Monosodium glutamate (MSG) treatment of neonatal mice results
in a selective damage to the arcuate nucleus (ARC) and
development of obesity with increased adiposity at sustained
body weight in the adulthood. Feeding pattern of the MSG obese
mice is unusual. Our previous results showed that after 24-h
fasting, MSG mice consumed negligible amount of food in several
hours and therefore, it was impossible to register the effect of
peptides attenuating food intake such as cholecystokinin (CCK) or
cocaine- and amphetamine-regulated transcript (CART) peptide.
To overcome this problem, two findings were used: firstly,
orexigenic effect of neuropeptide Y (NPY) was attenuated both
by CCK or CART peptide in lean fed mice and secondly,
orexigenic effect of NPY was preserved in fed rats with MSG
obesity. In this study, short-term food intake in fed lean and MSG
obese C57BL/6 male mice was measured after simultaneous
central administration of orexigenic NPY with either CART peptide
or peripherally administered CCK. Anorexigenic action of
exogenous CART peptide was preserved in MSG obese mice. On
the other hand, satiety effect of exogenous CCK was completely
lost in MSG obese mice. In conclusion, effective leptin signaling
in ARC is necessary for satiety effect of CCK.
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