In mice, a type of gut bacteria called Sphingomonas paucimobilis moves to belly fat during inflammation and blocks the body’s ability to burn calories for heat by interfering with a key fat-burning chemical and its signaling pathway.
Scientific Claim
In mice, chronic inflammation induced by lipopolysaccharide increases the translocation of Sphingomonas paucimobilis from the gut to epididymal white adipose tissue, where it suppresses adaptive thermogenesis by reducing 15-HETE production and inhibiting AMPK phosphorylation, leading to decreased UCP1 expression and mitochondrial function.
Original Statement
“An adipose tissue‐resident bacterium Sphingomonas paucimobilis is identified as a potential inhibitor on the activation of brown fat and browning of inguinal WAT, resulting in defective adaptive thermogenesis... LPS and S. paucimobilis inhibit the production and release of 15‐HETE by suppressing its main metabolic enzyme 12 lipoxygenase (12‐LOX)... 15‐HETE directly binds to AMP‐activated protein kinase α (AMPKα) and elevates the phosphorylation of AMPK, leading to the activation of uncoupling protein 1 (UCP1) and mitochondrial oxidative phosphorylation (OXPHOS) complexes.”
Evidence Quality Assessment
Claim Status
overstated
Study Design Support
Design supports claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
While the mouse data show strong mechanistic associations, the claim uses definitive language ('suppresses', 'inhibits') implying direct causation in humans, which the human data cannot support. The human component is correlational only.
More Accurate Statement
“In mouse models of chronic inflammation, translocation of Sphingomonas paucimobilis to epididymal white adipose tissue is associated with reduced 15-HETE production and suppressed AMPK phosphorylation, leading to decreased UCP1 expression and impaired adaptive thermogenesis.”
Evidence from Studies
Supporting (1)
In mice with chronic inflammation, a specific gut bacterium called Sphingomonas paucimobilis ends up in fat tissue and blocks a key process that helps burn calories, by reducing a helpful molecule (15-HETE) that normally turns on energy-burning machinery in fat cells.