Insulin resistance caused by sympathetic nervous system over-activation, a paradigm-shifting study finds

SNS Overactivation Drives Insulin Resistance: The study revealed that overnutrition causes insulin resistance primarily through increased sympathetic nervous system (SNS) activity rather than through impaired cellular insulin signaling.

Insulin Resistance Prevention by Reducing SNS Activity: In a mouse model, reducing peripheral SNS activity protected against insulin resistance and glucose intolerance, even with a high-fat diet, demonstrating the potential for SNS modulation in preventing metabolic disorders.

Catecholamine Resistance from Chronic SNS Overactivation: Long-term high-fat diets in wild-type mice led to catecholamine resistance, where elevated norepinephrine levels no longer triggered normal physiological responses, worsening metabolic outcomes.

Adipose Tissue Dysfunction Linked to SNS Overactivity: Chronic SNS overactivation in high-fat diet-fed mice led to increased inflammation, fibrosis, and senescence in white adipose tissue, which impaired metabolic health, while mice with reduced SNS activity avoided these issues.

Potential Paradigm Shift in Type 2 Diabetes Management: This study suggests that targeting SNS overactivity may be a novel approach to managing insulin resistance and obesity-related metabolic disorders, potentially reshaping type 2 diabetes prevention strategies.