Insulinegevoeligheid is een onderwerp waar mensen in de fitnessbranche erg in geïnteresseerd zijn. Dit is gemakkelijk op te lossen zolang de pathofysiologische mechanismen die hieraan ten grondslag liggen bekend zijn, en die zullen in dit artikel kort worden beschreven. Serie supplementen die kunnen helpen bij het verbeteren van deze marker zal ook worden beschreven.
Op basis hiervan zal dus een reeks eenvoudige stacks worden besproken en aangeboden, die voor iedereen beschikbaar zijn en die kunnen worden gebruikt om de insulinegevoeligheid te verbeteren, afhankelijk van de fase waarin we ons bevinden.
Glucose-intolerantie
On average, a healthy adult human has approximately 90mg/dL glucose in an 8-hour fasting state; the normal level varies from 70 to 110mg/dL, with each measurement between 110 and 125mg/dL qualifying as pre-diabetes and from 126mg/dL as diabetes.
Insulin is excreted by the pancreas in response to the changes observed in blood glucose levels, so although glucose levels remain more or less within a few limits throughout the day, insulin levels fluctuate quite a bit, depending on the meals we make.
Insulin has a receptor on the cell membrane in tissues such as muscles where, once it binds, a cascade of molecular signaling is initiated (with Akt phosphorylation as the final step) with the aim of inducing the migration of glucose transporters (GLUT) from the cytoplasm to the cell membrane to absorb glucose.
And what happens when the glucosepiegel is low? For that, the alvlesesklier is not alone bètacellen the insuline afscheiden, but also alfacellen the glucagon afscheden.
Glucagon is a hormone that has different functions, but all with the same goal: to stimulate the production and release of glucose and to inhibit glycolysis (combustion of glucose).
Summarising:
- It stimulates the amount of amino acids that the liver absorbs to produce glucose (neoglucogenesis).
- It stimulates the release of catecholamines.
- Stimulates the release of liver glycogen in the form of glucose.
- Stimulation of the production of ketone bodies.
Has been remarkable to Glucagon that the envious ervan is not regulated on the basis of bloodglucose, but on the basis of the envents of insuline door de bètacellen van de alvlesesklier. So as they “zien” that the alvlesklier insuline afscheidt, art je seggen that then intuitively feel that de glucosespiegel is high and therefore non-scheiden, as she is in it that de bètacellen naarjks insuline afscheiden, shees that de glucoseegel is low and goes to work.
Diabetes type 2
Now that this has been more or less explained, we can move on to the next point and that is explaining what the hell type 2 diabetes is.
Type 2 diabetes, or insulin-resistant diabetes (because you are resistant to insulin), is characterized by a combination of
insulin resistance
This is the phenomenon where when insulin binds to its receptor on the surface of the cell membrane, the intensity at which the intracellular signaling cascades are produced is weaker, resulting in less insulin being displaced. GLUT receptors per unit of insulin, remember when the transport of fats to mitochondria was inhibited and the amount of fatty acids in the cell increased?
This causes insulin resistance.
Therefore, taking into account the normal physiology of the human being, which is responsible for insulin resistance is nothing more and nothing less than a calorie surplus, since insulin resistance is nothing more than a cellular defense mechanism against excessive calorie consumption, since by preventing glucose from entering the cell, it increases fatty acid oxidation, reducing lipotoxicity due to lipid accumulation and thus lipoapoptosis (cell death caused by excessive lipid accumulation). Scherer in 2010, it is known that there is a positive correlation between adipose tissue (it must be well vascularized and have a high proliferation capacity to be considered metabolically healthy adipose tissue) and insulin sensitivity, i.e.that extremely obese individuals are extremely sensitive to insulin. Extremely obese individuals are extremely sensitive to insulin, although this is another topic to talk about.
Disfunctie van alvleeskliercellen
If you have understood the above information, this will be very easy for you.
Do you remember the accumulation of fats in the cell? Well, this causes what is called ectopic fat deposition (in addition to the release of several unwanted adipokines), which is nothing more than the accumulation of fat outside the subcutaneous adipose tissue (visceral fat), this fat is extremely “unhealthy”, so it produces, among other things, the aforementioned lipotoxicity and therefore lipoapoptosis.
When did zich front test in the alvlesesklier, in de bètacellen, it does suggest that deze no longer handles function and there is less good reageren on alteration in the bloodglucose. interest is also that hastebic money before the alfacellen of the alvlesklier; due to lipotoxicity is being used to be the reason why diabenici, ze constantly have glucagon afscheden (hyperglucagonemia), which is why diabenici, zelfs when ze fasten, zgels glucone
This is also why medications like Metformin or Berberine work so well; because they inhibit liver neoglucogenesis.
Behoud en verbeter je insulinegevoeligheid
First of all, it should be noted that lifestyle changes have much more significant effects than supplements: so remember that it is essential to first analyze and recognize which factors can negatively affect them and solve them as quickly as possible. (Otherwise, the best thing you can do with supplements (and medications) is slow progression.
Before delving into the supplements, understand their key underlying mechanisms:
AMPK
In the medical world, AMPK is often seen as the antagonist of mTOR, that is, the hero who, as it were, puts an end to the pro-carcinogenic rule of the malignant mTOR. Others, like most of the FItnes community, see AMPK as the enemy to be defeated because it negatively impacts the increase in muscle mass, and mTOR as the hero of the film… and I think it goes without saying that neither of these two points of view is correct, right?
AMPK and mTOR are not even antagonistic per se, at least not for the average person, that is, people who train regularly. For example, after training, mTOR expression is at its peak, which occurs in the presence of increased AMPK expression.
What seems a paradox at first glance is actually easy to explain if, instead of looking at the characteristic downstream effects of mTOR and AMPK, we pay more attention to the conditions in which they are activated.
With the activation of mTOR by the abundance of nutrients, specific protein and even more specific leucine, one would not expect that there would be an increase in AMPK at the same time. After all, the latter is expressed when a cell detects a nutrient deficiency in the form of an increase in ADP (indicative of ATP use) and a decrease in ATP level. The reaction, that is, increased expression of AMPK, will have further effects on glucose uptake and fatty acid oxidation, both of which contribute to the restoration of normal ATP levels in the cell.
Both AMPK and mTOR operate in a highly localized manner. Exercise-induced glucose uptake is therefore muscle-specific, which should be obvious, because on exercise ADP levels only rise in the muscle. Supplements that mimic this effect, on the other hand, work systemically.
Therefore, agents such as alpha-lipoic acid or Metformin (which act systemically) will increase glucose uptake in both muscle and adipose tissue (Moini, 2002). After training and at other times, where glucose uptake is already high and, more importantly, muscle specific, it is not necessarily the best idea to try to “intensify” the effects by using a class of supplements that are often mislabeled as “insulin mimetics”.
PPAR-gamma
If you read about the effects each of the different PPARs has, you can easily deduce that if you block PPAR gamma, you can inhibit energy absorption by adipose tissue.
This, which at first glance seems like the straw, is not as beneficial as you think. For example, it is very likely that CLA-induced PPAR-gamma blockade (in rodents) is also responsible for the higher tendency to develop NAFLD in rodents.
Fedor & Co.’s results show that these effects can be enhanced when the PPAR gamma suppressor (i.e. conjugated linoleic acid) is combined with a supplement that has the opposite effects on the liver; DHA from fish oil.
The latter, like many of the older diabetes drugs, is a PPAR-G agonist.
Whether PPAR-gamma blockade is good or bad naturally depends on the scenario we are talking about. For a low-fat individual who moves regularly and wants to limit the accumulation of body fat in a hypercaloric diet as much as possible, it may be a good thing because hardly, thanks to exercise and controlling their body fat percentage, accumulation of fat at the liver and visceral level generally occurs.
However, in the case of obese and sedentary people, especially in the context of a hypercaloric diet, these would be completely contraindicated.
Paradoxical as it sounds, the antidiabetic effects of thiazolidinediones (TZDs), which are PPAR-gamma activators, which are still used to “treat” (or rather, “control”) diabetes and other diseases that present in the form of insulin resistance, exert their effects at the expense of increased fat storage in the body. The latter can be quite pronounced.
Hoe weet ik of ik insulineresistent ben?
Normally it is often said that if you feel lethargic after a carbohydrate-rich meal or if you see that high consumption of this “covers” you, you are resistant to insulin.
Personally, I would say that if these are the main signals you rely on to determine your glucose tolerance status, chances are you’re misdiagnosed.
To assess your glucose sensitivity status, one of the best and least invasive ways is simply a HOMA-IR measurement (which is nothing more than a value taken based on your insulin level and fasting glucose), and if possible, combine these with a cortisol measurement to rule out the possibility of a false positive from a dawn phenomenon due to the stress of doing the test (although even in the worst case the HOMA-IR should be within normal parameters).
Conclusie
Our glucose support supplement GDA Glucose Support has been specially formulated to be used synergistically with the above recommendations for glusosis sensitivity.