Obesity dysregulates fasting-induced changes in glucagon secretion
Open accessAbstract
Hyperglucagonemia, a hallmark in obesity and insulin resistance promotes hepatic glucose output, exacerbating hyperglycemia and thus predisposing to the development type 2 diabetes. As such, glucagon signaling is a key target for new therapeutics to manage insulin resistance. We evaluated glucagon homeostasis in lean and obese mice and people. In lean mice, fasting for 24 h caused a rise in glucagon. In contrast, a decrease in serum glucagon compared to baseline was observed in diet-induced obese mice between 8 and 24 h of fasting. Fasting decreased serum insulin in both lean and obese mice. Accordingly, the glucagon:insulin ratio was unaffected by fasting in obese mice but increased in lean mice. Re-feeding (2 h) restored hyperglucagonemia in obese mice. Pancreatic perfusion studies confirm that fasting (16 h) decreases pancreatic glucagon secretion in obese mice. Consistent with our findings in the mouse, a mixed meal increased serum glucagon and insulin concentrations in obese humans, both of which decreased with time after a meal. Consequently, fasting and re-feeding less robustly affected glucagon:insulin ratios in obese compared to lean participants. The glucoregulatory disturbance in obesity may be driven by inappropriate regulation of glucagon by fasting and a static glucagon:insulin ratio.
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In people with obesity, fasting and postprandial glucagon levels are higher compared to those with normal body weight.
“Similarly, in people with obesity, fasting and postprandial glucagon levels are higher compared to those with normal body weight [19].”
From Tirzepatide as monotherapy improved markers of beta-cell function and insulin sensitivity in type 2 diabetes (SURPASS-1). (2023) · cites this paper as [19]
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- Authors
- Stern, J. H., Smith, G. I., Chen, S., Unger, R. H., Klein, S., & Scherer, P. E.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Washington University in St. Louis (US)
- Corresponding author
- Scherer, Philipp E
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- Published
- 2019-11
- Volume
- 243
- Issue
- 2
- Pages
- 149-160
- ISSN
- 0022-0795 (ISSN-L)
- 1479-6805
- PMC
- PMC6994388
- OpenAlex
- W2970161534
- Cited by
- 84
- References
- 65
- Citations by year
- 2026: 13 · 2025: 13 · 2024: 12 · 2023: 18 · 2022: 13 · 2021: 10 · 2020: 4 · 2018: 1
- FWCI
- 6.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- VUBIR (Vrije Universiteit Brussel) (submittedVersion)
- Funders
- Pershing Square Foundation
- Novo Nordisk
- National Institutes of Health (5p60dk020579-35, DK20579, DK56341, P01-DK088761-01, RR024992, UL1TR002345)
- National Institute on Aging (K99AG055649, R00AG055649)
- National Institute of Diabetes and Digestive and Kidney Diseases (F32DK107058, R01DK055758, P01DK088761, P60-DK-020579, P30DK056341, R01DK099110, P30DK020579)
- National Center for Research Resources (UL1RR024992)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Physiology › Dietary Effects on Health
- Keywords
- obesity, glucagon secretion, fasting, hyperglucagonemia, glucagon/insulin ratio, insulin resistance, type 2 diabetes, hepatic glucose production, refeeding, diet-induced obesity, mixed meal, pancreatic perfusion, glucoregulation
- MeSH terms
- Adult, Animals, Blood Glucose, Diabetes Mellitus, Type 2, Fasting, Female, Glucagon, Humans, Hyperglycemia, Insulin, Insulin Resistance, Male, Mice, Inbred C57BL, Middle Aged, Obesity, Pancreas, Body Mass Index
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