Analysis Tools|
Allele Symbol Allele Name Allele ID |
Prdm16tm1.1Brsp targeted mutation 1.1, Bruce M Spiegelman MGI:5564782 |
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| Summary |
7 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• tamoxifen-treated mice do not show overt cardiac phenotypes, even 36 weeks after induction
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• postnatal lethality before P7
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice exhibit progressive cardiac dysfunction leading to death before P7
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• thinner left ventricle compact myocardium starting from E15.5
• however, thickness of right ventricle compact myocardium is normal
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• mice develop biventricular noncompaction
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• mice exhibit clefts at the apices of the hearts as early as E15.5
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• thinner interventricular septum starting from E15.5
• however, thickness of right ventricle compact myocardium is not different
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• enlarged left ventricle is seen as early as E15.5
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• mice exhibit progressive cardiac dysfunction
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• severe cardiac contractile dysfunction in P0 to P3 neonates
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• reduction in proliferating cardiomyocytes in left ventricle compact myocardium and interventricular septum at both E13.5 and E15.5
• however, no differences in cardiomyocyte apoptosis are seen
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• echocardiography shows severe cardiac contractile dysfunction in P0 to P3 neonates, increased left ventricle chamber size, and thinned interventricular septum
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• left ventricular noncompaction cardiomyopathy
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• thinner left ventricle compact myocardium starting from E15.5
• however, thickness of right ventricle compact myocardium is normal
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• severe cardiac contractile dysfunction in P0 to P3 neonates
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• reduction in proliferating cardiomyocytes in left ventricle compact myocardium and interventricular septum at both E13.5 and E15.5
• however, no differences in cardiomyocyte apoptosis are seen
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• left ventricular noncompaction cardiomyopathy
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• reduction in proliferating cardiomyocytes in left ventricle compact myocardium and interventricular septum at both E13.5 and E15.5
• however, no differences in cardiomyocyte apoptosis are seen
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| left ventricular noncompaction | DOID:0060480 |
OMIM:604169 |
J:326525 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• pale axillary and cervical brown adipose tissue depots
• however, tissue mass is not altered
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• in the interscapular brown adipose tissue of mice older than 6 months
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• in the interscapular brown adipose tissue of mice older than 6 months
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• whitening in mice older than 6 months with increased size of the tissue, a switch from multilocular to unilocular morphology, and increased lipid content
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• in unstimulated interscapular brown adipose tissue
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• whitening in mice older than 6 months with increased size of the tissue, a switch from multilocular to unilocular morphology, and increased lipid content
• 3 week old mice fed a high-fat diet exhibit loss of normal brown adipocyte morphology unlike wild-type mice
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• in mice older than 6 months
• however, juvenile mice exhibit normal sized brown adipose tissue depots
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• precipitous drop in body temperature following exposure to cold
• however, diet-induced thermogenesis is normal
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• precipitous drop in body temperature following exposure to cold
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• at all ages
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• in unstimulated interscapular brown adipose tissue
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• with poorly organized cristae in unstimulated interscapular brown adipose tissue
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• reduced basal in interscapular brown adipose tissue
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in the interscapular brown adipose tissue of mice older than 6 months
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• pale in 3 month old mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• subcutaneous adipose tissue contains larger adipocytes and fewer smaller multiocular UCP1+ adipocytes relative to control mice following cold exposure
• subcutaneous adipose tissue from mice following 6 weeks on high fat diet has increased numbers of crown like structures, however, there are no changes in visceral (abdominal) fat
• subcutaneous adipose tisse from mice following 6 weeks on high fat diet has increased numbers of CD11b+F4/80+ macrophages
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• subcutaneous fat mass from male mice after 16 weeks on high fat diet is increased to twice that of controls, epididymal and brown adipose tissue are unchanged
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• body composition analysis after 16 weeks on high fat diet indicates increased fat mass with no change in lean body mass
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• subcutaneous fat mass is doubled as compared to controls after 16 weeks on high fat diet; epididymal and BAT masses are unchanged
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• subcutaneous adipocytes from male mice after 18 weeks on high fat diet exhibit a 33% increase in mean adipocyte area
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• O2 consumption is reduced in subcutaneous adipose pads, but not in brown adipose pads, at baseline (36% reduced) and following stimulation with a beta-adrenergic agonist (49% reduced)
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• glucose uptake is reduced in subcutaneous fat (79% decrease) and visceral fat (53% decrease) after 6 weeks on high fat diet as compared to controls
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• subcutaneous adipocytes exhibit a blunted response to stimuli such as isoproterenol that induce a thermogenic gene program (beige adipocytes)
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• mice exhibit increased weight gain after 16 weeks on high-fat, high-carbohydrate diet relative to control mice
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• subcutaneous adipose tissue from mice following 6 weeks on high fat diet has increased numbers of CD11b+F4/80+ macrophages, but macrophage numbers in visceral adipose tissue and spleen are unchanged
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• increased fasting plasma insulin levels (55%) in mice after 6 weeks on high fat diet
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• unlike controls, mutant mice do not exhibit increased O2 consumption following stimulation with a beta-adrenergic agonist
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• mice exhibit an increased respiratory exchange ratio (RER), but no increase in O2 consumption
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• a reduced glucose infusion rate (64% of controls) is observed in mice after 6 weeks on high fat diet
• decreased whole body glucose uptake is observed in mice after 6 weeks on high fat diet
• clamped insulin levels do not increase as much as controls in mice after 6 weeks on high fat diet
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• increased liver tryglycerides are observed in mice after 6 weeks on high fat diet as compared to controls
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• subcutaneous adipose tissue from mice following 6 weeks on high fat diet has increased numbers of CD11b+F4/80+ macrophages, but macrophage numbers in visceral adipose tissue and spleen are unchanged
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• subcutaneous fat mass from male mice after 16 weeks on high fat diet is increased to twice that of controls, epididymal and brown adipose tissue are unchanged
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• increased liver tryglycerides are observed in mice after 6 weeks on high fat diet as compared to controls
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• after 6 weeks on high fat diet
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• glucose uptake is reduced in subcutaneous fat (79% decrease) and visceral fat (53% decrease) after 6 weeks on high fat diet as compared to controls
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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 12/10/2024 MGI 6.24 |
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