Article Abstract:
Mutant mice lacking neuropeptide Y (NPY) show normal feeding and inhibition by leptin, but are more prone to seizures. The mutant mice maintain normal body weight despite the absence of NPY. Leptin causes an immediate and significant suppression of food intake. The lack of defects in feeding shows that other peptides control feeding in the absence of NPY. The tendency of the mutants to have seizures shows that NPY is involved in the suppression of hippocampal glutamate secretion.
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Article Abstract:
Injection of the mouse obese (ob) gene product (mOB) into ob/ob obese mice suppresses food intake leading to decrease of body weight of mice. The mOB gene product inhibits the release of neuropeptide Y (NPY) by the hypothalamus. A low concentration of NPY decreases feeding and the insulin and corticosterone levels. The OB receptors in the hypothalamus are probably the arcuate nucleus. The OB gene regulates food intake and body weight in thin and genetically obese mice.
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Article Abstract:
The crystal structure of a human mutant obese gene protein (leptin-E100) at 2.4 A resolution has been established as a four-helix bundle. Leptin-E100 includes IL-6, IL-11, IL-12, LIF, G-CSF, CNTF and oncostatin M cytokines. Diffraction data, genetic sequences, ribbon diagrams and MIR phasing statistics are given to illustrate research findings. Research techniques include multiple isomorphous replacement and solvent flattening.
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