other tissues. The study challenges the traditional view that VAT is the primary contributor to metabolic complications in obesity. It shows that VAT may simply be a marker of IHTG, which is more directly linked to metabolic disease. The findings suggest that IHTG is an independent predictor of insulin resistance and dyslipidemia, and that changes in CD36 expression in adipose tissue and skeletal muscle may play a role in the pathogenesis of ectopic triglyceride accumulation and metabolic disease. The study also highlights the importance of IHTG as a marker of metabolic complications associated with obesity.A study by Elisa Fabbrini and colleagues found that intrahepatic triglyceride (IHTG) content, not visceral adipose tissue (VAT), is a better marker of metabolic complications associated with obesity. The research compared groups of obese individuals with varying IHTG levels but similar VAT volumes, and vice versa. Using stable isotope tracer techniques and euglycemic-hyperinsulinemic clamps, they assessed insulin sensitivity and very-low-density lipoprotein-triglyceride (VLDL-TG) secretion rates. They also evaluated tissue biopsies to examine factors involved in ectopic triglyceride accumulation. The study found that individuals with higher IHTG had significantly lower insulin sensitivity in the liver, adipose tissue, and skeletal muscle, and a much higher VLDL-TG secretion rate compared to those with normal IHTG. Additionally, adipose tissue CD36 expression was lower, while skeletal muscle CD36 expression was higher in those with higher IHTG. These findings suggest that IHTG, not VAT, is a better marker of metabolic dysfunction in obesity. The study also indicates that alterations in tissue fatty acid transport may contribute to ectopic triglyceride accumulation by redirecting plasma fatty acid uptake from adipose tissue to other tissues. The study challenges the traditional view that VAT is the primary contributor to metabolic complications in obesity. It shows that VAT may simply be a marker of IHTG, which is more directly linked to metabolic disease. The findings suggest that IHTG is an independent predictor of insulin resistance and dyslipidemia, and that changes in CD36 expression in adipose tissue and skeletal muscle may play a role in the pathogenesis of ectopic triglyceride accumulation and metabolic disease. The study also highlights the importance of IHTG as a marker of metabolic complications associated with obesity.