First;y Eurekalert is an open access media company. Anyone can publish in it and there is no requirement for papers to be peer reviewed or independant. It is a pay per publish outfit. So articles in it shpuld be viewed as not being gold plated fact.
Secondly, this study was a mouse study, and these are often found to be unreliable in assuming that humans follow the same pathway. The use of standard mouse chow san introduce errors by itself, since it is not what mice normally eat. Then the mice are usually gentically modified mice specially bred to have certain characteristics that can skew the research. Also, where a diabetes topic is being tested, the diabetes is usually induced chemically to mimic diabetes, and is not the same as human metabolic syndrome.
The Keck School of Medicine used to be a faculty within USC university, but was renamed following a major donation from the W.M Keck foundation, which continues to fiund it, It is a private faculty and runs its own private clinics in the area. The W M Keck foundation is a family based organisation associated with the petroleum industry.
As has already been mentioned, the curent understanding of endocrinology is that it is not LDL per se that is harmful. LDL is just a transport vehicle for lipids, but when it is damaged by free radicals, radiation etc, then it fragments into small dense LDL (sLDL) which the HDL cannot recognise, and does not collct for recycling in the liver. So sLDL remains in the bloodstream and is not easily removed by the body since it is now an alien component and becomes the main constituent of plaque in the arteries.
Recent studies at Newcastle ac et al has shown that an ultra low calorie or a low carb ketogenic diet can remove the fatty buildup due to NAFLD, and so it seems to imply that having carbs is to blame for the buildup in the liver and that a high fat diet in its own is not to blame. Meta studies also show that having a low LDL score can actually shorten life expectancy as can having very high LDL (bathtub curve) so it seems we need a moderate level of fat in our diet. Again, using mouse research may not emulate the human condition and may be misleading.
A metastudy of a large human database gives a good indication of how we are dealing with it in the real world. It seems that not only were they feeding the mice high fat diet they were adding extra cholesterol to it. How does that work? humans do not use dietary cholesterol since it is alien, but we make our own cholesterol with our individual biomarkers. Something here raises my hackles, since it seems wrong test method. They started with a hypothesis, and seem to be forcing the condition to prove the hypothesis, but in doing so go against what in most people is a natural body function.
Here is the actual paper
https://www.ncbi.nlm.nih.gov/pubmed/30516830