Adipokine Secretion in Diabetes

Adipokines are signaling molecules secreted by adipose tissue that play a crucial role in regulating metabolism and inflammation. In diabetes, altered adipokine secretion significantly impacts insulin sensitivity and glucose homeostasis. Key adipokines include leptin, which promotes satiety and regulates energy balance, and adiponectin, which enhances insulin sensitivity and has anti-inflammatory properties. In diabetic patients, levels of leptin are often elevated, while adiponectin levels are decreased, contributing to insulin resistance and chronic inflammation. This imbalance can worsen metabolic disturbances, leading to increased risk of cardiovascular disease and other complications. Understanding the role of adipokines in diabetes offers potential therapeutic targets for improving metabolic health. Strategies to restore adipokine balance, such as weight loss, exercise, and pharmacotherapy, may enhance insulin sensitivity and reduce the risk of diabetes-related complications.

Committee Members
Speaker at Diabetes  2026 - Mahir Khalil Ibrahim Jallo

Mahir Khalil Ibrahim Jallo

Gulf Medical University, Canada
Speaker at Diabetes  2026 - F Buck Willis

F Buck Willis

Christian College of Medicine, Belize
Speaker at Diabetes  2026 - Anil Harrison

Anil Harrison

Midwestern University, United States
Speaker at Diabetes  2026 - Wan Rosli Wan Ishak

Wan Rosli Wan Ishak

Universiti Sains Malaysia, Malaysia
Diabetes 2026 Speakers
Speaker at Diabetes  2026 - Mahir Khalil Ibrahim Jallo

Mahir Khalil Ibrahim Jallo

Gulf Medical University, Canada
Speaker at Diabetes  2026 - F Buck Willis

F Buck Willis

Christian College of Medicine, Belize
Speaker at Diabetes  2026 - Anil Harrison

Anil Harrison

Midwestern University, United States
Speaker at Diabetes  2026 - David Navazio

David Navazio

Gentell, United States
Speaker at Diabetes  2026 - Sujith Rajan

Sujith Rajan

NYU Long Island School of Medicine, United States
Speaker at Diabetes  2026 - David Petch

David Petch

utR Biotech, Canada
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