Hepatic fat content is a determinant of postprandial triglyceride levels in type 2 diabetes mellitus patients with normal fasting triglyceride

In vivo characterization of the liver fat 1H MR spectrum

“…(4) estimated that peaks 1 and 2 contained 15% of the total fat signal. Their 15% value has been widely used to correct for inferred fat under the water peak (7,30–32), but differs considerably from the value of 8.6% derived from our study. From Table 1, the fat under the water peak is equal to 2 × ndb + 5.…”

Comparison of free fructose and glucose to sucrose in the ability to cause fatty liver

“…Both diets induced fatty liver and increased hepatic TG content, although this tended to be worse in the FG group. We also documented that postprandial levels of TGs positively correlated with fatty liver score and intrahepatic TGs; similar findings have been observed in human studies [10, 30, 35]. In this regard, it is known that the maximal effects of fructose on TGs are best observed in the postprandial state, and recent studies by Stanhope et al [41] have shown that this is particularly true in overweight humans fed fructose.…”

“…Recent studies showed that 59% of TG within hepatocytes arose from the plasma-free fatty acid pool in the fed state [10]. Interestingly, three studies have shown that postprandial hypertriglyceridemia correlates with fat liver content [25, 30, 35]. In one study of patients with type-II diabetes mellitus and normal fasting TG, the increase in postprandial TG levels was directly predicted by the amount of hepatic fat [30].…”

“…Interestingly, three studies have shown that postprandial hypertriglyceridemia correlates with fat liver content [25, 30, 35]. In one study of patients with type-II diabetes mellitus and normal fasting TG, the increase in postprandial TG levels was directly predicted by the amount of hepatic fat [30]. In this regard, the administration of fructose-sweetened beverages providing 25% of the daily caloric intake for 10 weeks was shown to increase hepatic de novo lipogenesis and reduce postprandial lipoprotein lipase activity suggesting that both mechanisms may contribute to fructose-induced postprandial hypertriglyceridemia [41].…”

Difference between Fasting and Nonfasting Triglyceridemia; the Influence of Waist Circumference

“…In subjects with increased visceral adiposity and concomitant insulin resistance, increased lipolysis of visceral adipocytes that is presumably caused by insulin resistance contributes to the increase in postprandial delivery of fatty acids to the portal circulation 16,35) . Another possible explanation may be that excess liver fat content plays a dominant role in postprandial hypertriglyceridemia in subjects with expanded waist circumference 36,37) . It is reported that hepatic TG represents the driving force for very-low-densitylipoprotein (VLDL) assembly and that secretion of large VLDL increases with increasing liver fat content 38) .…”