A pharmacist's perspective on health and metabolic disease
Along with many other experts, I see little value in measuring fasting insulin. However, my reasons may differ to others. One reason is that fasting insulin does not generally reflect post-prandial insulin levels. Although we are not as bad as Hobbits for continuously eating, many of us spend more time in the post-prandial state than we do in the fasted state. This means that understanding our post-prandial insulin status has more meaning for our overall metabolic health than our fasting insulin levels.
Another challenge for using fasting insulin is understanding insulin secretion itself.
Insulin is released from the beta cells of the pancreas in a basal and bolus fashion. In the basal state, we maintain a low level of insulin in the blood, enough to maintain homeostasis. However, if blood glucose levels increase, a bolus of insulin is released in order to restore balance.
Many people think that insulin is secreted from the pancreas in a steady and continuous stream with an increased amount when higher blood glucose levels are detected.
However, insulin actually is secreted from the pancreas in oscillations or waves. As there is a limited amount of research on these oscillations, it is hard to get a complete understanding. We believe that there is a slow rhythmic wave to insulin secretion over 80-180 minutes (the ‘slow’ oscillation). This ultradian rhythm (more than one repeat within a 24 hour cycle) appears to be controlled by our autonomic nervous system.
The slow wave is modulated by a “fast” oscillation, with a rise and fall in insulin levels every 5-15 minutes. This latter rhythm seems to be determined by our personal metabolic state, especially our degree of insulin sensitivity, with a less frequent waves seeming to indicate a higher degree of insulin sensitivity.
This Dual Oscillation Model, has also been referred to as the Metronome Model¹ and it means that your insulin secretion pattern is more likely to look something like this……..
What influences the frequency and magnitude of these waves is still being debated, although the usual suspects of food, sleep, pollution, exercise, and stress are all there. What we do know is faster or more irregular oscillations, indicate a higher degree of insulin resistance.
The more important question is why is insulin secreted in this pulsatile fashion?
It comes back to insulin receptors. After insulin binds to a GLUT4 receptor, the GLUT4 is “internalised” (readsorbed) by the cell, and there is a latent period before a new GLUT4 is retransported to the cell surface again. Also, the number of receptors increases and decreases depending on how much insulin is available.
If there is a constant supply of insulin, it is more likely that the GLUT4 will be internalised and in a latent period within the cell. Also, the more you expose the cell to insulin (or many other substances), the less it responds, a process known as deregulation. Having periods of time with no insulin secretion gives the cells a chance to rest, upregulate GLUT4 and return them to cell surface. This maintains your sensitivity to insulin.
It is believed that the islet cells have a very complex system of cell-to-cell communication to allow them to coordinate the insulin secretion. This communication becomes even more complex as it is believed that the pancreas coordinates with the liver as well!
Perhaps this is why fatty liver disease and lots of fat in the pancreas cause so many metabolic issues. The fat could be clogging up the communication pathways, and this is why there is often such as dramatic improvement in health once fatty liver or fat in the pancreas has been resolved.
So, insulin is secreted in a dual oscillation manner, where there is a slow wave modulated by a fast wave. These waves are controlled by both electrical and metabolic activity, and are needed to prevent down-regulation of GLUT4 transporters, and helps to maintain our insulin sensitivity.
¹Satin, L. S., Butler, P. C., Ha, J., & Sherman, A. S. (2015). Pulsatile insulin secretion, impaired glucose tolerance and type 2 diabetes. Molecular Aspects of Medicine, 42, 61-77.