Ananda Basu, M.D.Glucagon is a pancreatic hormone that increases blood sugar. It normally works with insulin to maintain glucose levels, but this regulation is impaired in diabetes.
Those with Type 1 diabetes (T1D) have higher glucagon levels right after eating than healthy individuals, but the reason why had not been determined.
Using a novel glucagon isotope tracer, UAB researchers found that changes in postprandial (post-meal) glucagon concentrations in T1D are due to increased rates of glucagon secretion during the early postprandial period, i.e., during the first two hours after a meal. Scientists suggest strategies that decrease early postprandial glucagon fluxes could improve postprandial glucose concentrations in T1D.
Their findings, “Postprandial Glucagon Metabolism in Healthy and Type 1 Diabetes” were published in the February 2026 issue of Diabetes, the peer-reviewed flagship journal of the American Diabetes Association.
The study’s corresponding author is Ananda Basu, M.D., program director of the NIH-funded Diabetes Research Center, S. Richardson Hill, Jr. Endowed Professor in the UAB Department of Medicine Division of Endocrinology, Diabetes and Metabolism, and associate director at the UAB Comprehensive Diabetes Center. Basu is an expert in developing innovative isotope modeling techniques to study whole body and regional metabolism and physiology in humans with and without diabetes.
The objective of this study was to use the isotope dilution method to determine postprandial glucagon turnover. Scientists first characterized glucagon kinetics—glucagon secretion, distribution, and clearance—during steady-state in nine individuals with no diabetes (ND) and 12 individuals with T1D.
They then applied the isotope dilution technique to measure postprandial glucagon metabolism after a mixed meal in a cohort of 16 individuals with T1D and 16 healthy control participants.
“We have directly demonstrated that higher early postprandial glucagon concentrations in individuals with T1D are due to higher rates of glucagon secretion,” Basu said. “This technique can therefore be applied to directly probe pancreatic alpha-cell function and glucagon in a variety of conditions, including but not limited to, Type 2 diabetes, prediabetes, metabolic dysfunction-associated steatohepatitis, and drug effects.”
Basu said, to the best of his knowledge, the use of a glucagon isotope to measure glucagon turnover has never been conducted before in humans or in animals.
“We believe this tracer can be applied to gain further knowledge about glucagon metabolism in Type 2 diabetes, during exercise, in those with hypoglycemia and hypoglycemia unawareness, and to explore the effects of glucagon-like peptide 1 (GLP-1) and dual and triple agonists on glucagon production and clearance,” he said.
Other study authors include Rita Basu, M.D., Endowed Professor of Diabetes Science in the UAB Division of Endocrinology, Diabetes and Metabolism and UCDC senior scientist, and collaborators from the University of Virginia, Mayo Clinic in Rochester, Minnesota, and the University of Padova in Italy.
The work was supported by grants from the National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, and National Cancer Institute.
Read the full article in Diabetes.