AI Article Synopsis
- nAChRs are known for their role in neuronal signaling but are also found in nonneuronal cells, including those involved in metabolism, like pancreatic islets and adipose tissues.
- In a study of α7β2nAChR(-/-) mice, it was found that there were no significant issues with insulin secretion or sensitivity, but these mice showed lower blood sugar levels, increased lean and bone mass, and reduced fat storage.
- The metabolic benefits in α7β2nAChR(-/-) mice were connected to higher spontaneous physical activity, especially in vertical movements, unlike α7nAChR(-/-) mice, which displayed glucose intolerance and inflammation-related issues.
Article Abstract
Nicotinic acetylcholine receptors (nAChRs) are pentameric ligand-gated cation channels well characterized in neuronal signal transmission. Moreover, recent studies have revealed nAChR expression in nonneuronal cell types throughout the body, including tissues involved in metabolism. In the present study, we screen gene expression of nAChR subunits in pancreatic islets and adipose tissues. Mice pancreatic islets present predominant expression of α7 and β2 nAChR subunits but at a lower level than in central structures. Characterization of glucose and energy homeostasis in α7β2nAChR(-/-) mice revealed no major defect in insulin secretion and sensitivity but decreased glycemia apparently unrelated to gluconeogenesis or glycogenolysis. α7β2nAChR(-/-) mice presented an increase in lean and bone body mass and a decrease in fat storage with normal body weight. These observations were associated with elevated spontaneous physical activity in α7β2nAChR(-/-) mice, mainly due to elevation in fine vertical (rearing) activity while their horizontal (ambulatory) activity remained unchanged. In contrast to α7nAChR(-/-) mice presenting glucose intolerance and insulin resistance associated to excessive inflammation of adipose tissue, the present metabolic phenotyping of α7β2nAChR(-/-) mice revealed a metabolic improvement possibly linked to the increase in spontaneous physical activity related to central β2nAChR deficiency.
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| http://dx.doi.org/10.1016/j.ymgme.2014.03.003 | DOI Listing |
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