Chronic exposure to Low dose bacterial lipopolysaccharide inhibits leptin signaling in ... - 0 views
www.ncbi.nlm.nih.gov/...PMC4523075
LPS lipopolysaccharides leptin CCK cholecystokinin metabolism weight appetite diet nutrition inflammation
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Obesity and models of obesity induced by ingestion of HF-diet in rodents are associated with chronically elevated circulating levels of LPS
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chronic low-dose administration of LPS induces leptin-resistance in vagal afferent neurons and abolition of CCK-induced inhibition of food intake
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HF fat feeding has been shown to enhance gastrointestinal permeability promoting the translocation of LPS to the circulation
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LPS leads to an increase in SOCS3 expression [20]. SOCS3 is a negative regulator of leptin signaling
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the data provides a mechanism linking changes in gut microbiota induced by ingestion of HF diets to dysregulation of food intake and body weight
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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.
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SOCS3 is an important mechanism by which leptin resistance develops in vagal afferent neurons and coincides with the onset of hyperphagia
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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
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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.