What’s Up with Beta Cells?

Beta Cells: The Leading Stars in Diabetes Mellitus

Beta cells live within clusters called the “islets of Langerhans” in the pancreas (Salpeter & Dor, 2006). These cells are responsible for the production of insulin. However, in both T1D and T2D, these cells fail to produce enough insulin to maintain normal blood sugars. Insulin is an anabolic hormone, meaning it acts to build up proteins and energy in the body. Like a car, insulin picks up sugar molecules within the blood and takes them to places they need to be (like the muscles, liver, and fat) in order to produce and store energy, as well as rebuild and repair muscles. 

Without the car to get the sugar where it needs to go, sugar starts to build up in the bloodstream and cause complications. As these sugar molecules build up in the blood, it leads to high blood sugars (hyperglycemia) and causes the blood to become thick and sticky, preventing blood from flowing easily to key parts of your body that have smaller vessels (kidneys, eyes, nerves), leading to decreased function. 

Therefore, with beta cell dysfunction, there is a lack of insulin production leading to hyperglycemia.

What Happens to Beta Cells in T1D?

In T1D, the beta cells are mistakenly attacked by your own body as foreign invaders; this is referred to as an autoimmune condition. In a similar way as to how our bodies fight off infections, with T1D, the body produces autoantibodies that attack the beta cells in the pancreas (American Diabetes Association). When enough beta cells are destroyed, the pancreas is unable to make insulin or makes so little that you have to provide external insulin to survive. Shortly after diagnosis, one goes into a “honeymoon” period because there are still some functional cells that will occasionally produce insulin, but this timeline is different for everyone. This “honeymoon” period is similar to using your phone in low-power mode. It still works, but at a lesser capacity and it may surprise you how long it lasts; however, the phone will eventually run out of battery and require a steady source of power. In T1D, that steady source of power is external insulin as the beta cells begin to lose that power to produce insulin. 

What Happens to Beta Cells in T2D?

The best way to think of insulin is like a key to a door; the door being the target tissues – muscles, liver, and fat. Normally, insulin will open the door to allow sugar into these tissues and out of the blood. In T2D, something happens to these keys and the door that does not allow the sugar in. This phenomenon is referred to as insulin resistance. While a certain percentage of insulin resistance is associated with lifestyle and dietary factors, such as increased weight, excess carbohydrate intake, and lack of physical activity, it can also be influenced by genetics, family history, and hormonal changes. For instance, some individuals may have a key that may not fit “perfectly” into the lock and requires more effort than others (or damaged insulin or insulin receptors on target tissues). In these cases, you may be doing “everything right,” but you simply have a defective key (insulin) or lock (insulin receptor).

It is said that insulin resistance is present up to 10-15 years prior to the development of T2D (Freeman, Acevedo & Pennings, 2023). Because the body isn’t using insulin effectively, the beta cells in the pancreas work harder to keep blood sugar in a normal range. Over time, the beta cells get tired and can’t make enough insulin anymore. High blood sugar and stress in the body can make this worse. If this stress keeps happening, the beta cells can become damaged and stop working properly altogether requiring external insulin. T2D isn’t caused by one thing, and it’s never about blame. It’s a complex condition that develops over time, and everyone’s body responds differently.

Is There a Way to Not Kill off the Main Character?

The conversation towards a cure will always be around preservation of beta cells and while a cure does not currently exist, preservation of beta cell function prior to complete destruction could alleviate progression of diabetes. There have been various clinical trials focused on immunotherapies that aim to retrain the antibodies to not attack the beta cells in an attempt to preserve their function for a longer period of time. Talk to your provider to learn more about what is currently approved by the FDA, and what’s coming down the pipeline.

In T2D, interventions that reduce body fat, such as exercise and GLP-1 receptor agonists (like Wegovy or Zepbound, for example), and a diet low in simple carbohydrates to prevent hyperglycemia provide the best evidence to slow or stop the deterioration of beta cells. 

References

American Diabetes Association. (n.d.). Understanding type 1 diabetes. Understanding Type 1 Diabetes | ADA. https://diabetes.org/about-diabetes/type-1 

Freeman AM, Acevedo LA, Pennings N. Insulin Resistance. [Updated 2023 Aug 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507839/

Park, Y. J., & Woo, M. (2019). Pancreatic β cells: Gatekeepers of type 2 diabetes. Journal of Cell Biology, 218(4), 1094–1095. https://doi.org/10.1083/jcb.201810097 

Salpeter, S. J., & Dor, Y. (2006). Pancreatic cells and their progenitors. Methods in Enzymology, 322–337. https://doi.org/10.1016/s0076-6879(06)19013-8