To address whether PKA stimulators-mediated leptin suppression may be required for their regulation of MSC differentiation, namely induction of adipogenesis and inhibition of osteogenesis, we investigate whether the effects of PKA stimulators would be blocked by adding leptin exogenously.
We have used multiple convergent methods, including making lean mice obese, by adding leptin systemically and by restoring LepR to the DMH of LepR-deficient mice.
In addition, other joint effect combinations assessed by adding leptin, CRP, IL-6, and/or SAA into the full model adjusted for metabolic syndrome variables in addition to primary exposure to adiponectin did not improve diabetes prediction.
The sOB-R assay was not affected by adding up to 300 μg/L recombinant leptin to plasma samples.
Obesity, it seemed, might be caused by a leptin deficiency, and treating it might be as simple as supplying fat people with the hormone.
The mechanism by which obASC-derived leptin promotes alterations to the biology of BCCs was investigated by inhibiting leptin expression by stably transfecting lnASCs and obASCs with a leptin shRNA construct.
This suggests a possible vicious cycle in which the stimulation of CRP production by leptin leads to the production of greater quantities of a leptin antagonist, thereby being a potential mechanism contributing to leptin resistance seen in obese subjects.
Leptin was measured by a human leptin radioimmunoassay kit.
Phosphorylation of VEGFR2, p38MAPK and Akt, and COX-2 induction in cells challenged with leptin were blocked by a specific leptin peptide receptor antagonist.
