Background: CART (cocaine-and amphetamine-regulated transcript) peptide and cholecystokinin (CCK) are neuromodulators involved in feeding behavior. This study is based on previously found synergistic effect of leptin and CCK on food intake and our hypothesis on a cooperation of the CART peptide and CCK in food intake regulation and Fos activation in their common targets, the nucleus tractus solitarii of the brainstem (NTS), the paraventricular nucleus (PVN), and the dorsomedial nucleus (DMH) of the hypothalamus.
In this study, susceptibility of inbred C57BL/6 and outbred NMRI
mice to monosodium glutamate (MSG) obesity or diet-induced
obesity (DIO) was compared in terms of food intake, body
weight, adiposity as well as leptin, insulin and glucose levels.
MSG obesity is an early-onset obesity resulting from MSGinduced lesions in arcuate nucleus to neonatal mice. Both male
and female C57BL/6 and NMRI mice with MSG obesity did not
differ in body weight from their lean controls, but had
dramatically increased fat to body weight ratio. All MSG obese
mice developed severe hyperleptinemia, more remarkable in
females, but only NMRI male mice showed massive
hyperinsulinemia and an extremely high HOMA index that pointed
to development of insulin resistance. Diet-induced obesity is a
late-onset obesity; it developed during 16-week-long feeding with
high-fat diet containing 60 % calories as fat. Inbred C57BL/6
mice, which are frequently used in DIO studies, both male and
female, had significantly increased fat to body weight ratio and
leptin and glucose levels compared with their appropriate lean
controls, but only female C57BL/6 mice had also significantly
elevated body weight and insulin level. NMRI mice were less
prone to DIO than C57BL/6 ones and did not show significant
changes in metabolic parameters after feeding with high-fat diet.
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