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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Plin5tm1e(KOMP)Wtsi
targeted mutation 1e, Wellcome Trust Sanger Institute
MGI:4363886
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Plin5tm1e(KOMP)Wtsi/Plin5tm1e(KOMP)Wtsi involves: C57BL/6N MGI:5903929


Genotype
MGI:5903929
hm1
Allelic
Composition
Plin5tm1e(KOMP)Wtsi/Plin5tm1e(KOMP)Wtsi
Genetic
Background
involves: C57BL/6N
Cell Lines EPD0301_4_E04
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plin5tm1e(KOMP)Wtsi mutation (0 available); any Plin5 mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• 52% reduction in cardiac triacylglycerol content, along with a marked reduction of lipid droplets stained by ORO in the heart

homeostasis/metabolism
• 52% reduction in cardiac triacylglycerol content, along with a marked reduction of lipid droplets stained by ORO in the heart
• ~11% decrease in whole-body fatty acid oxidation
• however, no significant alterations in fatty acid uptake, fatty acid oxidation or esterification of extracellular-derived fatty acids in isolated skeletal (soleus) muscle under basal or forskolin-stimulated conditions
• pulse-chase experiments on primary myotubes from skeletal muscle show that oxidation of triacylglycerol-derived fatty acids is increased concomitant with increased depletion of the 14C labeled triacylglycerol, indicating degradation of triacylglycerol in skeletal muscle
• however, mitochondrial content and function are not enhanced in either isolated myotubes or intact skeletal muscle
• respiratory exchange ratio is increased, as assessed by indirect calorimetry
• glucose tolerance is improved on a low-fat diet (LFD), as shown by an attenuated blood glucose excursion after glucose administration
• glucose tolerance is markedly enhanced on a high-fat diet (HFD), with HFD-fed mice showing comparable glucose tolerance to LFD-fed wild-type mice
• skeletal muscle glycogen content is reduced following hyperinsulinemic euglycemic clamp
• both hepatic glucose production and insulin sensitive gluconeogenic gene expression are reduced during insulin clamp conditions, suggesting improved hepatic insulin sensitivity
• mice become insulin resistant due to reduced insulin stimulated glucose disposal in skeletal muscle and adipose tissue, but maintain insulin sensitivity in the liver
• reduced skeletal muscle insulin sensitivity, observed during hyperinsulinemic euglycemic clamps, is associated with ceramide accumulation
• sphingomyelin levels are increased in cultured myotubes
• ceramide level is increased by 53% in skeletal muscle, whereas diacylglycerol levels remains normal
• ceramide, dihydro- and hexosyl-ceramide levels are increased in cultured myotubes, whereas other lipid types such as phospholipids and sterols are mostly normal
• however, no evidence of ER stress, inflammation or oxidative stress in skeletal muscle
• significant reduction of triacylglycerol content in red quadriceps (oxidative) skeletal muscle
• however, no significant alterations in mixed quadriceps or liver triacylglycerol content
• ~11% increase in whole-body carbohydrate oxidation
• however, no significant alteration in glucose oxidation in isolated skeletal (soleus) muscle
• 24 h fasted mice fail to show lipid droplet staining in skeletal muscle, indicating increased intramyocelluar lipolysis and an inability to expand the intramyocellular triacylglycerol pool

muscle
• 52% reduction in cardiac triacylglycerol content, along with a marked reduction of lipid droplets stained by ORO in the heart
• skeletal muscle glycogen content is reduced following hyperinsulinemic euglycemic clamp
• significant reduction of triacylglycerol content in red quadriceps (oxidative) skeletal muscle
• however, no significant alterations in mixed quadriceps or liver triacylglycerol content

adipose tissue
• glucose uptake is reduced in white adipose tissue

cellular
• glucose uptake is reduced in white adipose tissue
• ~11% decrease in whole-body fatty acid oxidation
• however, no significant alterations in fatty acid uptake, fatty acid oxidation or esterification of extracellular-derived fatty acids in isolated skeletal (soleus) muscle under basal or forskolin-stimulated conditions
• pulse-chase experiments on primary myotubes from skeletal muscle show that oxidation of triacylglycerol-derived fatty acids is increased concomitant with increased depletion of the 14C labeled triacylglycerol, indicating degradation of triacylglycerol in skeletal muscle
• however, mitochondrial content and function are not enhanced in either isolated myotubes or intact skeletal muscle





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last database update
11/19/2024
MGI 6.24
The Jackson Laboratory