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Article

Heterozygous Nme7 Mutation Affects Glucose Tolerance in Male Rats

1
Laboratory of Transgenic Models of Diseases, Division BIOCEV, Institute of Molecular Genetics of the Czech Academy of Sciences, 252 50 Vestec, Czech Republic
2
Institute of Biology and Medical Genetics, First Faculty of Medicine, Charles University, and General University Hospital, 128 00 Prague, Czech Republic
3
Czech Centre for Phenogenomics, Institute of Molecular Genetics of the Czech Academy of Sciences, v.v.i., 252 50 Vestec, Czech Republic
4
Department of Molecular Endocrinology, Institute of Endocrinology, 116 94 Prague, Czech Republic
*
Author to whom correspondence should be addressed.
Academic Editor: David Q.-H. Wang
Received: 22 June 2021 / Revised: 15 July 2021 / Accepted: 17 July 2021 / Published: 18 July 2021
Complex metabolic conditions such as type 2 diabetes and obesity result from the interaction of numerous genetic and environmental factors. While the family of Nme proteins has been connected so far mostly to development, proliferation, or ciliary functions, several lines of evidence from human and experimental studies point to the potential involvement of one of its members, NME7 (non-metastatic cells 7, nucleoside diphosphate kinase 7) in carbohydrate and lipid metabolism. As a complete lack of Nme7 is semilethal in rats, we compared morphometric, metabolic, and transcriptomic profiles of standard diet-fed heterozygous Nme7+/− on male rats vs. their wild-type Nme7+/+ controls. Nme7+/− animals showed increased body weight, adiposity, higher insulin levels together with decreased glucose tolerance. Moreover, they displayed pancreatic islet fibrosis and kidney tubular damage. Despite no signs of overt liver steatosis or dyslipidemia, we found significant changes in the hepatic transcriptome of Nme7+/− male rats with a concerted increase of expression of lipogenic enzymes including Scd1, Fads1, Dhcr7 and a decrease of Cyp7b1 and Nme7. Network analyses suggested possible links between Nme7 and the activation of Srebf1 and Srebf2 upstream regulators. These results further support the implication of NME7 in the pathogenesis of glucose intolerance and adiposity. View Full-Text
Keywords: metabolic syndrome; pancreatic fibrosis; animal models metabolic syndrome; pancreatic fibrosis; animal models
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MDPI and ACS Style

Šedová, L.; Prochazka, J.; Zudová, D.; Bendlová, B.; Včelák, J.; Sedlacek, R.; Šeda, O. Heterozygous Nme7 Mutation Affects Glucose Tolerance in Male Rats. Genes 2021, 12, 1087. https://0-doi-org.brum.beds.ac.uk/10.3390/genes12071087

AMA Style

Šedová L, Prochazka J, Zudová D, Bendlová B, Včelák J, Sedlacek R, Šeda O. Heterozygous Nme7 Mutation Affects Glucose Tolerance in Male Rats. Genes. 2021; 12(7):1087. https://0-doi-org.brum.beds.ac.uk/10.3390/genes12071087

Chicago/Turabian Style

Šedová, Lucie, Jan Prochazka, Dagmar Zudová, Běla Bendlová, Josef Včelák, Radislav Sedlacek, and Ondřej Šeda. 2021. "Heterozygous Nme7 Mutation Affects Glucose Tolerance in Male Rats" Genes 12, no. 7: 1087. https://0-doi-org.brum.beds.ac.uk/10.3390/genes12071087

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