NDLI: Enhanced glucose tolerance in pancreatic-derived factor (PANDER) knockout C57BL/6 mice

Content Provider	PubMed Central
Author	Moak, Shari L. Dougan, Grace C. Marelia, Catherine B. Danse, Whitney A. Fernandez, Amanda M. Kuehl, Melanie N. Athanason, Mark G. Burkhardt, Brant R.
Copyright Year	2014
Abstract	Pancreatic-derived factor (PANDER; also known as FAM3B) is a uniquely structured protein strongly expressed within and secreted from the endocrine pancreas. PANDER has been hypothesized to regulate fasting and fed glucose homeostasis, hepatic lipogenesis and insulin signaling, and to serve a potential role in the onset or progression of type 2 diabetes (T2D). Despite having potentially pivotal pleiotropic roles in glycemic regulation and T2D, there has been limited generation of stable animal models for the investigation of PANDER function, and there are no models on well-established genetic murine backgrounds for T2D. Our aim was to generate an enhanced murine model to further elucidate the biological function of PANDER. Therefore, a pure-bred PANDER knockout C57BL/6 (PANKO-C57) model was created and phenotypically characterized with respect to glycemic regulation and hepatic insulin signaling. The PANKO-C57 model exhibited an enhanced metabolic phenotype, particularly with regard to enhanced glucose tolerance. Male PANKO-C57 mice displayed decreased fasting plasma insulin and C-peptide levels, whereas leptin levels were increased as compared with matched C57BL/6J wild-type mice. Despite similar peripheral insulin sensitivity between both groups, hepatic insulin signaling was significantly increased during fasting conditions, as demonstrated by increased phosphorylation of hepatic PKB/Akt and AMPK, along with mature SREBP-1 expression. Insulin stimulation of PANKO-C57 mice resulted in increased hepatic triglyceride and glycogen content as compared with wild-type C57BL/6 mice. In summary, the PANKO-C57 mouse represents a suitable model for the investigation of PANDER in multiple metabolic states and provides an additional tool to elucidate the biological function and potential role in T2D.
Related Links	http://dx.doi.org/10.1242/dmm.016402
Ending Page	1315
Page Count	9
Starting Page	1307
File Format	PDF
ISSN	17548411
e-ISSN	17548411
Journal	Disease Models & Mechanisms
Issue Number	11
Volume Number	7
Language	English
Publisher	The Company of Biologists Limited
Publisher Date	2014-11-01
Access Restriction	Open
Rights Holder	The Company of Biologists Limited
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Microbiology Medicine Biochemistry, Genetics and Molecular Biology

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