Zitat:
Do very-low-carbohydrate diets cause insulin resistance?
Despite concern that very-low-carbohydrate diets, especially if high in saturated fat, might lead to insulin resistance, the link between saturated fat and insulin resistance is tenuous.
Further, data from three recent studies that used the insulin clamp technique indicate that very-low-carbohydrate diets do not have an adverse effect on glucose metabolism or insulin resistance.
Collectively, these studies indicate that very-low-carbohydrate diets alter the effects of insulin on oxidative and nonoxidative glucose disposal, favoring storage of glucose as glycogen in muscle. They also appear to prevent insulin-stimulated inhibition of lipid oxidation.
Data from these studies do not support the notion that very-low-carbohydrate diets exacerbate the risk of type 2 diabetes and insulin resistance; rather, they actually show a potential favorable effect as evidenced by decreased basal endogenous glucose production and improved insulin-stimulated nonoxidative glucose disposal.
Was das Thema der freien Fettsäuren angeht, so ist es letztendlich auch nicht uninteressant, dass gerade bei einer Ernährung mit hohem GI die Menge der freien Fettsäuren über den gesamten Tag geringer ist als bei einer Ernährung mit geringem GI, dennoch führt nicht die geringglykämische Ernährung eher zum Diabetes, sondern die hochglykämische.
Zitat:
Although low-carbohydrate diets tend to normalize insulin and blood glucose levels in many
individuals, a little known effect is increased insulin resistance when carbohydrates are refed.
There is little research concerning the physiological effects of refeeding carbohydrates after longterm ketogenic dieting although fasting has been studied to some degree. Early ketogenic diet literature mentions a condition called "alloxan" or "starvation diabetes", referring to an initial insulin resistance when carbohydrates are reintroduced to the diet following carbohydrate restriction (2).
In brief, the initial physiological response to carbohydrate refeeding looks similar to what is seen in Type II diabetics, namely blood sugar swings and hyperinsulinemia. This type of response is also seen in individuals on a CKD. It should be noted that this response did not occur universally in research, being more prevalent in those who had preexisting glucose control problems. As well, exercise appears to affect how well or poorly the body handles carbohydrates during refeeding.
One hypothesis for this effect was that ketones themselves interfered with insulin binding and glucose utilization but this was shown not to be the case (3,4). In fact, ketones may actually improve insulin binding (2). The exact reason for this "insulin resistance" was not determined until much later. The change was ultimately found to be caused by changes in enzyme levels, especially in those enzymes involved in both fat and carbohydrate burning (5). High levels of free fatty acid levels also affect glucose transport and utilization (6).
Long periods of time without carbohydrate consumption leads to a down regulation in the enzymes responsible for carbohydrate burning. Additionally, high levels of free fatty acids in the bloodstream may impair glucose transport (6).
This change occurs both in the liver (5) and in the muscle (5,7). During carbohydrate refeeding, the body upregulates levels of these enzymes but there is a delay during which the body may have difficulty storing and utilizing dietary carbohydrates. This delay is approximately 5 hours to upregulate liver enzyme levels and anywhere from 24-48 hours in muscle tissue (8,9).
While there is a decrease in carbohydrate oxidation in the muscle, this is accompanied by an increase in glycogen storage (7).
These time courses for enzyme up-regulation correspond well with what is often seen in individuals on a CKD, which is really nothing more than a ketogenic diet followed by carbohydrate refeeding done on a weekly basis. Frequently, individuals will report the presence of urinary ketones during the first few hours of their carb-loading period, seeming to contradict the idea that carbohydrates always interrupt ketosis...
When carbohydrates are refed after even a few days of a ketogenic diet, the insulin response is higher than it would be under normal dietary conditions (38). This is probably due to the slight insulin resistance which occurs during a ketogenic diet, discussed in chapter 7.
Hyperinsulinemia also increases the transport of some amino acids into muscle (39). These metabolic effects might contribute to muscle growth during the carb-up.
PPS: