"Insulin is important in the regulation of blood sugar, but its importance has been exaggerated because of the diabetes/insulin industry. Insulin itself has been found to account for only about 8% of the "insulin-like activity" of the blood, with potassium being probably the largest factor. There probably isn't any process in the body that doesn't potentially affect blood sugar."
-Dr. Ray Peat
When I initially read this quotation posted by one of Dr. Peat’s ardent followers on Facebook, it caught my attention because I was under the impression that insulin was the dominant factor in regulating blood glucose levels.
Normally, when blood levels increase, the β-cells of the pancreatic islets secrete insulin into the bloodstream, where it binds to insulin receptors on organs and tissues throughout the body. The adipose tissue, liver, and muscles are the principle sites that insulin exerts its actions on. In effect, insulin is a storage hormone that rapidly clears nutrients out of the bloodstream.
(1) In the fat tissue, insulin suppresses the mobilization of fatty acids and promotes the synthesis of fatty acids & triglycerides.
(2) In the liver, insulin inhibits gluconeogenesis and glycogen breakdown and stimulates glucose oxidation and glycogen synthesis.
(3) In the muscles, insulin stimulates amino acid uptake & protein synthesis.
According to some of the most widely read physiology textbooks, in the absence of insulin all of the above processes become impaired, and fatty acids and amino acids are released in large amounts into the bloodstream from the adipose tissue and muscles, respectively. In the liver, the fatty acids are used to generate ketone bodies and the amino acids, substrates for gluconeogenesis, are used to make glucose. Because insulin stimulates the use of the ketone bodies by cells in the body, and because fatty acids flow to the liver at high rates, the ketone bodies accumulate in the bloodstream, leading to acidosis, coma, death.
I think most people are also aware of the experiments in isolated segments of animal tissue, in which blood glucose levels are incrementally increased in the absence of insulin. In these experiments, despite increasing blood glucose concentrations by up to 800 mg% (which is 10x greater than the normal fasting blood glucose concentrations), the levels of glucose inside cells don’t change. In other words, without insulin, regardless of how high blood glucose levels rise, the entry of glucose into cells is prevented, and this is attendant to a rise in NEFA and ketone body concentrations.
More recently, based on better (and more physiological) experiments, it’s been suggested that there could be constitutively active glucose transporters; in other words, proteins embedded in the plasma membrane that in an insulin-independent manner transport glucose into cells (Sonksen, 2001). These transport proteins are regulated by the unequal distribution of free glucose molecules between the blood and inside the cell (i.e., the concentration gradient across the plasma membrane), and the efficiency with which the glycolytic enzymes function.
So it’s possible insulin assumes a secondary/conditional role in the regulation of blood glucose levels under some circumstances. In the fasting state, when blood glucose levels fall, glucose is transported into cells with, at the most, very little help from insulin; this process is only limited by the rate at which the glycolytic enzymes function.
But when blood glucose levels rise, as in after a carbohydrate-laden meal, the beta-cells secrete insulin, and insulin (1) suppresses the mobilization of fatty acids, (2) suppresses hepatic glucose production, and (3) stimulates the recruitment of glucose transport proteins to the plasma membrane, whereby insulin-targeted cells sprout exponentially more glucose transport proteins. In this way, glucose is cleared as rapidly as it rises in the blood because of insulin’s permissive effects, such that blood glucose levels don’t fall out of range too much.
So, although insulin may not be the be-all and end-all regulator of the rate at which glucose is transported into cells, it is by no means a minor player as asserted by Dr. Peat. (Actually insulin is a protective compensatory adaptation to the rising levels of the counterregulatory hormones that occurs naturally with aging.)
As to potassium, it’s known that inappropriately dosed insulin injections can uncomfortably lower blood potassium levels (hypokalemia), as insulin shifts potassium into cells.
By neutralizing ROS, potassium has also been postulated to improve insulin sensitivity (Ando, Matsui, Fujita, & Fujita, 2010). Though this is not having insulin-like action. (As an aside, to date the use of antioxidants to treat diabetes has been abysmally unsuccessful.)
Then again, high potassium levels (hyperkalemia), in turn stimulates the secretion of aldosterone which could worsen insulin sensitivity (Kraus, Jäger, Meier, Fasshauer, & Klein, 2005); this is the same mechanism by which salt-restricted diets induce insulin resistance (Garg et al., 2011).
Potassium has another important role in blood glucose regulation in the β-cells. Without going into too much detail, when blood glucose levels rise, the β-cells uptake glucose, and glucose is then oxidized to generate ATP. ATP thereafter binds the ATP-sensitive potassium channels located in the plasma membrane, which upon this interaction with ATP, close, enabling potassium to accumulate intracellularly. As a result, the membrane depolarizes, and this stimulates the opening of the voltage-gated calcium channels, which then allow calcium to move into the β-cell in droves, triggering insulin secretion.
It’s conceivable that a deficiency of potassium could impair insulin’s action (e.g., diuretics that deplete potassium have been shown to induce insulin resistance). But as far as potassium having insulin-like action, I don’t see any evidence for this.
Insulin’s actions are blocked by elevated levels of NEFA and the counterregulatory hormones, in which case, the resulting inhibition of certain glycolytic enzymes blocks the procession of glycolysis, leading to the accumulation of free glucose molecules, which could diffuse out into the extracellular space by way of the glucose transporters. This plays an important regulatory role whilst fasting (a period of time when glucose availability is limited) and in stressful times, by preventing glucose from being used up too quickly...otherwise, shock would manifest.
Insulin can be conceived to boost, in a permissive manner, the clearance of glucose from the blood so that after eating a carbohydrate-laden meal, per the mechanisms described above, blood glucose levels don’t fall out of range too much or for too long. Gastrointestinal hormones play a role in blood glucose regulation as well, but it does so by potentiating the stimulation of insulin secretion from the pancreatic beta-cells.
In conclusion, insulin occupies a major role in blood glucose regulation—not a measly one. A rise in glucose is always quickly accompanied by a rise in insulin in the bloodstream, and insulin suppresses the factors that inhibit the rapid clearance & oxidation of glucose, which are processes that would occur too inefficiently otherwise, that is if glucose were to stimulate its own uptake and oxidation. A situation like this would only occur during a fast or ketogenic diet, cases where fasting glucose levels would run parallel with low insulin levels, prompting a slow and controlled rate of glucose use. This is the scenario that Dr. Peat is probably alluding to.
References
Ando, K., Matsui, H., Fujita, M., & Fujita, T. (2010). Protective effect of dietary potassium against cardiovascular damage in salt-sensitive hypertension: possible role of its antioxidant action. Current vascular pharmacology, 8(1), 59–63. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/19485915
Garg, R., Williams, G. H., Hurwitz, S., Brown, N. J., Hopkins, P. N., & Adler, G. K. (2011). Low-salt diet increases insulin resistance in healthy subjects. Metabolism: clinical and experimental, 60(7), 965–8. doi:10.1016/j.metabol.2010.09.005
Kraus, D., Jäger, J., Meier, B., Fasshauer, M., & Klein, J. (2005). Aldosterone inhibits uncoupling protein-1, induces insulin resistance, and stimulates proinflammatory adipokines in adipocytes. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme, 37(7), 455–9. doi:10.1055/s-2005-870240
Sonksen, P. H. (2001). Insulin, growth hormone and sport. The Journal of endocrinology, 170(1), 13–25. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11431133