A Swift Kick in the ASP
ASP is another hormone secreted by fat cells, with several effects. First, ASP can increase LPL activity, making fatty acids available for transport into the fat cells. Second, ASP increases the expression of glucose transporters in fat cells, allowing them to bring in the glucose required to store fat. So ASP plays roughly the same role as insulin in fat storage, but rather than being generated by the pancreas in response to carbohydrates, is generated by the fat cells themselves. Better yet, ASP stimulates the production of triglycerides inside the fat cells. But what causes ASP to be secreted?
The answer, at least in test-tubes, is chylomicrons. When fat cells are exposed to chylomicrons they generate lots of ASP. By contrast, exposing the same cells to glucose, fatty acids, VLDL, HDL, or LDL elicits little ASP response. Further, the ASP response exhibits both a time and concentration dependence on chylomicron concentration.
This is an important clue. As discussed above, chylomicrons are the first step in transporting dietary fats into the body. When you eat a lot of fat, you make more chylomicrons, which causes the fat cells to make more ASP, which stimulates greater fat storage. But the chylomicrons only hang around for a relatively short time, being converted in the liver to VLDL. The receptor for VLDL (VLDL-R), when activated, does increase LPL activity, but to my knowledge does not stimulate glucose transport into fat cells. Thus the fat in VLDL is available to be used for energy, because the LPL frees the fatty acids for transport across cell membranes; but without some other hormonal signal (e.g. insulin), rather little of this fat can be stored in adipose tissue.
Two questions then arise in the context of a low-carbohydrate/high-fat diet. The most obvious one is "can I get fat by eating too much fat?" Taubes lays out the case that overconsumption of carbohydrates drives fat storage through the action of insulin, but can overconsumption of fat do the same via the action of ASP? When viewed with the most narrow lens, the answer is clearly "yes". While insulin's effects on LPL and glucose transport are considerably stronger than ASP, ASP does ultimately trigger the same conditions leading to fat storage. So if you eat enough fat for a long enough time, in principle you will become obese.
While it may be hard to gain fat through a high-fat diet, it is likely possible to keep on a certain level of body-fat. Low-carbohydrate diets are known to "stall", where the last 20 or so pounds just won't come off, regardless of carbohydrate restriction. I suspect our friend ASP plays a crucial role here. The low insulin levels on a low-carb diet will allow the fat cells to free fatty acids, but if you are consuming enough fat, at some point this effect will be balanced by that of ASP, and voila, no more fat loss.