Adult Type 3 Adenylyl Cyclaseâ Deficient Mice Are Obese

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dc.contributor.authorWang, Zhenshan
dc.contributor.authorLi, Vicky
dc.contributor.authorChan, Guy C. K.
dc.contributor.authorPhan, Trongha
dc.contributor.authorNudelman, Aaron S.
dc.contributor.authorXia, Zhengui
dc.contributor.authorStorm, Daniel R.
dc.contributor.corporatenameDepartment of Neurology
dc.contributor.corporatenameCollege of Graduate Studies
dc.contributor.editorTsien, Joe Z.
dc.date.accessioned2012-10-26T16:26:44Z
dc.date.available2012-10-26T16:26:44Z
dc.date.issued2009-09-11en_US
dc.description.abstractBackground: A recent study of obesity in Swedish men found that polymorphisms in the type 3 adenylyl cyclase (AC3) are associated with obesity, suggesting the interesting possibility that AC3 may play a role in weight control. Therefore, we examined the weight of AC3 mice over an extended period of time.
dc.description.abstractWe discovered that AC3-/- mice become obese as they age. Adult male AC3-/- mice are about 40% heavier than wild type male mice while female AC3-/- are 70% heavier. The additional weight of AC3-/- mice is due to increased fat mass and larger adipocytes. Before the onset of obesity, young AC3-/- mice exhibit reduced physical activity, increased food consumption, and leptin insensitivity. Surprisingly, the obesity of AC3-/- mice is not due to a loss of AC3 from white adipose and a decrease in lipolysis.
dc.description.abstractConclusions/Significance: We conclude that mice lacking AC3 exhibit obesity that is apparently caused by low locomotor activity, hyperphagia, and leptin insensitivity. The presence of AC3 in primary cilia of neurons of the hypothalamus suggests that cAMP signals generated by AC3 in the hypothalamus may play a critical role in regulation of body weight.
dc.identifier.citationPLoS One. 2009 Sep 11; 4(9):e6979en_US
dc.identifier.doi10.1371/journal.pone.0006979en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmcidPMC2735775en_US
dc.identifier.pmid19750222en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/572
dc.rightsWang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectResearch Articleen_US
dc.subjectPharmacologyen_US
dc.subjectNeuroscience/Neurobiology of Disease and Regenerationen_US
dc.subjectDiabetes and Endocrinology/Obesityen_US
dc.titleAdult Type 3 Adenylyl Cyclaseâ Deficient Mice Are Obeseen_US
dc.typeArticleen_US
html.description.abstractBackground: A recent study of obesity in Swedish men found that polymorphisms in the type 3 adenylyl cyclase (AC3) are associated with obesity, suggesting the interesting possibility that AC3 may play a role in weight control. Therefore, we examined the weight of AC3 mice over an extended period of time.
html.description.abstractWe discovered that AC3-/- mice become obese as they age. Adult male AC3-/- mice are about 40% heavier than wild type male mice while female AC3-/- are 70% heavier. The additional weight of AC3-/- mice is due to increased fat mass and larger adipocytes. Before the onset of obesity, young AC3-/- mice exhibit reduced physical activity, increased food consumption, and leptin insensitivity. Surprisingly, the obesity of AC3-/- mice is not due to a loss of AC3 from white adipose and a decrease in lipolysis.
html.description.abstractConclusions/Significance: We conclude that mice lacking AC3 exhibit obesity that is apparently caused by low locomotor activity, hyperphagia, and leptin insensitivity. The presence of AC3 in primary cilia of neurons of the hypothalamus suggests that cAMP signals generated by AC3 in the hypothalamus may play a critical role in regulation of body weight.
refterms.dateFOA2019-04-09T21:12:14Z

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