Obesity-associated insulin resistance adversely affects skin function

Area of Science:

• Dermatology
• Metabolic Syndrome
• Molecular Biology

Background:

• Obesity is linked to various health complications, including potential alterations in skin structure and function.
• Understanding the molecular mechanisms connecting metabolic dysfunction to skin health is crucial.

Purpose of the Study:

• To investigate the functional and molecular changes in skin associated with obesity.
• To elucidate the role of insulin signaling and glucose metabolism in obesity-induced skin alterations.

Main Methods:

• Comparative analysis of skin function and gene expression in mice fed a control versus high-fat diet (HFD).
• Assessment of insulin responsiveness in skin and skeletal muscle.
• In vitro studies on keratinocytes to analyze the impact of insulin signaling inhibition and glucose levels.

Main Results:

• High-fat diet-fed mice showed severe obesity, impaired skin barrier function, and reduced levels of aquaporin-3, keratins, and desmosomal proteins.
• Insulin signaling was attenuated in the skin and skeletal muscle of obese mice.
• Inhibition of insulin signaling in keratinocytes decreased keratin expression and barrier function; high glucose increased cell-cycle arrest markers.

Conclusions:

• Obesity-associated skin dysfunction stems from structural fragility, impaired glycerol transport, and altered epidermal cell proliferation.
• Cutaneous insulin resistance and hyperglycemia are significant contributors to these obesity-related skin changes.