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Obesity dysregulates fasting-induced changes in glucagon secretion
Jennifer H Stern1, Gordon I Smith2, Shiuwei Chen1
1Touchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
The Journal of Endocrinology
|August 28, 2019
Summary
Obesity disrupts normal glucagon regulation during fasting, leading to a static glucagon:insulin ratio. This impaired hormonal balance contributes to hyperglycemia and type 2 diabetes risk.
Area of Science:
- Endocrinology
- Metabolic research
- Diabetes pathophysiology
Background:
- Hyperglucagonemia is linked to obesity, insulin resistance, and hyperglycemia, increasing type 2 diabetes risk.
- Glucagon signaling is a critical therapeutic target for managing insulin resistance.
Purpose of the Study:
- To investigate glucagon homeostasis and the glucagon:insulin ratio in lean versus obese states during fasting and refeeding.
- To understand the role of glucagon dysregulation in obesity-related metabolic disturbances.
Main Methods:
- Comparative analysis of serum glucagon and insulin levels in lean and diet-induced obese mice under fasting and refeeding conditions.
- Pancreatic perfusion studies in mice to assess glucagon secretion.
- Evaluation of glucagon and insulin responses to a mixed meal in obese humans.
Main Results:
- Obese mice showed decreased serum glucagon during prolonged fasting, unlike lean mice, resulting in an unchanged glucagon:insulin ratio.
- Refeeding normalized hyperglucagonemia in obese mice, while fasting decreased pancreatic glucagon secretion.
- Obese humans exhibited blunted changes in glucagon:insulin ratios post-meal compared to lean individuals.
Conclusions:
- Fasting and refeeding exhibit altered glucagon dynamics in obesity.
- A static glucagon:insulin ratio in obesity may contribute to impaired glucose regulation.
- Dysregulated glucagon signaling is a key factor in the pathophysiology of obesity and type 2 diabetes.
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