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Nathan Goodyear

Chronic exposure to Low dose bacterial lipopolysaccharide inhibits leptin signaling in ... - 0 views

  • Obesity and models of obesity induced by ingestion of HF-diet in rodents are associated with chronically elevated circulating levels of LPS
  • chronic low-dose administration of LPS induces leptin-resistance in vagal afferent neurons and abolition of CCK-induced inhibition of food intake
  • HF fat feeding has been shown to enhance gastrointestinal permeability promoting the translocation of LPS to the circulation
  • ...9 more annotations...
  • LPS leads to an increase in SOCS3 expression [20]. SOCS3 is a negative regulator of leptin signaling
  • We observed a significant increase in energy intake in the LPS-treated rats
  • the data provides a mechanism linking changes in gut microbiota induced by ingestion of HF diets to dysregulation of food intake and body weight
  • SOCS3 is an important mechanism by which leptin resistance develops in vagal afferent neurons and coincides with the onset of hyperphagia
  • Chronic low-dose LPS treatment induced TLR4 activation and MyD88 signaling in vagal afferent neurons, associated with increased SOCS3 expression and reduced leptin-signaling, characterized by the absence of leptin-induced pSTAT3.
  • We demonstrate that this chronic low dose LPS is sufficient to induce leptin–resistance in vagal afferent neurons, reduced sensitivity to the satiating effects of CCK, and loss of vagal afferent plasticity
  • it suggests that the increase in food intake and body weight we observed at week 6 in the LPS treated rats may be caused by LPS-induced leptin resistance.
  • chronic LPS treatment of mice for four weeks increased body weight
  • chronic LPS treatment of mice for four weeks increased subcutaneous fat
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    Very interesting study.  High fat diet in rats induced gut flora change that resulted in LPS which induced appetite through leptin resistance and reduced cholecystokinin signaling.
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