Relationship Between β-Cell Mass and Fasting Blood Glucose Concentration in Humans
- Robert A. Ritzel, MD1,
- Alexandra E. Butler, MD1,
- Robert A. Rizza, MD2,
- Johannes D. Veldhuis, MD2 and
- Peter C. Butler, MD1
- 1Larry Hillblom Islet Research Center, UCLA David Geffen School of Medicine, Los Angeles, California
- 2Division of Endocrinology, Mayo Clinic, Rochester, Minnesota
- Address correspondence reprint requests to Peter C. Butler, MD, Larry Hillblom Islet Research Center, UCLA David Geffen School of Medicine, 24-130 Warren Hall, 900 Veteran Ave., Los Angeles, CA 90095-7073. E-mail: pbutler{at}mednet.ucla.edu
In type 2 diabetes there is a progressive defect of insulin secretion that precedes the development of hyperglycemia (1). This defect appears to be at least in part due to a deficit in β-cell mass (2–4). Several therapeutic strategies are now being proposed that may reverse the defect in β-cell mass in people with type 2 diabetes, for example glucagon-like peptide 1 or glucagon-like peptide 1–like surrogates (5). However, the relationship between β-cell mass and the blood glucose in humans is uncertain. Here we report the relative β-cell volume in pancreata obtained at autopsy from people with well-documented blood glucose concentrations in life.
RESEARCH DESIGN AND METHODS
Mean β-cell volume, β-cell replication, and β-cell apoptosis for the case subjects included in this analysis have been reported previously (3). Here we now show the individual data points for blood glucose versus relative β-cell volume in obese case subjects who were nondiabetic, had impaired fasting glucose, or had type 2 diabetes. Pancreatic tissue was processed and immunostained for insulin, and the relative β-cell volume was quantified as previously described (3). The relative β-cell volume was used as a surrogate for β-cell mass since whole- pancreas weight is not available.
Selection of the study subjects from autopsy files was previously described (3). In brief, all case subjects included were obese (BMI …
