Related Experiment Video
Updated: May 30, 2026
08:47
Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
Published on: December 7, 2017
Circulating glucagon is associated with inflammatory mediators in metabolically compromised subjects
Francisco J Ortega1, José M Moreno-Navarrete, Mónica Sabater
1Service of Diabetes, Endocrinology and Nutrition (UDEN), Institut d'Investigació Biomédica de Girona (IdIBGi), Hospital of Girona Dr Josep Trueta, Girona, Spain.
European Journal of Endocrinology
|July 30, 2011
Summary
In obesity, elevated glucagon correlates with inflammation markers like IL-6 and CFB, impacting triglyceride levels. Weight loss reduces glucagon, suggesting a link between inflammation and metabolic dysfunction.
Area of Science:
- Endocrinology
- Metabolic Syndrome
- Immunology
Background:
- Obesity is linked to chronic low-grade inflammation and metabolic changes.
- Acute phase mediators influence circulating hormones, but the glucagon-inflammation link in obesity is unclear.
Purpose of the Study:
- To investigate the association between circulating glucagon and inflammatory parameters in obesity.
- To explore the role of glucagon in the metabolic dysregulation associated with obesity.
Main Methods:
- Cross-sectional and longitudinal studies involving 316 obese subjects.
- Analysis of glucagon, glucose/lipid metabolism, interleukin-6 (IL6), and complement factor B (CFB).
- Evaluation of weight loss effects on these parameters in a separate cohort.
Main Results:
- Glucagon correlated with glucose, HbA1c, triglycerides, IL6, and CFB in obese subjects with altered glucose tolerance.
- Glucagon and CFB independently predicted fasting triglyceride variance in obese individuals.
- Weight loss significantly reduced glucagon, triglycerides, and CFB levels.
Conclusions:
- Acute phase reactants (IL6, CFB) are associated with fasting glucagon in metabolically compromised individuals.
- Glucagon may mediate the link between inflammation and metabolic parameters in obesity-related inflammation.
Related Concept Videos
01:15Hypoglycemia and Glucagon
Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
01:16Hormones Regulating Blood Glucose
Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
In addition to accelerating glucose uptake and utilization, insulin has...
01:24Glucagon-like Receptor Agonists
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
01:02Glucose Homeostasis: Regulation of Blood Glucose
Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
01:27Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...
Insulin and C-peptide are co-secreted in...
01:24Type II Diabetes II: Pathophysiology
PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.