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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Mlxipltm1Kuy
targeted mutation 1, Kosaku Uyeda
MGI:3043871
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Mlxipltm1Kuy/Mlxipltm1Kuy B6.129S6-Mlxipltm1Kuy/J MGI:6297092
hm2
Mlxipltm1Kuy/Mlxipltm1Kuy involves: 129S6/SvEvTac * C57BL/6J MGI:3043880


Genotype
MGI:6297092
hm1
Allelic
Composition
Mlxipltm1Kuy/Mlxipltm1Kuy
Genetic
Background
B6.129S6-Mlxipltm1Kuy/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mlxipltm1Kuy mutation (1 available); any Mlxipl mutation (36 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• mice exhibit a significant weight loss when fed a high fructose diet (60% fructose, 10% starch), showing a 20% reduction in body weight after 5 days on the diet
• body weight recovers within 6 days after switching back to the control diet

digestive/alimentary system
• cecum weight is increased in mice fed a high fructose diet
• on day 3 of a high fructose diet, mice exhibit enlarged ceca that contains fluid
• by day 5 and through day 7 of the high fructose diet, mice exhibit enlarged, red intestines and extremely distended ceca that contain both fluid and gas
• colon length is increased in mice fed a high fructose diet
• fecal pellets are decreased in high fructose fed mice
• mice fed a high fructose diet develop severe diarrhea
• fructose levels in feces are 2-fold higher in mice fed a high fructose diet, indicating development of fructose intolerance
• plasma alanine transaminase, aspartate transaminase, and lactate dehydrogenase, indicators of liver injury, are not increased in mutant mice fed a high fructose diet unlike in wild-type mice that show an increase in their levels, indicating resistance to liver damage by high fructose diet due to impaired fructose absorption
• on the high fructose diet, lactate levels in the intestine are not increased as in wild-type mice and lactate levels in the liver are decreased in mutants indicating impaired fructose conversion into lactate in the intestine but not the liver

behavior/neurological
• average daily food intake is lower in mice fed a high fructose diet
• food intake is decreased by more than 50% within 1-2 days after starting the high fructose diet and increases right after switching back to the control diet

homeostasis/metabolism
• males exhibit a lower blood glucose levels when fed a high fructose diet
• females exhibit a slight increase in blood glucose levels when fed a high fructose diet
• plasma cholesterol levels are decreased in mutant mice on both a control diet and the high fructose diet
• plasma triglyceride levels are decreased in mutant mice on both a control diet and the high fructose diet
• mice exhibit lower body temperature when fed a high fructose diet
• liver triglyceride levels are decreased in mutant mice on both a control diet and the high fructose diet

liver/biliary system
• liver triglyceride levels are decreased in mutant mice on both a control diet and the high fructose diet

mortality/aging
• mice fed a high fructose diet become moribund in 2 weeks
• mice younger than 5 weeks that are fed the high fructose diet become moribund within a few days

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
irritable bowel syndrome DOID:9778 J:273754




Genotype
MGI:3043880
hm2
Allelic
Composition
Mlxipltm1Kuy/Mlxipltm1Kuy
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mlxipltm1Kuy mutation (1 available); any Mlxipl mutation (36 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• on a high starch diet liver weight are about 40% greater in homozygous mice compared to wild-type mice probably as a result of increased glycogen stores in homozygous mice

mortality/aging
• on a 70% sucrose diet homozygous mice die in less than 1 week
• on a high-fructose diet homozygous mice die within a few days
• on a standard chow diet homozygous mice have a normal life span

adipose tissue
• on a standard diet homozygous mice have lower brown fat weights
• on a standard diet homozygous mice have lower epididymal fat weights

homeostasis/metabolism
• on a 70% sucrose diet homozygous mice develop hypothermia
• plasma glucose levels are somewhat elevated
• plasma insulin levels are somewhat elevated
• on a high-starch diet plasma insulin levels increase significantly compared to homozygous mice on a standard diet or wild-type mice on either diet
• liver glycogen levels are elevated but muscle glycogen levels are not elevated
• liver glycogen levels are elevated further on a high-starch diet
• on a high-starch diet homozygous mice are moderately insulin resistant
• on a high starch diet plasma cholesterol is significantly lower compared to wild-type mice on the same diet
• hepatic fatty acid synthesis rates are 65% lower in homozygous mice
• on either a standard or high-starch diet plasma free fatty acid levels are about 50% that in wild-type mice on the same diet
• on a 70% sucrose diet free fatty acid levels decline further in homozygous mice

liver/biliary system
• on a high starch diet liver weight are about 40% greater in homozygous mice compared to wild-type mice probably as a result of increased glycogen stores in homozygous mice
• liver glycogen levels are elevated but muscle glycogen levels are not elevated
• liver glycogen levels are elevated further on a high-starch diet
• hepatic glucose levels are increased
• hepatic pyruvate/phosphoenolpyruvate ratio is decreased indicating inhibition of hepatic glycolysis





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
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last database update
01/18/2022
MGI 6.17
The Jackson Laboratory