Back to the Basics: Insulin and the GI

buff guy curling dumbbellby: Marc Collins

Back to the Basics: Insulin and the GI , Insulin can either be your best friend or your worst enemy. Insulin’s main role is to control the storage of nutrients. In fat cells it promotes fat storage. In the liver it promotes glycogen and fat storage and, most importantly, in the muscle it promotes growth! No wonder this hormone intrigues both those trying to lose weight and those trying to gain muscle. It’s also not a surprise that some use exogenous insulin…however stupid I personally feel that is. But never mind that right now. Insulin is also the hormone that’s secretion is most easily influenced by diet. Insulin responds primarily to glucose, but other stimuli, such as gut hormones secreted in response to food, also influence insulin secretion.

Simply put, the role of insulin is to decide when and where you store nutrients. So whether you are looking to get big or trim down, controlling your insulin levels should be more than a minor concern.

The Glycemic Index (GI)

When you eat carbohydrates, they eventually end up in your bloodstream as glucose. This is true of all carbohydrates. The difference is that some carbohydrate sources are absorbed and increase blood glucose faster than others. The faster carbohydrates raise your blood glucose, the higher glycemic index (GI) they have. The ability of ingested glucose to increase blood glucose is given a value of 100. All other foods are given values in relation to this. For example, sweet potatoes are assigned a value of 54, meaning it can raise blood glucose 55% as well as glucose. In general, foods below 55 are considered low GI while foods above 70 are considered high GI.

A better measurement is the insulin index. This indicates the ability of a food to increase plasma insulin. I know what some of you are thinking: isn’t that the same thing? Well, not exactly. As I mentioned earlier, there are factors other than plasma glucose that increase insulin release. Let’s take milk for example. The glycemic index is rather low. However, it has been shown to induce an insulin response similar to very high glycemic index foods. That’s reason enough for me to put it in my post-workout shake (high insulin post-workout is beneficial for muscle gain – more on this later). As a side note, dairy calcium has separate beneficial effects on weight loss, not to mention the multitude of vitamins and minerals.

The Science of Insulin Release

Insulin is secreted by the pancreas in response to a glucose stimulus. The higher the glucose concentration in the blood, the more insulin the pancreas will release. Glucose enters pancreatic beta cells (the ones that secrete insulin) through GLUT2 transporters. These differ from the GLUT4 transporters of other cells (such as adipose and skeletal muscle) in that GLUT2 transporters have a much higher Km – making them highly susceptible to glucose availability. In contrast, the GLUT transporters of other cells are primarily regulated by insulin levels. I recommend anyone who doesn’t care much about glucose metabolism to skip the next 3 paragraphs.

Upon entering the beta cell, glucose undergoes glycolysis and is transformed to pyruvate. The rate-limiting step of this process is glucokinase (GK). This is important because many factors upregulate or downregulate the activity / expression of this enzyme. Pyruvate is then further broken down in the mitochondria to yield ATP. However, the ATP in beta cells is not used for energy as such. Rather, it serves to stimulate insulin release. This is mediated through closure of the K+ATP channels and subsequent opening of the voltage gated calcium channels. Calcium is the primary stimulus for insulin release.

That said, there are many other factors that affect insulin release. However, many of these cannot in themselves stimulate insulin release. The majority of them only potentiate (read increase) glucose-stimulated insulin secretion (GSIS). Sympathetic input decreases insulin release while parasympathetic input increases insulin release. The effect of sympathetic input is apparent when one is exercising. When exercising (sympathetic input is high), there is no need for insulin release so it seems natural for such input to decrease insulin secretion. On the other hand, when one is laying on one’s ass watching the ball game, that’s a perfect time to store nutrients.

Gut hormones also potentiate insulin release. When food is ingested, hormones such as CCK, GLP1 and GIP are released. These hormones aid insulin release provided the pancreas is also stimulated by glucose. This is the reason that infused (read injected) glucose does not have the same effect on insulin release as ingested glucose. For the scientifically inclined, these act on G-coupled receptors affecting either adenylate cyclase / PKA or the PLC pathways. PKA affects numerous steps of insulin release such as the K+ channel and Ca++ channel as well as being involved in the movement/release of the insulin granule. PLC leads to the formation of PKC and IP3. PKC acts similarly to PKA in the pancreas while IP3 acts on the endoplasmic reticulum, increasing intracellular calcium. I won’t go into any other pathways since I don’t see the point and there is still much to be determined. Plus, I’m too lazy.

Probably the most important mediator of insulin secretion in the long term is the type of fats we consume. Polyunsaturated (good) fats have been shown to maintain/improve pancreatic function while saturated (bad) fats impair function. These effects are thought to be mediated partly via transcription factors (such as the PPAR family and SREBP1c) and the subsequent effect on expression and/or activity of key enzymes in glycolysis and the TCA cycle. However, effects of free fatty acids (FFA) on the hypothalamus have also been implicated in insulin release in both the short- and long-term (and in hepatic glucose production I might add).

So why is any of this important? Loss of beta cell function is a bad thing because dysregulated insulin secretion is known to cause insulin resistance, diabetes, and obesity. I won’t go into the mechanisms behind this now as it is quite complicated. Nevertheless, suffice it to say that maintaining your ability to secrete insulin is important and the easiest thing we can do to ensure this is chow down the polyunsaturated fats (i.e. fish oil or SesaThin) and lay off the saturated fats (i.e. Burger King).

Insulin Resistance

The importance of insulin resistance is obvious. If you are dieting, insulin resistance will cause more muscle loss and less fat loss. If you are bulking, insulin resistance will lead to decreased muscle gain and increased fat gain.

Insulin resistance refers to when the cells of your body (adipose, liver, muscle) become resistant to the effects of insulin. This means it will take more insulin to clear the blood of glucose. Needless to say, this will result in more insulin being released for a given concentration of glucose. It is important to note that skeletal muscle is much quicker to become insulin resistant than adipose tissue. So, even though your insulin levels are higher, the anabolic effect of insulin on muscle remains the same. The effect on adipose stores, however, is increased. This puts you in a situation where storing fat is favoured while gaining muscle is stable or reduced. There is much research being done in this area. Let’s now look at some of the things you can do to limit insulin resistance (i.e. increase insulin sensitivity in muscle).

Low carbohydrate diets promote insulin resistance. This means that the Atkins diet and ketogenic diets are extremely detrimental to the anabolic effects of insulin. This is one reason that when people come off these diets they tend to gain fat very easily. Your muscle cells are resistant to insulin so more insulin must be released to rid the blood of excess glucose. Adipose stores will respond to the elevated insulin by storing triglycerides (i.e. fat).


I’m going to take this opportunity to rant a little about low carbohydrate diets, despite the fact that it is somewhat off-topic. The weight loss is real, but most of the weight (at least initially) is water. When you reduce carbohydrate intake, you are depleting glycogen (storage form of glucose) from your liver and muscle. As glycogen is your primary energy source, athletic performance will obviously suffer. Okay, back to weight loss. Each gram of glycogen is stored with ~3grams of water. By losing 1lb of glycogen, the scale will tell you that 3lbs were lost. After a carbohydrate refeed, the glycogen and water will return. This is why the mirror is much more trustworthy than the scale. Low carbohydrate diets have also been shown to lower testosterone levels. This is detrimental to both muscle hypertrophy and sexual function.

Resistance training enhances muscle glucose uptake (up to 24 hrs post-exercise). The effect is much less pronounced with aerobic training. This is partly due to increased blood flow to the particular muscle exercised (lasts 2-3 hours). Obviously, larger muscles will have a greater effect than smaller ones. Those who exercise regularly will have greater insulin sensitivity than sedentary (read lazy) individuals. This is partly attributable to increased muscle glycogen storage and reduced insulin resistance.

Hot tubs may also become your friend. By increasing blood flow to your muscles, mean plasma glucose was shown to decrease and patients lost weight. A weight loss of ~2kg a day was observed in a study with spending only 30 minutes in a hot tub for 3 weeks.

Unsaturated fatty acids have also been shown to reduce insulin resistance. This means your muscles will more easily be stimulated by insulin, and in turn that less insulin will be released to control blood glucose. Less insulin means less stimulus for fat storage. GLA (high concentrations found in borage oil, also found in hemp oil and evening primrose oil) in particular have been found to have beneficial effects on insulin resistance.

John Berardi recommends taking 600mg alpha-lipoic acid and 6-10 grams DHA and EPA (the omega 3s in fish oil) post-exercise. He also lists chromium as a supplement able to increase insulin sensitivity. I haven’t researched this myself, so you’ll have to take his word for it.

Who Cares?

Okay, so what does all this mean in real life. As I’ve already mentioned, insulin release is easily manipulated by diet. High GI meals rapidly induce insulin release while lower GI meals cause a much lower insulin response. Throughout the day, insulin spikes are conducive to fat accumulation. This is a bad thing. In addition, insulin spikes are rapidly followed (2-4hrs later) by slight hypoglycemia (low blood glucose). This hypoglycemia is corrected primarily by glucagon and somewhat by epinephrine, which is detrimental to muscle protein. By eating frequently, this response is negated.

If, for example, you were to consume a high GI meal before bed, not only would you increase fat accumulation (insulin causes glucose to be stored as fat) but you would also become hypoglycaemic early while you sleep. This would increase the time the counter-regulatory hormones (i.e. glucagon) would be breaking down muscle protein. A high fat/protein meal would serve to decrease gastrointestinal absorption, not only limiting insulin response but also ensuring adequate plasma amino acids to prevent muscle breakdown.

Post-workout, however, is a time when insulin release is desirable. By adding glucose to a post-workout shake, you get the maximal insulin release at the time you want it most. Maltodextrin or maltose can also be used (in fact, they have a slightly higher GI than glucose). Alternatively, if you wish to reduce carbohydrate intake, BCAAs and glutamine may also be used to induce an insulin response. Leucine is the primary amino acid in BCAAs known to induce this response, but the effects of the other 2 BCAAs may also help. These affect insulin release via metabolism (not through G-proteins) so a maximal glucose stimulus is not required. Insulin also stimulates the uptake of creatine by muscles. This is why many pre-mixed creatine products contain dextrose (and also why many advocate consuming creatine post-exercise). Creatine powders may also have other ingredients.

Another thing to consider is the effect of epinephrine on insulin secretion. Since epinephrine negates the insulin response, even low to moderate exercise following a meal (this is obviously not applicable to your post-workout meal) would blunt the insulin response and decrease fat storage.

Final Thoughts

Here, I have outlined some of the basics to consider regarding insulin, diet and exercise. There are many theories and diet plans that revolve around insulin (and, on a somewhat related note, leptin). I suggest reading “Carbohydrate Cycling” by Twin Peak to anyone thinking about attempting a low-carbohydrate type diet. I hope some of what I have written helps someone in diet planning, or at least re-evaluate his or her outlook on carbohydrates (no, they are not the devil).

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