Type 2 diabetes has become a pervasive public health prob-lem. The etiology of the disease has not been fully defined but appears to involve abnormalities in peripheral and central nervous system pathways, as well as prominent inflamma-tory components. Because nicotinic acetylcholine receptors (nAChRs) are known to interact with anti-inflammatory path-ways and have been implicated in control of appetite and body weight, as well as lipid and energy metabolism, we examined their role in modulating biological parameters associated with the disease. In a model of type 2 diabetes, the homozygous leptin-resistant db/db obese mouse, we measured the effects of a novel 7 nAChR-selective agonist [5-methyl-N-[2-(pyridin-3-ylmethyl)-1-azabicyclo[2.2.2]oct-3-yl]thiophene-2-carbox-amide (TC-7020)] on body mass, glucose and lipid metabolism
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