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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Sphkaptm1.1Nina
targeted mutation 1.1, Nobuya Inagaki
MGI:6449058
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Sphkaptm1.1Nina/Sphkaptm1.1Nina Not Specified MGI:6473655


Genotype
MGI:6473655
hm1
Allelic
Composition
Sphkaptm1.1Nina/Sphkaptm1.1Nina
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sphkaptm1.1Nina mutation (0 available); any Sphkap mutation (87 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• glucose-stimulated insulin secretion (GSIS) at high (16.7 mM) glucose concentration in the presence of 10 nM exendin-4 is similar to that in the absence of exendin-4 indicating that exendin-4 enhanced insulin secretion is absent in mutant islets, unlike in wild-type islets where exendin-4 induces a 2.0-fold increase in GSIS at 16.7 mM glucose
• GSIS is ~2.5-fold higher than that in wild-type mice under high glucose (11.1 mM and 16.7 mM) conditions, with no differences in islet insulin content
• GSIS in pancreatic islets is increased by ~5.5-fold and 14.4-fold at 11.1 mM and 16.7 mM glucose, respectively, relative to that at 2.8 mM glucose, whereas GSIS is increased by ~3.2-fold and 7.3-fold, respectively, in wild-type mice
• sphingosine kinase activity is normal at 2.8 mM and 16.7 mM glucose and ATP and cAMP content are similarly increased in mutant and wild-type islets
• depolarization-evoked, PKA and cAMP-mediated insulin secretion are unaffected
• GSIS is similarly augmented by IBMX (a non-selective phosphodiesterase (PDE) inhibitor) in mutant and wild-type islets
• under a 2 g/kg body weight intraperitoneal glucose tolerance test (IpGTT), blood glucose levels are significantly lower than those in wild-type mice at 30 and 60 min, and tend to be even lower at 120 min; blood glucose area under the curve is reduced by 15%
• under a 2 g/kg body weight IpGTT, plasma insulin levels in the presence of 10 nM exendin-4 are significantly lower at 10 and 15 min than those in wild-type mice, while insulin-AUC is similar to that in wild-type mice at 0-120 min
• under a 2 g/kg body weight IpGTT, plasma insulin levels are higher than those in wild-type mice at 15 and 60 min and insulin area under the curve is increased by 1.24-fold

endocrine/exocrine glands
• glucose-stimulated insulin secretion (GSIS) at high (16.7 mM) glucose concentration in the presence of 10 nM exendin-4 is similar to that in the absence of exendin-4 indicating that exendin-4 enhanced insulin secretion is absent in mutant islets, unlike in wild-type islets where exendin-4 induces a 2.0-fold increase in GSIS at 16.7 mM glucose
• GSIS is ~2.5-fold higher than that in wild-type mice under high glucose (11.1 mM and 16.7 mM) conditions, with no differences in islet insulin content
• GSIS in pancreatic islets is increased by ~5.5-fold and 14.4-fold at 11.1 mM and 16.7 mM glucose, respectively, relative to that at 2.8 mM glucose, whereas GSIS is increased by ~3.2-fold and 7.3-fold, respectively, in wild-type mice
• sphingosine kinase activity is normal at 2.8 mM and 16.7 mM glucose and ATP and cAMP content are similarly increased in mutant and wild-type islets
• depolarization-evoked, PKA and cAMP-mediated insulin secretion are unaffected
• GSIS is similarly augmented by IBMX (a non-selective phosphodiesterase (PDE) inhibitor) in mutant and wild-type islets





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last database update
10/29/2024
MGI 6.24
The Jackson Laboratory