Beta Cell Preservation

Preserving beta cell function has become one of the most important and rapidly evolving topics in endocrinology. Once viewed as an unavoidable decline—rapid in type 1 diabetes (T1D) and gradual yet progressive in type 2 diabetes (T2D)—the loss of beta cell function is now understood as a dynamic process that can, in certain circumstances, be slowed, stabilized, or partially protected. Advances in the retraining of our immune system (immunotherapies), early detection, genetics, and metabolic interventions have reshaped our understanding of what beta cell preservation can look like today and what may be possible in the near future.

Beta Cell Preservation in T1D

Are my Beta Cells Thriving or Just Barely Surviving?

In order to preserve beta cells, it is important to identify early on that there is an attack on these cells. This is done by screening for autoantibodies, cells that have been misinformed that the beta cells are foreign and a threat to the body that must be attacked. 

There are a few different ways to screen for autoantibodies:

• Ask your PCP to send a lab order to your commercial laboratory
• Find a research program, such as TrialNet for free screening of relatives with T1D
• At-home testing kits via Enable Biosciences or ASK. 

By identifying your risk early, the options towards preservation of beta cells are greater because there are still a vast majority that are functioning within the body. 

How Can We Keep Beta Cells Surviving AND Thriving?

So you got screened and have autoantibodies that are positive for T1D. Now what? Immunotherapies that aim to retrain the immune system to not attack the beta cells have been researched. 

Immunotherapy: The goal of immunotherapy in T1D is to retrain the CD3 cells that are attacking the beta cells to not perceive the beta cells as a threat anymore. This does not stop the destruction of beta cells, but rather slows it down to preserve the function for a longer period of time. While this enables preservation of beta cells, it is important to note that it is not a cure. Talk to your provider to learn more about what is currently approved by the FDA, and what’s coming down the pipeline.

Overview of the “Honeymoon Phase”

The “honeymoon phase” is a phase of partial remission in T1D in which the beta cell function partially recovers due to the initiation of insulin therapy relieving the stress on beta cells of elevated blood sugars (Martino et al., 2024). It is important to note that at the time of T1D diagnosis, about 30% of beta cells remain functional. During this period, it is normal for insulin requirements to decrease. Although the honeymoon phase is temporary, its existence underscores the potential for targeted interventions to extend or strengthen natural insulin production. Efforts to prolong this period—using immunotherapy, metabolic stabilization, and anti-inflammatory strategies—remain a major focus of research.

With higher pancreatic beta cell reserves there are associated improved glycemic control, reduced incidence of low blood sugars, reduced likelihood of diabetic ketoacidosis, and reduced risk of microvascular complications (retinopathy, nephropathy or neuropathy). Therefore, there is benefit in preserving beta cells.

What Does the Future Look Like for Beta Cells? 

There are many clinical trials that aim to preserve beta cells in different ways. For instance, Antithymocyte globulin (ATG), is another immunotherapy with a shorter course for administration and a more generic change in T cell function. Whether a treatment is approved and cleared by the FDA or in early stages of research, it is important to know about these treatments to contribute to the science focused on finding a cure. You can learn more about clinical trials here. 

Beta Cell Preservation in T2D

Do I have Insulin Resistance? 

Unlike T1D which is an autoimmune condition, T2D is a metabolic disorder, meaning, autoantibodies are not present and early identification is accomplished by measuring c-peptide or glycemic control via HbA1c or oral glucose tolerance test (OGTT). It is important to note that T2D involves beta cell dysfunction due to insulin resistance caused by genetic, hormonal, familial history and/or lifestyle factors. Therapeutic aims are to reduce the beta cell workload and improve the responsiveness of the body to the insulin being produced. Weight loss and lifestyle changes can improve or partially restore the beta cell function. 

Is Insulin Resistance Causing my Beta Cells to Barely Survive?

Type 2 diabetes (T2D) isn’t driven by the immune system like type 1—it’s largely caused by insulin resistance, meaning your body’s cells don’t respond well to the insulin being produced. The good news? If T2D is identified early, you have powerful tools to protect your beta cells and even potentially reverse progression. Hooray—you might not even need medication!

• Lifestyle Modifications: 
  • Diet: Diets that are low in simple carbohydrates will help in preserving beta cells because of the lack of need to release as much insulin with meals. As such, the beta cells do not need to work as hard to overcome resistance. 
  • Exercise: Exercise acts as a natural insulin booster! When you exercise, the muscles contract and use the sugar for energy.  Over time, because of the need for sugar by the muscles, they become MORE sensitive to the insulin. 
• Medications (if needed): 
  • Incretin-based therapies (Wegovy, Zepbound, etc.) mimic natural gut hormones and
    • stimulate insulin secretion after meals
    • reduce appetite and support weight loss
    • reduce the stress on beta cells over time
  • Metformin
    • decreases sugar production by the liver
    • improves insulin sensitivity at target tissue sites

On the Horizon

Beyond what has already been approved, there are other medications being studied that have a broader effect or a more targeted approach in both T1D and T2D. In addition, there have been some talks regarding stem-cell beta cell transplants. While it seems like T1D takes the forefront in research for a cure, there is a lot of research and clinical trials that are focused on identifying less invasive means of GLP-1 therapy, such as oral antigens and also focusing on triple hormone therapy (GLP, GIP, and Glucagon). 

The future holds much promise for the future of diabetes.

Sources

Leichter, S. B., Felton, J. L., Geno Rasmussen, C., Rizzuto, P., Bellini, N., Ebekozien, O., & Schulman-Rosenbaum, R. (2025). Establishing Screening Programs for Presymptomatic Type 1 Diabetes: Practical Guidance for Diabetes Care Providers. The Journal of clinical endocrinology and metabolism, 110(8), 2371–2382. https://doi.org/10.1210/clinem/dgaf194

Martino, M., Galderisi, A., Evans-Molina, C., & Dayan, C. (2024). Revisiting the pattern of loss of β-cell function in preclinical type 1 diabetes. Diabetes, 73(11), 1769–1779. https://doi.org/10.2337/db24-0163 

Yang, J., & Wei, R. (2024). The future is on the way: β cell function preservation for type 1 diabetes. Med, 5(1), 4–6. https://doi.org/10.1016/j.medj.2023.11.003