Insulin: How Circadian Rhythms Shape Metabolism
Insulin is a key hormone that keeps our blood sugar in check and orchestrates how our bodies use and store energy. It is often called the “master controller” of metabolism, influencing the processing of carbohydrates, fats, and proteins.¹
But insulin’s actions do not occur in a vacuum, they’re intertwined with our body’s internal clock. A “master clock” in the brain’s suprachiasmatic nucleus (SCN) synchronizes subsidiary clocks throughout the body (in organs like the liver, muscle, fat, and pancreas).² This clockwork makes sure that various processes (hormone levels, metabolism, sleep-wake cycles, etc.) rise and fall at optimal times of day. As previous posts have explored the daily patterns of cortisol and melatonin, we will now examine how insulin fits into this circadian orchestra. We’ll see how insulin secretion and cellular sensitivity to insulin fluctuate over a normal day, and how our circadian rhythm prepares the body to handle food during daylight and to fast at night. Finally, we’ll delve into what happens when this timing is thrown off, disrupting insulin’s rhythm and contributing to insulin resistance, type 2 diabetes, and metabolic syndrome.
Insulin’s Role In The Body
To appreciate insulin’s circadian pulse, it helps to start with a clear picture of what insulin does. After a carbohydrate-containing meal, blood sugar levels climb, and this spike in glucose prompts the β-cells in the pancreas to secrete insulin into the bloodstream. Insulin acts like a key, unlocking cells so they can take in glucose to burn for energy now or store for later. In the liver, insulin signals a shutdown of glucose production (since plenty is coming in from the meal). In muscle and fat tissue, insulin triggers cells to soak up glucose from the blood. Insulin also inhibits the breakdown of fat (a process called lipolysis) and stimulates protein synthesis in muscles. Together, these actions make insulin a storage hormone: it helps store excess nutrients when they are abundant (after eating) and restricts the release of more fuel into the blood. Under normal conditions, the insulin–glucagon system, where glucagon acts in opposition to insulin, keeps blood glucose tightly regulated, ensuring energy is available when needed and storing excess to prevent spikes or dips.
It’s important to note that insulin is only part of the metabolism story. In the morning, cortisol naturally rises as part of the wake-up routine, nudging the liver to release glucose to help energize the body for the day. Insulin typically works in concert with these rhythms: as morning glucose levels rise, insulin steps in to distribute that fuel to tissues. In the night, melatonin surges and communicates with the pancreas by binding to receptors on β-cells; thereby directly and temporarily suppressing insulin release.³ This makes sense biologically, as it ensures our glucose remains steady during the period we are sleeping and therefore fasting. This is one of several factors that explain why the pancreas secretes more insulin for a given blood sugar level during the biological daytime than at night.²
But the insulin secretion rhythm is only part of the story, the other is the rhythm of insulin sensitivity.
Your body’s response to insulin isn’t the same at all hours of the day, it too follows a circadian pattern. Our cells are more sensitive to insulin earlier in the day and relatively more resistant in the evening. What does this mean? If you eat the same meal for breakfast and then again for dinner, the dinner will produce a higher blood glucose spike than the breakfast, even with the same amount of insulin released. In other words, glucose tolerance is better in the morning, while in the evening, the body doesn’t respond as effectively to insulin. Again, this circadian rhythm is driven by the brain’s master clock (SCN), tuning the body’s insulin responses in anticipation of daytime feeding and nighttime fasting.²
These insulin release and sensitivity rhythms are an evolutionary adaptation, optimizing our metabolism for when food is typically available (during daylight).
What Happens When The Clock Is Out Of Sync
The story of insulin shows that timing matters. Our bodies have evolved to expect a roughly 24-hour cycle of behaviour: active days and restful nights. Insulin is deeply woven into this fabric, ensuring we efficiently handle nutrients when they are abundant to maintain homeostasis (balance).. When we live in sync with our internal clocks, sleeping at night, eating during daylight, and keeping a regular daily schedule, we give insulin the best chance to do its job properly. Modern life, unfortunately, often throws a spanner into this finely tuned system. Circadian disruption refers to disturbances in our normal 24-hour biological rhythms. This can happen due to shift work (being awake and active at night and trying to sleep during the day), travel across time zones, irregular sleep schedules, or anything that results in irregular, ill-timed, or minimal light exposure. A growing mountain of research shows that disrupting circadian rhythms can lead to insulin resistance. In this condition, cells no longer respond well to insulin, causing blood sugar to remain elevated. Insulin resistance is a hallmark of type 2 diabetes and often precedes it by years, and it is a core feature of metabolic syndrome (the cluster of high blood sugar, high blood pressure, abnormal cholesterol, and obesity).¹
On a hopeful note, the powerful influence of circadian rhythms means that lifestyle adjustments in timing can markedly improve metabolic health.
Dr. Jonathan Moustakis
Co-founder and CTO of Lume Health
References:
Catalano F, De Vito F, Cassano V, Fiorentino TV, Sciacqua A, Hribal ML. Circadian Clock Desynchronization and Insulin Resistance. Int J Environ Res Public Health. 2022 Dec 20;20(1):29. doi: 10.3390/ijerph20010029. PMID: 36612350; PMCID: PMC9819930.
Lee DY, Jung I, Park SY, Yu JH, Seo JA, Kim KJ, Kim NH, Yoo HJ, Kim SG, Choi KM, Baik SH, Kim NH. Attention to Innate Circadian Rhythm and the Impact of Its Disruption on Diabetes. Diabetes Metab J. 2024;48(1):37-52.
Stumpf, I., Mühlbauer, E., & Peschke, E. (2008). Involvement of the cGMP pathway in mediating the insulin-inhibitory effect of melatonin in pancreatic beta-cells. Journal of pineal research, 45(3), 318–327. https://doi.org/10.1111/j.1600-079X.2008.00593.x
