Summary of “Special Edition: What's Next—An Update on Beta Cell Function”

Podcast: Diabetes Core Update
Date: November 10, 2025
Host: Dr. Neil Skolnick (A)
Guest: Dr. Melina Bellin (B), Professor of Pediatric Endocrinology and Surgery, University of Minnesota Masonic Children’s Hospital

Episode Overview

This special edition explores the latest advancements in beta cell function—key for insulin production within the pancreas—and their significance in evolving diabetes care. Dr. Melina Bellin offers a state-of-the-art update on beta cell biology, measurement, preservation, regeneration, and replacement, highlighting clinical and research breakthroughs relevant for both Type 1 and Type 2 diabetes.

Key Discussion Points & Insights

1. Pancreatic Anatomy and Islet Cell Basics ([01:22]–[03:03])

• The pancreas has two main components:
  • Exocrine (~98%): Produces digestive juices (acinar and ductal cells).
  • Endocrine/Islet: Clusters of hormone-producing cells scattered throughout.
• Islet cell types and main functions:
  • Beta cells: Insulin and C-peptide (focus in diabetes)
  • Alpha cells: Glucagon (raises blood sugar)
  • PP cells: Pancreatic polypeptide (less often discussed)
• Islets are highly vascular, enabling efficient hormone delivery.

Memorable Quote:

“The area of the pancreas that we're interested in as endocrinologists … are the islets. And the islets are clusters … roughly, you could think of an average islet being about a cluster of a thousand cells.”
—Dr. Bellin [02:01]

2. Beta Cell Dysfunction in Type 1 vs. Type 2 Diabetes ([03:03]–[04:42])

• Type 1: Autoimmune destruction leads to near-total beta cell loss; patients make virtually no insulin.
• Type 2: Beta cell inability to meet metabolic demands; ranges from severe insulin deficiency (low C-peptide) to high insulin production that remains insufficient due to resistance.
• Central message: All diabetes forms involve some beta cell failure, but mechanisms and clinical manifestations differ.

Memorable Quote:

“In type 2 diabetes … the beta cell can't produce enough insulin to meet all the demands ... there’s a lot of heterogeneity in different patients.”
—Dr. Bellin [03:35]

3. Beta Cell Preservation: Early Detection and Intervention ([04:42]–[06:43])

• Shift toward early intervention in Type 1: Aim to catch at-risk individuals (pre-symptomatic stages 1/2) before irreversible beta cell loss.
• Focus of current research: Biomarker identification and immunotherapies to halt or slow autoimmune destruction.

Memorable Quote:

“I think where the field is moving … is how do we intervene earlier, right, to protect that beta cell so we don't lose the beta cell function and then have to replace it with insulin therapy?”
—Dr. Bellin [05:18]

4. Regeneration and Replacement Therapies ([07:02]–[13:06])

• Pancreas transplantation: The classic (since 1960s) but limited by surgical risks and need for immunosuppression.
• Islet cell transplantation: Less invasive (infusion into the liver). Benefits select, high-risk patients but is limited by cell supply and need for anti-rejection drugs.
• Stem cell–derived islets: Currently in clinical trials. Allows near-unlimited cell source, with hope for future therapies needing little or no immunosuppression (via genetic editing or encapsulation).
• Challenges with encapsulated cells: Protecting cells from immune attack without depriving them of oxygen and nutrient supply.

Memorable Quote:

“The amazing thing … once you have a stem cell line, you can make many, many, many, many islet products … almost an unlimited number of islets to treat many patients who have diabetes.”
—Dr. Bellin [11:12]

5. Measurement of Beta Cell Function ([14:53]–[16:47])

• C-peptide is preferred over insulin for assessing endogenous beta cell activity, especially in patients on exogenous insulin.
• C-peptide measured fasting or postprandially can help distinguish between types of diabetes, particularly to clarify ambiguous cases (e.g., possible LADA).

Memorable Quote:

“When you look at C peptide, you're looking at the insulin someone's own body is making and you're not picking up any of the insulin they're taking.”
—Dr. Bellin [15:46]

6. When to Test Beta Cell Function—Clinical Scenarios ([16:47]–[19:37])

• Example: Adult (BMI 27, age 40, atypical profile) with elevated glucose; consider C-peptide and autoantibodies to distinguish Type 2 from LADA.
• Management implications: Low C-peptide suggests insulin deficiency, supporting early insulin initiation.

7. Screening and Preserving Beta Cell Function in Early Type 1 Diabetes ([19:37]–[22:07])

• Benefits of screening at-risk populations: Prevents DKA at presentation, identifies candidates for beta cell–preserving therapies (e.g., teplizumab).
• Teplizumab: FDA-approved immunotherapy that can delay clinical T1D onset by years when used in presymptomatic (stage 2) patients.

Memorable Quote:

“We may have ways to protect those beta cells … to either slow down or prevent the progression to symptomatic type 1.”
—Dr. Bellin [20:44]

8. Clinical Stages of Type 1 Diabetes ([22:07]–[24:14])

• Stage 1: Autoantibodies present, normal glucose
• Stage 2: Autoantibodies + mild glucose abnormalities
• Stage 3: Clinical diagnosis—requires insulin
• Stage 4: Complete loss of beta cell function

9. Whom to Screen & How ([25:31]–[28:49])

• Strongest screening recommendation for first-degree relatives (age 0–45) of people with T1D (risk ~5%).
• Also consider screening second-degree relatives and those with other autoimmune conditions.
• How: Test for GAD, insulin, IA2, ZnT8 antibodies.
• Next steps: Positive antibody results should trigger referral to endocrinology for monitoring/dysglycemia assessment.
• The future may see primary care playing a greater role in interpretation and next steps as more therapies and screening become widespread.

10. Final Thoughts ([29:51]–[30:17])

• The field is rapidly evolving, likely to transform diabetes care within a decade.
• Emphasis on staying up to date and embracing forthcoming innovations.

Memorable Quote:

“It's really going to just change how we think about and treat diabetes over the next decade.”
—Dr. Bellin [30:08]

Timestamps for Important Segments

• Islet cell basics: [01:22]–[03:03]
• Type 1 vs. Type 2 beta cell loss: [03:03]–[04:42]
• Beta cell preservation: [04:42]–[06:43]
• Replacement/regeneration advances: [07:02]–[13:06]
• Stem-cell derived islets: [10:01]–[13:06]
• Beta cell function testing (C-peptide): [14:53]–[16:47]
• Clinical application/ambiguous T2D vs. LADA: [16:47]–[19:37]
• Screening for early Type 1 and candidate selection: [19:37]–[28:49]
• Teplizumab impact: [28:49]–[29:51]
• Big picture/future of the field: [30:02]–[30:17]

Notable Quotes

“What can we do to keep that beta cell healthy?”
—Dr. Bellin [05:23]

“The future looking approach would be finding ways to overcome those barriers of cell supply and immunosuppression to be able to replace cells in more people than we can right now.”
—Dr. Bellin [09:36]

“Once you have a treatment that's really successful in type 1, then people are going to start taking that and saying, like, okay, so what can we do for people with type 2 diabetes?”
—Dr. Bellin [14:17]

“Right now if someone has autoantibodies that are positive, they do get referred to us ... I think future looking, you can imagine a standard of care where ... there may be enough people who are positive ... that there isn't capacity to refer them all.”
—Dr. Bellin [27:37]

Takeaway

This episode offers a comprehensive update for clinicians on the state and future of beta cell function research—from foundational pancreas biology to the cutting edge of screening, preservation, and cell-based therapies. As innovations move from trial to practice, greater emphasis on early detection and intervention will likely transform diabetes care for both T1D and T2D in years to come.