The following are pieces of the article that I found the most interesting. Remember, if you don't have access to scholarly databases and want to read the article, you should be able to get a log-in for your local public library's proxy and then be able to look up journal articles.
1.) Low glycogen promotes insulin action, whereas high glycogen promotes insulin resistance. Glycogen is primarily elevated by eating carbohydrates.
"Prevention of glycogen synthesis, by fasting or feeding a low-carbohydrate/high-fat diet, results in a persistence of contraction and insulin-mediated glucose transport that lasts as long as carbohydrates are not consumed. This line of work shows that low glycogen promotes increased insulin action, whereas high glycogen promotes insulin resistance."
2.) People who are metabolically damaged respond more positively to restricting carbohydrate intake than people who are not metabolically damaged.
"That patients with MetS [metabolic syndrome] might be particularly sensitive to carbohydrate restriction was suggested by Cornier et al.  who compared the response of obese insulin-sensitive and obese insulin-resistant subjects randomized to either a high-carbohydrate (60%) or lower carbohydrate (40%) diet. Weight loss was similar for the insulin-sensitive group irrespective of carbohydrate level. The most striking result was that only the insulin-resistant group showed a major change in any lipid parameter with a 42% average decrease in TG on lower carbohydrate, and a 27% increase on higher carbohydrate. That individuals with MetS or insulin resistance syndrome respond better to restricting carbohydrates than fat is consistent with intolerance to carbohydrate as the fundamental metabolic problem."
3.) The saturated fat levels in your blood are higher when eating carbohydrates. Go figure.
"If carbohydrate intake were low enough to decrease levels of glucose and insulin, however, a high SFA intake would be processed very differently. We recently showed, for example, a disconnect between dietary SFA and plasma levels of SFA apparently due to the regulatory role of dietary carbohydrate in controlling de novo lipogenesis (DNL)...
A notable result was that, despite a 3-fold higher intake of dietary saturated fat during the VLCKD [very low carb], saturated fatty acids in TG [triglyceride] and cholesteryl ester were significantly decreased compared to subjects consuming the LFD [low fat diet]. That this was due to a decrease in DNL [de novo lipogenesis] was shown by a corresponding reduction in palmitoleic acid (16:1n-7), an endogenous indicator of this process."
4.) Glucose, independent of insulin, also has an effect on fat storage.
"Expression of the lipogenic genes occurs without any apparent effect of insulin indicating one way in which glucose directly regulates nutrient partitioning."
5.) It's not about calories per se.
"It is worth noting that many changes in lipid metabolism during fasting are due to the specific removal of carbohydrate as opposed to a general elimination of calories."
6.) This was the most interesting one. Insulin resistance occurs in the muscles and liver first, and when this happens, your body has no choice but to convert the glucose in your blood stream into fat (either de novo lipogenesis or manufacture of triglycerides). This is an interesting concept on a few levels. One thing is, any studies done on people who are NOT insulin resistant could be IRRELEVANT for those who are.
("There are truths which are not for all men, nor for all times."--Voltaire)
"The fate of a dietary carbohydrate load in lean insulin-resistant and insulin-sensitive men was determined using a combination of 1H and 13C NMR spectroscopy to assess liver and muscle triglyceride and glycogen synthesis, respectively, and deuterium enrichment to assess de novo lipogenesis. The insulin-resistant men showed impaired skeletal muscle and hepatic glycogen formation following intake of dietary carbohydrate. Consistent with the paradigm presented in Fig. 1, dietary carbohydrate in the insulin-resistant group was instead diverted toward hepatic DNL [de novo lipogenesis] and TG [triglyceride] synthesis that contributed to a significant increase (60%) in plasma TG levels."
7.) A short study probably shows jack when it comes to metabolism.
"The time course of metabolic adaptations is also variable; some lipolytic adaptations occur within a week (e.g., gene expression of FAT/CD36 and b HAD) while others take longer (e.g., FABP and CPT I). Several weeks may be necessary for complete switch to optimal fat utilization."
8.) Fatty acid oxidation is increased with carbohydrate restriction. According to Lippincott's Illustrated biochemistry text, fatty acid oxidation is the primary source of fuel when starving. We know that decreased carbohydrate intake is similar to starving when it comes to how your body mobilizes fat stores.
"The hormonal changes that accompany carbohydrate restriction, fasting or continued physical activity lead to inhibition of glycogen synthesis and inactivation of acetyl-CoA carboxylase and a fall in malonyl-CoA levels which, in turn, relieves inhibition of carnitine transport and thereby stimulates fatty acid oxidation."
All very interesting stuff.