*Hepatic Lipid Homeostasis in NAFLD DOI: http://dx.doi.org/10.5772/intechopen.108168*

concentrations [82, 83], there do not exist a definite positive correlation between plasma TG concentrations and the hepatic steatosis. In response to excess hepatic fat, NAFLD patients actually secrete more VLDL-TG than do subjects without NAFLD. ApoB100 and MTTP are associated with VLDL secretion, and serve as key components in hepatic VLDL secretion and in maintaining hepatic lipid homeostasis. The transcription of MTTP could be upregulated by PPARα and its expression parallels with ApoB100 secretion, while insulin could reduce hepatic lipid secretion by inducing ApoB100 degradation and suppressing MTTP synthesis, which downregulates both ApoB100 and MTTP [83, 84]. In normal liver, high level of insulin levels during post-prandial state facilitates the mobilization of dietary lipids rather than hepatic VLDL, while the selective hepatic insulin resistance in NAFLD may induce insulin to stimulate DNL without inhibiting VLDL production, indirectly increasing the secretion of VLDL. Although VLDL particles overproduction has been reported in patients with NAFLD, ApoB100 secretion is unchanged. Further study demonstrated that VLDL particles secreted as a more TG-rich and larger form than those in normal people [85]. Notably, while intrahepatic lipid accumulation increases VLDL-TG secretion, when hepatic fat content exceeded 10%, the capacity of VLDL-TG secretion is unable to compensate the lipid metabolic homeostasis. Besides, compared to no disease controls, NAFLD patients with more advanced steatosis had lower MTTP levels, which indicate that lipids accumulation may impair lipid secretion [81].

The association between dietary structure and VLDL secretion has been identified in several studies, which suggest the more significant effect of sugar than that of fat and carbohydrate on VLDL secretion. A study compared the influence of sugarenriched diet and less sugar diet, which found that the former could significantly increase the VLDL1-TG production rate in patients with or without NAFLD [86], while the VLDL2 production rate increased only after the high sugar diet in NAFLD [86]. While for dietary fat, study found that the level of monounsaturated FAs in the diet may not affect the production of VLDL1 and VLDL2 in patients with mild hypercholesterolemia [87]. Moreover, study demonstrated that although high-carbohydrate diet could induce higher VLDL-TG concentrations and a lower VLDL-TG uptake than control diet in normal or hypertriglyceridemia individuals, two groups did not have different responses [88].
