Comments:
- 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. - Nathan Goodyear
Highlights and Sticky Notes:
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
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
Tags:LPS, lipopolysaccharides, leptin, CCK, cholecystokinin, metabolism, weight, appetite, diet, nutrition, inflammation
