Lymphocyte Antigen 6G Mediates Vagotomy-Associated Reduction in Body Weight

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Dysregulation of adipocyte function is an important component of metabolic and cardiovascular diseases. It is increasingly evident that interorgan neuroimmune crosstalk in adipose tissue maintains adipose tissue functionality, yet the molecular mechanisms are incompletely understood. The vagus nerve regulates numerous physiological functions, including inflammation and weight control, even in tissues lacking direct cholinergic innervation. In this study, we examined whether vagal signaling is involved in maintaining baseline homeostasis in epididymal white adipose tissue (eWAT) by investigating how disrupting vagus signaling affects adipose tissue physiology. As expected, vagotomized male animals had lower body weight and epididymal white adipose tissue mass as compared with controls. Vagotomized animals showed increased Ly6G + cell infiltration in eWAT. Interestingly, vagotomy-associated weight loss was significantly attenuated in neutrophil-deficient Ly6G cre Mcl1 fl/fl mice and in mice treated with repeated injections of anti-Ly6G antibodies. Together, these observations indicate that there is a Ly6G-mediated vagotomy-associated reduction in weight and reveal that Ly6G + cells participate in the regulation of eWAT energy homeostasis.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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