How liver manage fat of different origins: dietary, de novo synthesis, release from adipose tissue

Overview of hepatic fatty acid metabolism in the postprandial state. Fatty acids enter a pool where they may be partitioned into oxidation (1) or esterification (2) pathways. There are TG storage and secretory pools. Fatty acids liberated from the hydrolysis of TG in the secretory TG pool, or TG particles, may then be partitioned to a storage TG pool (3). TG in the secretory pool is utilised for very low-density lipoprotein (VLDL) production (4) which enters systemic circulation. It remains unclear if fatty acids liberated from the TG pools enter oxidation pathways (dotted line, (5)). Abbreviations: TG, triglyceride; VLDL, very low-density lipoprotein; DNL, de novo lipogenesis; FA, fatty acid; NEFA, non-esterified fatty acids; ApoB, apolipoprotein B; 3OHB, 3-hydroxybutyrate; ER, endoplasmic reticulum.

For instance if you have big fat stores, if you eat lot of sugars and no fat, your liver will synthetize VLDL... Despite your fat intake is very low.
Second example if you are on a low carb diet, if your BMI and W/H ratio are normal your liver has less sources of de novo lipogenesis, less free fatty acids released by fat stores and will only rely on your fat intake to synthesize VLDL.

"Determining the contribution of specific fatty acid sources (Figure 1) can be achieved with the use of stable-isotope tracers. Using a multi-tracer approach Donnelly et al. [48] determined the contribution of specific sources of fatty acid to liver and VLDL-TG in NAFLD patients (n = 8). After five days of labeling, they reported there was no difference in the contribution of fatty acids originating from systemic NEFA, DNL or diet to liver and VLDL-TG [48]. On the basis of this observation, the authors suggested that VLDL-TG may be used as a surrogate marker of the liver TG/fatty acid pool [48]. Dietary fatty acids have been reported to contribute 2%–28% of VLDL-TG [48,49,50,51]. Fatty acids originating from systemic NEFA contribute 45%–75% and from hepatic DNL fatty acids contribute 13%–37% to VLDL-TG [48,49,50,51]. The wide-range in findings may be explained by differences in the length of the postprandial phase, the type of test meal fed and hepatic uptake, and/or alterations in the turnover time of the hepatic TG pool, which may be influenced by size of the pool."

Some insights in the different sources of hepatic synthesis of VLDL.

And this remark:
"These data demonstrate that the most important contributing factor to whether liver fat accumulation occurs is the amount of total energy consumed, rather than the composition of the diet. Notably, liver fat decreases more rapidly when a hypo-caloric diet devoid of carbohydrate is consumed, compared to calorie restriction alone [62,64]."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4245577/