Phenotypes associated with this allele

• Allele Symbol: Tg(Nr5a1-cre)2Lowl
• Allele Name: transgene insertion 2, Bradford B Lowell
• Allele ID: MGI:3617314
• Summary: 4 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Lepr^tm1.1Chua/Lepr^tm1.1Chua Tg(Nr5a1-cre)2Lowl/0 Tg(Pomc1-cre)16Lowl/0	involves: 129 * C57BL/6J * FVB	MGI:3663493
cn2	Lepr^tm1.1Chua/Lepr^tm1.1Chua Tg(Nr5a1-cre)2Lowl/0	involves: 129 * C57BL/6J * FVB	MGI:3663483
cn3	Slc17a6^tm1Lowl/Slc17a6^tm1Lowl Tg(CAG-Bgeo/GFP)21Lbe/0 Tg(Nr5a1-cre)2Lowl/0	involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * FVB	MGI:4442973
cn4	Mc3r^tm1Butl/Mc3r^tm1Butl Tg(Nr5a1-cre)2Lowl/0	involves: C57BL/6J * FVB/NJ	MGI:5302396

Genotype
MGI:3663493

cn1

• Allelic Composition: Lepr^tm1.1Chua/Lepr^tm1.1Chua; Tg(Nr5a1-cre)2Lowl/0; Tg(Pomc1-cre)16Lowl/0
• Genetic Background: involves: 129 * C57BL/6J * FVB

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

adipose tissue

increased total body fat amount ( J:105327 )

• increase in fat mass

abnormal fat pad morphology ( J:105327 )

• size of fat pads (perigonadal, perirenal, and mesenteric) is increased

abnormal gonadal fat pad morphology ( J:105327 )

abnormal mesenteric fat pad morphology ( J:105327 )

abnormal renal fat pad morphology ( J:105327 )

growth/size/body

obese ( J:105327 )

• weigh significantly more than mice lacking Lepr only in SF1 neurons or POM1 neurons

homeostasis/metabolism

increased circulating leptin level ( J:105327 )

Genotype
MGI:3663483

cn2

• Allelic Composition: Lepr^tm1.1Chua/Lepr^tm1.1Chua; Tg(Nr5a1-cre)2Lowl/0
• Genetic Background: involves: 129 * C57BL/6J * FVB

adipose tissue

increased total body fat amount ( J:105327 )

• increase in fat mass but no difference in lean mass

abnormal fat pad morphology ( J:105327 )

• size of fat pads (perigonadal and perirenal) is increased

abnormal gonadal fat pad morphology ( J:105327 )

• size of perigonadal fat pads is increased

abnormal renal fat pad morphology ( J:105327 )

• size of perirenal fat pads is increased

growth/size/body

increased body weight ( J:105327 )

• 15% increase in body weight at 20 weeks of age compared to controls; degree of obesity is about 20% of that seen in homozygous Lepr^tm1.2Chua mice

increased susceptibility to diet-induced obesity ( J:105327 )

• rapidly gain weight when fed a high-fat diet compared to controls; weight gain is reflected by increases in fat mass

• when switch from a regular chow to a high-fat diet at 8 weeks of age, mutants gain substantially greater amounts of weight than controls

homeostasis/metabolism

increased circulating leptin level ( J:105327 )

abnormal energy expenditure ( J:105327 )

• show marked impairment in ability to activate diet-induced thermogenesis in response to a high-fat diet

increased susceptibility to diet-induced obesity ( J:105327 )

• rapidly gain weight when fed a high-fat diet compared to controls; weight gain is reflected by increases in fat mass

• when switch from a regular chow to a high-fat diet at 8 weeks of age, mutants gain substantially greater amounts of weight than controls

nervous system

abnormal nervous system electrophysiology ( J:105327 )

• leptin has no effect on either membrane potential or firing rate of neurons unlike in controls which show depolarization and increased firing rate in response to leptin

behavior/neurological

increased food intake ( J:105327 )

• fail to suppress food intake over time when fed a high fat diet

Genotype
MGI:4442973

cn3

• Allelic Composition: Slc17a6^tm1Lowl/Slc17a6^tm1Lowl; Tg(CAG-Bgeo/GFP)21Lbe/0; Tg(Nr5a1-cre)2Lowl/0
• Genetic Background: involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * FVB

adipose tissue

increased body fat mass ( J:129860 )

• when fed a high fat diet, mice exhibit a slight increase in fat stores

behavior/neurological

increased food intake ( J:129860 )

• when fed a high fat diet, mice exhibit a slight increase in food intake

growth/size/body

increased body fat mass ( J:129860 )

• when fed a high fat diet, mice exhibit a slight increase in fat stores

increased body weight ( J:129860 )

• mice exhibit a greater increase in weight when fed a high fat diet compared to wild-type mice

homeostasis/metabolism

hypoglycemia ( J:129860 )

• after a 24 hour fast, mice exhibit decreased blood glucose levels (males, 55+/-3 compared to 68+/-5 mg/dl in wild-type mice; females 53+/-2 compared to 67+/-5 mg/dl in wild-type mice)

• acute administration of insulin induces hypoglycemia

abnormal hormone level ( J:129860 )

• mice exhibit impaired fasting-mediated increase in pancreatic hormone glucagon

decreased circulating adrenaline level ( J:129860 )

• following hypoglycemia, mice fail to exhibit an increase in plasma epinephrine levels

decreased circulating glucagon level ( J:129860 )

• during fasting and following hypoglycemia, mice fail to exhibit an increase in plasma glucagons compared to wild-type mice

decreased physiological sensitivity to xenobiotic ( J:129860 )

• glucose plasma levels fail to increase following central administration of 2-deoxyglucose as in wild-type mice

• however, the hyperhagic response initiated by central administration of 2-deoxyglucose is normal

nervous system

abnormal excitatory postsynaptic currents ( J:129860 )

• neurons do not possess any glutamatergic excitatory postsynaptic current

Genotype
MGI:5302396

cn4

• Allelic Composition: Mc3r^tm1Butl/Mc3r^tm1Butl; Tg(Nr5a1-cre)2Lowl/0
• Genetic Background: involves: C57BL/6J * FVB/NJ

growth/size/body

decreased lean body mass ( J:178147 )

• on a standard chow diet

adipose tissue

abnormal adipose tissue amount ( J:178147 )

• increase in fat mass in mice on a standard diet is attenuated compared to homozygous mice not expressing the cre transgene

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:178147 )

N • unlike in homozygous mice not expressing the cre transgene, hyperinsulinemia, reduced energy expenditure per kg of body weight and reduced respiratory exchange ratio are not seen

abnormal circulating leptin level ( J:178147 )

• hyperleptinemia is partially attenuated compared to homozygous mice not expressing the cre transgene

decreased circulating triglyceride level ( J:178147 )

• lower levels of total triglycerides

abnormal energy homeostasis ( J:178147 )

• under a restricted feeding protocol more food is required to protect mice from weight loss exceeding 15% of initial body weight

behavior/neurological

abnormal locomotor activation ( J:178147 )

• partial rescue of reduced activity compared to homozygous mice not expressing the cre transgene

• food anticipatory activity is attenuated