All Phenotypes Tg(Pomc1-cre)16Lowl MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Tg(Pomc1-cre)16Lowl
transgene insertion 16, Bradford B Lowell
MGI:3640616

Summary

24 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Htr2c^tm1Jke/Y Tg(Pomc1-cre)16Lowl/0	B6.Cg-Htr2c^tm1Jke Tg(Pomc1-cre)16Lowl	MGI:3841490
cn2	Insr^tm1Khn/Insr^tm1Khn Lepr^tm1.1Chua/Lepr^tm1.1Chua Tg(Pomc1-cre)16Lowl/0	involves: 129 * 129S4/SvJae * 129S6/SvEvTac * C57BL/6J * FVB/N	MGI:5471586
cn3	Lepr^tm1.1Chua/Lepr^tm1.1Chua Tg(Pomc1-cre)16Lowl/0	involves: 129 * C57BL/6J * FVB	MGI:3640618
cn4	Lepr^tm1.1Chua/Lepr^tm1.1Chua Tg(Nr5a1-cre)2Lowl/0 Tg(Pomc1-cre)16Lowl/0	involves: 129 * C57BL/6J * FVB	MGI:3663493
cn5	Gt(ROSA)26Sor^{tm1(Sirt1)Ktm}/Gt(ROSA)26Sor⁺ Tg(Pomc1-cre)16Lowl/0	involves: 129 * C57BL/6J * FVB/N	MGI:5586724
cn6	Gt(ROSA)26Sor^{tm2(Sirt1)Ktm}/Gt(ROSA)26Sor⁺ Tg(Pomc1-cre)16Lowl/0	involves: 129 * C57BL/6J * FVB/N	MGI:5586726
cn7	Lepr^tm1.1Chua/Lepr^tm1.1Chua Tg(Pomc1-cre)16Lowl/0	involves: 129 * FVB	MGI:5142227
cn8	Lepr^tm1.1Chua/Lepr^tm1.1Chua Tg(Pomc1-cre)16Lowl/0 Tg(Pomc1-hrGFP)1Lowl/0	involves: 129 * FVB	MGI:5142226
cn9	Glp2r^tm1.1Xfg/Glp2r^tm1.1Xfg Tg(Pomc1-cre)16Lowl/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N	MGI:5446804
cn10	Gt(ROSA)26Sor^{tm2(Foxo1)Jnk}/Gt(ROSA)26Sor⁺ Pdpk1^tm1Maka/Pdpk1^tm1Maka Tg(CAG-cat,-lacZ)11Miya/0 Tg(Pomc1-cre)16Lowl/0	involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N	MGI:4820872
cn11	Gt(ROSA)26Sor^{tm1(Foxo1)Jnk}/Gt(ROSA)26Sor⁺ Pdpk1^tm1Maka/Pdpk1^tm1Maka Tg(CAG-cat,-lacZ)11Miya/0 Tg(Pomc1-cre)16Lowl/0	involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N	MGI:4820871
cn12	Pdpk1^tm1Maka/Pdpk1^tm1Maka Tg(CAG-cat,-lacZ)11Miya/0 Tg(Pomc1-cre)16Lowl/0	involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N	MGI:4820873
cn13	Rock1^tm1.1Itl/Rock1^tm1.1Itl Tg(Pomc1-cre)16Lowl/0	involves: 129S4/SvJaeSor * C57BL/6 * FVB/N	MGI:5543676
cn14	Rock1^tm1.1Itl/Rock1^tm1.1Itl Tg(Npy-hrGFP)1Lowl/0 Tg(Pomc1-cre)16Lowl/0	involves: 129S4/SvJaeSor * C57BL/6 * FVB/N	MGI:5543677
cn15	Htr2c^tm2Jke/Y Tg(Pomc1-cre)16Lowl/0 Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺	involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * FVB/N	MGI:5569627
cn16	Nhlh2^tm2Thbr/Nhlh2^tm2Thbr Tg(Pomc-EGFP)1Low/0 Tg(Pomc1-cre)16Lowl/0	involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J * FVB/N	MGI:5524040
cn17	Htr2c^tm2Jke/Htr2c^tm2Jke Tg(Pomc1-cre)16Lowl/0	involves: 129X1/SvJ * C57BL/6J * FVB/N	MGI:5569624
cn18	Htr2c^tm2Jke/Y Tg(Pomc1-cre)16Lowl/0	involves: 129X1/SvJ * C57BL/6J * FVB/N	MGI:5569623
cn19	Lepr^tm1Jke/Lepr^tm1Jke Tg(Pomc1-cre)16Lowl/0	involves: 129X1/SvJ * C57BL/6J * FVB/N	MGI:5426233
cn20	Gt(ROSA)26Sor^{tm1(CAG-Foxo1*)Jcbr}/Gt(ROSA)26Sor⁺ Pdpk1^tm1Jcbr/Pdpk1^tm1Jcbr Tg(Pomc1-cre)16Lowl/0	involves: C57BL/6 * FVB/N	MGI:3804312
cn21	Pdpk1^tm1Jcbr/Pdpk1^tm1Jcbr Tg(Pomc1-cre)16Lowl/0	involves: C57BL/6 * FVB/N	MGI:3804310
cn22	Tg(CAG-PPARG*,-tdTomato)#Sig/0 Tg(Pomc1-cre)16Lowl/0	involves: C57BL/6 * FVB/N * SJL	MGI:5912229
cn23	Tg(CAG-PPARG,-tdTomato)#Sig/0 Tg(Pomc1-cre)16Lowl/0	involves: C57BL/6 * FVB/N * SJL	MGI:5912228
tg24	Tg(Pomc1-cre)16Lowl/0	involves: 129 * C57BL/6J * FVB/N	MGI:3655815

Allelic Composition	Htr2c^tm1Jke/Y Tg(Pomc1-cre)16Lowl/0
Genetic Background	B6.Cg-Htr2c^tm1Jke Tg(Pomc1-cre)16Lowl

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Htr2c^tm1Jke mutation (1 available); any Htr2c mutation (13 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

mortality/aging

premature death ( J:147514 )

• mice exhibit a decreased survival rate compared to wild-type mice

• mice fed a regular diet exhibit decreased survival compared to mice fed a high fat diet

nervous system

tonic-clonic seizures ( J:147514 )

behavior/neurological

behavior/neurological phenotype ( J:147514 )

N	• mice exhibit normal food intake and locomotor activity levels

tonic-clonic seizures ( J:147514 )

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:147514 )

N	• mice exhibit normal leptin levels and anorexigenic responses to d-Fen and metachlorophenylpiperazine

adipose tissue

adipose tissue phenotype ( J:147514 )

N	• mice exhibit normal adiposity in response to a high fat diet

growth/size/body

growth/size/body region phenotype ( J:147514 )

N	• mice exhibit normal weight gain in response to a high fat diet

Allelic Composition	Insr^tm1Khn/Insr^tm1Khn Lepr^tm1.1Chua/Lepr^tm1.1Chua Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129 * 129S4/SvJae * 129S6/SvEvTac * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Insr^tm1Khn mutation (1 available); any Insr mutation (95 available)
Lepr^tm1.1Chua mutation (1 available); any Lepr mutation (122 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

adipose tissue

increased abdominal adipose tissue amount ( J:192274 )

• trend towards increased intra-abdominal adiposity at 4 months of age

increased fat cell size ( J:192274 )

• perigonadal adipocyte hypertrophy at 4 months of age

abnormal gonadal fat pad morphology ( J:192274 )

• perigonadal adipocyte hypertrophy at 4 months of age

• an increase in macrophage accumulation is seen in the perigonadal fat indicating inflammation

increased percent body fat/body weight ( J:192274 )

• percent body fat is increased in females at 4 months of age, however absolute body weight is not increased at this time

white adipose tissue inflammation ( J:192274 )

• an increase in macrophage accumulation is seen in the perigonadal fat, and macrophage marker analysis and cytokine expression indicates low-grade inflammation in adipose tissue

endocrine/exocrine glands

absent corpus luteum ( J:192274 )

• 45% of mice lack either corpora lutea or preovulatory follicles

absent mature ovarian follicles ( J:192274 )

• 45% of mice lack either corpora lutea or preovulatory follicles

ovary inflammation ( J:192274 )

• low-grade inflammation as indicated by increased IL-6 expression in the ovary

growth/size/body

decreased lean body mass ( J:192274 )

• percent lean body mass is decreased at 4 months of age

homeostasis/metabolism

hyperglycemia ( J:192274 )

• females are hyperglycemic before (at 3 months of age) and during pregnancy (at gestational days 12 and 15), without evidence of gestational glucose intolerance

increased circulating leptin level ( J:192274 )

• circulating levels of adipokine leptin are increased at 4 months of age

immune system

white adipose tissue inflammation ( J:192274 )

• an increase in macrophage accumulation is seen in the perigonadal fat, and macrophage marker analysis and cytokine expression indicates low-grade inflammation in adipose tissue

ovary inflammation ( J:192274 )

• low-grade inflammation as indicated by increased IL-6 expression in the ovary

liver inflammation ( J:192274 )

• low-grade inflammation as indicated by increased IL-1beta expression in the liver

liver/biliary system

liver inflammation ( J:192274 )

• low-grade inflammation as indicated by increased IL-1beta expression in the liver

reproductive system

absent corpus luteum ( J:192274 )

• 45% of mice lack either corpora lutea or preovulatory follicles

absent mature ovarian follicles ( J:192274 )

• 45% of mice lack either corpora lutea or preovulatory follicles

ovary inflammation ( J:192274 )

• low-grade inflammation as indicated by increased IL-6 expression in the ovary

decreased ovulation rate ( J:192274 )

• females exhibit reduced ovulation but show normal cycling suppression from fasting

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
polycystic ovary syndrome		DOID:11612	OMIM:184700	J:192274

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

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lepr^tm1.1Chua mutation (1 available); any Lepr mutation (122 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

growth/size/body

increased body weight ( J:105327 )

obese ( J:106354 )

• exhibit mild obesity with an increase in body weight at 10 weeks of age that is 18.2% that of homozygous Lepr^tm1.2Chua mice

adipose tissue

increased total body fat amount ( J:105327 , J:106354 )

• increase in fat mass (J:105327)

• exhibit increased body fat but no differences in food intake or energy expenditure (J:106354)

abnormal fat pad morphology ( J:105327 , J:106354 )

abnormal epididymal fat pad morphology ( J:106354 )

• epididymal fat pads are at least twice as large as in controls

abnormal gonadal fat pad morphology ( J:105327 )

• size of perigonadal fat pads is increased

abnormal mesenteric fat pad morphology ( J:105327 , J:106354 )

• size of mesenteric fat pads is increased (J:105327)

• mesenteric fat pads are at least twice as large as in controls (J:106354)

abnormal renal fat pad morphology ( J:105327 , J:106354 )

• size of perirenal fat pads is increased (J:105327)

• perirenal fat pads are at least twice as large as in controls (J:106354)

homeostasis/metabolism

increased circulating leptin level ( J:105327 , J:106354 )

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

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lepr^tm1.1Chua mutation (1 available); any Lepr mutation (122 available)
Tg(Nr5a1-cre)2Lowl mutation (1 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

♀	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 )

Allelic Composition	Gt(ROSA)26Sor^{tm1(Sirt1)Ktm}/Gt(ROSA)26Sor⁺ Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129 * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm1(Sirt1)Ktm} mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:209418 )

N	• mice exhibit normal hypothalamus-pituitary-adrenal and hypothalamus-pituitary-thyroid axes

increased adipose tissue noradrenaline turnover ( J:209418 )

• noradrenaline turnover in the white adipose tissue is increased in male mice compared to in control mice

• however, turnover in skeletal muscle is normal

decreased susceptibility to induced hypothermia ( J:209418 )

• mice tend to be cold-resistant for short-term exposure compared with control mice

• however, mice fed a high fat high sugar diet exhibit normal cold resistance

decreased circulating thyroxine level ( J:209418 )

• tend

increased energy expenditure ( J:209418 )

• male mice fed normal chow exhibit increased energy expenditure suggested by a tend toward higher oxygen consumption and lower locomotor activity compared with control mice

• however, mice fed a high fat high sugar diet exhibit normal energy expenditure

increased oxygen consumption ( J:209418 )

• trend in male mice fed normal chow

increased response to leptin ( J:209418 )

• mice exhibit improved leptin sensitivity compared with control mice

growth/size/body

growth/size/body region phenotype ( J:209418 )

N	• male and female mice fed normal chow exhibit normal body length • mice fed a high fat high sugar diet exhibit normal weight gain

decreased susceptibility to age related obesity ( J:209418 )

• in male, but not female, mice fed normal chow

adipose tissue

decreased total body fat amount ( J:209418 )

• in male, but not female, mice fed normal chow

• however, mice fed a high fat high sugar diet exhibit normal adiposity

decreased epididymal fat pad weight ( J:209418 )

• in male mice fed normal chow

increased adipose tissue noradrenaline turnover ( J:209418 )

• noradrenaline turnover in the white adipose tissue is increased in male mice compared to in control mice

• however, turnover in skeletal muscle is normal

behavior/neurological

behavior/neurological phenotype ( J:209418 )

N	• female and male mice exhibit normal food intake

decreased locomotor activity ( J:209418 )

• trend in male mice fed normal chow

• however, mice fed a high fat high sugar diet exhibit normal locomotion

Allelic Composition	Gt(ROSA)26Sor^{tm2(Sirt1)Ktm}/Gt(ROSA)26Sor⁺ Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129 * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm2(Sirt1)Ktm} mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

adipose tissue

adipose tissue phenotype ( J:209418 )

N	• mice fed normal chow exhibit normal epididymal white adipose tissue weight

behavior/neurological

behavior/neurological phenotype ( J:209418 )

N	• mice fed normal chow exhibit normal food intake and locomotor activity

growth/size/body

growth/size/body region phenotype ( J:209418 )

N	• mice fed normal chow exhibit normal susceptibility to age-associated weight gain and body length

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:209418 )

N	• mice fed normal chow exhibit normal oxygen consumption

Allelic Composition	Lepr^tm1.1Chua/Lepr^tm1.1Chua Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129 * FVB

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lepr^tm1.1Chua mutation (1 available); any Lepr mutation (122 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

nervous system

nervous system phenotype ( J:174691 )

N	• no change in spontaneous IPSC amplitude or frequency in Pomc1 neurons in slices is observed, indicating that Lepr deletion from postsynaptic Pomc1 neurons does not affect inhibitory tone

Allelic Composition	Lepr^tm1.1Chua/Lepr^tm1.1Chua Tg(Pomc1-cre)16Lowl/0 Tg(Pomc1-hrGFP)1Lowl/0
Genetic Background	involves: 129 * FVB

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lepr^tm1.1Chua mutation (1 available); any Lepr mutation (122 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
Tg(Pomc1-hrGFP)1Lowl mutation (1 available)

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

nervous system

nervous system phenotype ( J:174691 )

N	• addtion of leptin to neurons reduces the frequency of spontaneous (s)IPSCs in Pomc1 neurons by about 40%, similar to the inhibition observed in control neurons

Allelic Composition	Glp2r^tm1.1Xfg/Glp2r^tm1.1Xfg Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Glp2r^tm1.1Xfg mutation (0 available); any Glp2r mutation (39 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

digestive/alimentary system

abnormal gastrointestinal motility ( J:189593 )

• accelerated gastric emptying with a dramatic shortening of half-excretion time and lag phase for a liquid meal

behavior/neurological

increased eating frequency ( J:189593 )

• increase in meal frequency but not meal size

increased food intake ( J:189593 )

• higher food intake during the dark cycle

increased vertical activity ( J:189593 )

• during the dark cycle

growth/size/body

decreased lean body mass ( J:189593 )

• lean mass as a percent of body weight is decreased by 32 weeks of age

obese ( J:189593 )

• late onset obesity develops after 33 weeks of age

adipose tissue

increased percent body fat/body weight ( J:189593 )

• by 32 weeks of age

homeostasis/metabolism

increased oxygen consumption ( J:189593 )

• in fed mice during the dark cycle

abnormal metabolism ( J:189593 )

• increase in heat production by fed mice during the dark cycle

• however, at 12 weeks of age mice fasted for 4 h show similar metabolic activity (VO2, VCO2, and heat production) to controls under inactive conditions

Allelic Composition	Gt(ROSA)26Sor^{tm2(Foxo1)Jnk}/Gt(ROSA)26Sor⁺ Pdpk1^tm1Maka/Pdpk1^tm1Maka Tg(CAG-cat,-lacZ)11Miya/0 Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm2(Foxo1)Jnk} mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Pdpk1^tm1Maka mutation (0 available); any Pdpk1 mutation (138 available)
Tg(CAG-cat,-lacZ)11Miya mutation (0 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

adipose tissue

increased total body fat amount ( J:162892 )

• female mice exhibit a tended towards increased adiposity compared with wild-type mice

behavior/neurological

increased food intake ( J:162892 )

• mice exhibit increased food intake compared with wild-type mice and Pdpk1^tm1Maka/Pdpk1^tm1Maka Tg(CAG-cat-lacZ)11Miya Tg(Pomc1-cre)16Lowl mice

growth/size/body

increased body weight ( J:162892 )

• at 16 weeks, mice are significantly heavier than Pdpk1^tm1Maka/Pdpk1^tm1Maka Tg(CAG-cat-lacZ)11Miya Tg(Pomc1-cre)16Lowl mice

Allelic Composition	Gt(ROSA)26Sor^{tm1(Foxo1)Jnk}/Gt(ROSA)26Sor⁺ Pdpk1^tm1Maka/Pdpk1^tm1Maka Tg(CAG-cat,-lacZ)11Miya/0 Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm1(Foxo1)Jnk} mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Pdpk1^tm1Maka mutation (0 available); any Pdpk1 mutation (138 available)
Tg(CAG-cat,-lacZ)11Miya mutation (0 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

growth/size/body

increased body weight ( J:162892 )

• mice a tend towards increased in body weight compared with Pdpk1^tm1Maka/Pdpk1^tm1Maka Tg(CAG-cat-lacZ)11Miya Tg(Pomc1-cre)16Lowl mice

Allelic Composition	Pdpk1^tm1Maka/Pdpk1^tm1Maka Tg(CAG-cat,-lacZ)11Miya/0 Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdpk1^tm1Maka mutation (0 available); any Pdpk1 mutation (138 available)
Tg(CAG-cat,-lacZ)11Miya mutation (0 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

nervous system

increased pituitary gland apoptosis ( J:162892 )

• mice exhibit increased apoptosis in the pituitary compared with wild-type mice

increased corticotroph apoptosis ( J:162892 )

• mice exhibit a decrease in corticotrophs in the anterior pituitary due to apoptosis unlike in wild-type mice

• however, corticotroph development in the anterior pituitary at E18.5 is normal

increased melanotroph apoptosis ( J:162892 )

• mice exhibit a decrease in melanotrophs in the intermediate pituitary due to apoptosis unlike in wild-type mice

• however, melanotrophs development in the intermediate pituitary at E18.5 is normal

abnormal pituitary intermediate lobe morphology ( J:162892 )

• extremely thin

abnormal neuron physiology ( J:162892 )

• Pomc1 neurons exhibit a blunted influx of calcium ions in response to leptin compared with similarly treated wild-type neurons

homeostasis/metabolism

hypoglycemia ( J:162892 )

decreased circulating corticosterone level ( J:162892 )

• at 16 weeks in fed and fasted states

increased insulin sensitivity ( J:162892 )

decreased response to leptin ( J:162892 )

• following intraperitoneal leptin injection, mice exhibit a lesser decrease in body weight and food intake compared with similarly treated wild-type mice

adipose tissue

increased total body fat amount ( J:162892 )

• especially visceral fat mass

behavior/neurological

increased food intake ( J:162892 )

• food intake is increased compared to in wild-type mice

endocrine/exocrine glands

increased pituitary gland apoptosis ( J:162892 )

• mice exhibit increased apoptosis in the pituitary compared with wild-type mice

increased corticotroph apoptosis ( J:162892 )

• mice exhibit a decrease in corticotrophs in the anterior pituitary due to apoptosis unlike in wild-type mice

• however, corticotroph development in the anterior pituitary at E18.5 is normal

increased melanotroph apoptosis ( J:162892 )

• mice exhibit a decrease in melanotrophs in the intermediate pituitary due to apoptosis unlike in wild-type mice

• however, melanotrophs development in the intermediate pituitary at E18.5 is normal

abnormal pituitary intermediate lobe morphology ( J:162892 )

• extremely thin

cellular

increased pituitary gland apoptosis ( J:162892 )

• mice exhibit increased apoptosis in the pituitary compared with wild-type mice

increased corticotroph apoptosis ( J:162892 )

• mice exhibit a decrease in corticotrophs in the anterior pituitary due to apoptosis unlike in wild-type mice

• however, corticotroph development in the anterior pituitary at E18.5 is normal

increased melanotroph apoptosis ( J:162892 )

• mice exhibit a decrease in melanotrophs in the intermediate pituitary due to apoptosis unlike in wild-type mice

• however, melanotrophs development in the intermediate pituitary at E18.5 is normal

Allelic Composition	Rock1^tm1.1Itl/Rock1^tm1.1Itl Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129S4/SvJaeSor * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rock1^tm1.1Itl mutation (0 available); any Rock1 mutation (60 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

adipose tissue

increased total body fat amount ( J:204885 )

increased epididymal fat pad weight ( J:204885 )

increased mesenteric fat pad weight ( J:204885 )

increased renal fat pad weight ( J:204885 )

• perirenal

homeostasis/metabolism

increased circulating insulin level ( J:204885 )

• at 20 weeks

increased circulating leptin level ( J:204885 )

• at 20 weeks

insulin resistance ( J:204885 )

• modest defect in the ability of insulin to decrease blood glucose

behavior/neurological

increased food intake ( J:204885 )

decreased locomotor activity ( J:204885 )

• during the dark phase

• however, movement during the light phase is normal

growth/size/body

increased body weight ( J:204885 )

skeleton

skeleton phenotype ( J:204885 )

N	• mice exhibit normal femur length, bone mineral density and bone mineral content

Allelic Composition	Rock1^tm1.1Itl/Rock1^tm1.1Itl Tg(Npy-hrGFP)1Lowl/0 Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129S4/SvJaeSor * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rock1^tm1.1Itl mutation (0 available); any Rock1 mutation (60 available)
Tg(Npy-hrGFP)1Lowl mutation (1 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

nervous system

abnormal nervous system electrophysiology ( J:204885 )

• leptin fails to depolarize POMC+ neurons and increase firing rate unlike in control neurons

Allelic Composition	Htr2c^tm2Jke/Y Tg(Pomc1-cre)16Lowl/0 Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze}/Gt(ROSA)26Sor⁺
Genetic Background	involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm14(CAG-tdTomato)Hze} mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Htr2c^tm2Jke mutation (0 available); any Htr2c mutation (13 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

nervous system

abnormal nervous system electrophysiology ( J:207704 )

• ability of the serotonin receptor 2C agonist mCPP to depolarized Pomc-expressing neurons is abolished in mutants

Allelic Composition	Nhlh2^tm2Thbr/Nhlh2^tm2Thbr Tg(Pomc-EGFP)1Low/0 Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nhlh2^tm2Thbr mutation (0 available); any Nhlh2 mutation (13 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)
Tg(Pomc-EGFP)1Low mutation (1 available)

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

reproductive system

reproductive system phenotype ( J:199640 )

N	• mice exhibit normal uteri weight and fertility

nervous system

nervous system phenotype ( J:199640 )

N	• mice exhibit normal numbers of Gnrh+ neurons

growth/size/body

growth/size/body region phenotype ( J:199640 )

N	• mice exhibit normal weight

adipose tissue

adipose tissue phenotype ( J:199640 )

N	• mice exhibit normal visceral and subcutaneous fat depots

Allelic Composition	Htr2c^tm2Jke/Htr2c^tm2Jke Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129X1/SvJ * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Htr2c^tm2Jke mutation (0 available); any Htr2c mutation (13 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

mortality/aging

mortality/aging ( J:207704 )

N	• animals are born at Mendelian frequency and show no increased mortality compared to controls

growth/size/body

growth/size/body region phenotype ( J:207704 )

N	• when fed a regular chow diet, body weights of mutants are similar to controls at weaning and between 8 and 20 weeks of age

increased body weight ( J:207704 )

• HFHS-fed (high fat, high sugar) animals have significantly increased body weights at 4 weeks after introduction of this diet; at 20 weeks on the HFHS-diet, mutants are 25% heavier than controls due to adiposity

• 20 week-old mutants which had been fed an HFHS diet for 12 weeks have increased body weights compared to controls

increased susceptibility to diet-induced obesity ( J:207704 )

• HFHS-fed (high fat, high sugar) animals have significantly increased body weights at 4 weeks after introduction of this diet

• chow-fed mutants transitioned acutely to HFHS food display similarly increased body weights after 1 week of the new diet

behavior/neurological

increased food intake ( J:207704 )

• daily food intake is elevated relative to controls when fed a regular chow diet; when diet is transitioned to a high fat, high sugar (HFHS) diet for 1 week, food intake is significantly increased relative to controls

• 20 week-old mutants which had been fed an HFHS diet for 12 weeks show a higher food intake compared to controls

• administration of d-flenfluaramine or the more specific serotonin 2C receptor agonist mCPP strongly suppresses food intake in control mice, but mutants are not affected

hyperactivity ( J:207704 )

• total activity due to increased dark cycle activity is increased compared to controls when fed a regular chow diet

• 20 week-old mutants which had been fed an HFHS diet for 12 weeks show increased total physical activity compared to controls; this increase is restricted to the dark phase

• when animals are switched to a high fat high sugar diet for 1 week, physical activity does not increase relative to the chow diet

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:207704 )

N	• on a regular chow diet, mutants and controls have similar respiratory exchange ratios when fed a regular chow diet • chow-fed or HFHS-fed (high fat, high sugar) animals have similar circulating leptin levels

increased susceptibility to diet-induced obesity ( J:207704 )

• HFHS-fed (high fat, high sugar) animals have significantly increased body weights at 4 weeks after introduction of this diet

• chow-fed mutants transitioned acutely to HFHS food display similarly increased body weights after 1 week of the new diet

increased circulating glucose level ( J:207704 )

• at the beginning of the light phase (7 am), chow-fed mice show modestly higher glucose levels than controls; levels are significantly elevated in postabsorptive (4-5 hour morning-fasted animals) but not in overnight (12-24 h) fasted mice

• high fat, high sugar (HFHS) fed mutants also have elevated glucose levels in the postabsorptive period compared to HFHS-fed controls

hyperglycemia ( J:207704 )

increased circulating glucagon level ( J:207704 )

• higher plasma glucagon levels are detected in postabsorptive chow-fed mutants (4-5 hour morning-fasted); levels are comparable to controls with overnight fasting

• HFHS-fed (high fat, high sugar) animals do not show additionally increased plasma glucagon levels compared to chow-fed mutants

increased circulating insulin level ( J:207704 )

• higher plasma insulin levels are detected in postabsorptive chow-fed mutants (4-5 hour morning-fasted); levels are comparable to controls with overnight fasting

• HFHS-fed (high fat, high sugar) animals have a greater increase in plasma insulin compared to chow-fed mutants

increased energy expenditure ( J:207704 )

• increased energy intake and expenditure are observed when fed a regular chow diet

decreased oxygen consumption ( J:207704 )

• 20 week-old mutants which had been fed an HFHS diet for 12 weeks have lower oxygen consumption relative to body weight compared to controls on the same diet while carbon dioxide production is similar to controls

increased oxygen consumption ( J:207704 )

• VO2 (and VCO2) are increased compared to controls when fed a regular chow diet

• when animals are switched to a high fat high sugar diet for 1 week, oxygen consumption/ C02 production does not increase relative to the chow diet

abnormal respiratory quotient ( J:207704 )

• on the high fat high sugar diet for 1 week, respiratory exchange ratio (RER) is slightly decreased in mutants and controls compared to animals on a regular chow diet, but over a 24 hour period, mutants show a modest increase relative to controls

• 20 week-old mutants which had been fed an HFHS (high fat, high sugar) diet for 12 weeks have a higher RER during the dark phase

insulin resistance ( J:207704 )

• hyperinsulinemic-euglycemic clamp experiments in postabsorptive and overnight-fasted 8-9 week old mice show reduced insulin sensitivity

Allelic Composition	Htr2c^tm2Jke/Y Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129X1/SvJ * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Htr2c^tm2Jke mutation (0 available); any Htr2c mutation (13 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

behavior/neurological

increased food intake ( J:207704 )

• 20 week-old mutants which had been fed an HFHS diet for 12 weeks show a higher food intake compared to controls

• administration of d-flenfluaramine or the more specific serotonin 2C receptor agonist mCPP strongly suppresses food intake in control mice, but mutants are not affected

hyperactivity ( J:207704 )

• total activity due to increased dark cycle activity is increased compared to controls when fed a regular chow diet

• 20 week-old mutants which had been fed an HFHS diet for 12 weeks show increased total physical activity compared to controls; this increase is restricted to the dark phase

• when animals are switched to a high fat high sugar diet for 1 week, physical activity does not increase relative to the chow diet

growth/size/body

growth/size/body region phenotype ( J:207704 )

N	• when fed a regular chow diet, body weights of mutants are similar to controls at weaning and between 8 and 20 weeks of age

increased body weight ( J:207704 )

• 20 week-old mutants which had been fed an HFHS diet for 12 weeks have increased body weights compared to controls

increased susceptibility to diet-induced obesity ( J:207704 )

• HFHS-fed (high fat, high sugar) animals have significantly increased body weights at 4 weeks after introduction of this diet

• chow-fed mutants transitioned acutely to HFHS food display similarly increased body weights after 1 week of the new diet

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:207704 )

N	• on a regular chow diet, mutants and controls have similar respiratory exchange ratios when fed a regular chow diet • chow-fed or HFHS-fed (high fat, high sugar) animals have similar circulating leptin levels

increased susceptibility to diet-induced obesity ( J:207704 )

• HFHS-fed (high fat, high sugar) animals have significantly increased body weights at 4 weeks after introduction of this diet

• chow-fed mutants transitioned acutely to HFHS food display similarly increased body weights after 1 week of the new diet

increased circulating glucose level ( J:207704 )

• high fat, high sugar (HFHS) fed mutants also have elevated glucose levels in the postabsorptive period compared to HFHS-fed controls

hyperglycemia ( J:207704 )

increased circulating glucagon level ( J:207704 )

• higher plasma glucagon levels are detected in postabsorptive chow-fed mutants (4-5 hour morning-fasted); levels are comparable to controls with overnight fasting

• HFHS-fed (high fat, high sugar) animals do not show additionally increased plasma glucagon levels compared to chow-fed mutants

increased circulating insulin level ( J:207704 )

• higher plasma insulin levels are detected in postabsorptive chow-fed mutants (4-5 hour morning-fasted); levels are comparable to controls with overnight fasting

• HFHS-fed (high fat, high sugar) animals have a greater increase in plasma insulin compared to chow-fed mutants

increased energy expenditure ( J:207704 )

• increased energy intake and expenditure are observed when fed a regular chow diet

decreased oxygen consumption ( J:207704 )

increased oxygen consumption ( J:207704 )

• VO2 (and VCO2) are increased compared to controls when fed a regular chow diet

• when animals are switched to a high fat high sugar diet for 1 week, oxygen consumption/ C02 production does not increase relative to the chow diet

abnormal respiratory quotient ( J:207704 )

• 20 week-old mutants which had been fed an HFHS (high fat, high sugar) diet for 12 weeks have a higher RER during the dark phase

insulin resistance ( J:207704 )

• hyperinsulinemic-euglycemic clamp experiments in postabsorptive and overnight-fasted 8-9 week old mice show reduced insulin sensitivity

mortality/aging

mortality/aging ( J:207704 )

N	• animals are born at Mendelian frequency and show no increased mortality compared to controls

Allelic Composition	Lepr^tm1Jke/Lepr^tm1Jke Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129X1/SvJ * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lepr^tm1Jke mutation (2 available); any Lepr mutation (122 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:184572 )

N	• mice exhibit normal circulating glucagon levels in the fed and carbohydrate-refed state

increased circulating leptin level ( J:184572 )

• compared with wild-type mice

decreased circulating cholesterol level ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

increased circulating cholesterol level ( J:184572 )

• compared with wild-type mice

decreased circulating triglyceride level ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

increased circulating triglyceride level ( J:184572 )

• compared with wild-type mice

decreased carbon dioxide production ( J:184572 )

• compared with wild-type mice

increased carbon dioxide production ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

decreased oxygen consumption ( J:184572 )

• compared with wild-type mice

increased oxygen consumption ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

increased respiratory quotient ( J:184572 )

• compared with wild-type mice

abnormal glucose homeostasis ( J:184572 )

• mice exhibit normal basal glucose turnover compared with Lepr^tm1Jke homozygotes

• insulin-stimulated glucose disposal is impaired compared to in wild-type mice

• however, mice exhibit normal circulating glucose levels at 6, 8 and 12 weeks

increased insulin secretion ( J:184572 )

• in the pancreas compared with wild-type mice

decreased circulating glucose level ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

decreased circulating insulin level ( J:184572 )

• at 8 and 12 weeks compared with Lepr^tm1Jke homozygotes

increased circulating insulin level ( J:184572 )

• compared with wild-type mice

increased insulin sensitivity ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

decreased liver triglyceride level ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

increased liver triglyceride level ( J:184572 )

• compared with wild-type mice

growth/size/body

decreased body weight ( J:184572 )

• in male mice after 12 weeks compared with Lepr^tm1Jke homozygotes

obese ( J:184572 )

• in male mice between 4 and 12 weeks less severe after 12 weeks compared with wild-type mice

• in female mice

behavior/neurological

abnormal eating behavior ( J:184572 )

• compared with wild-type mice

hyperactivity ( J:184572 )

• during the dark phase compared with wild-type mice

adipose tissue

decreased total body fat amount ( J:184572 )

• in male mice at 20 weeks compared with Lepr^tm1Jke homozygotes

increased total body fat amount ( J:184572 )

• in male mice at 12 and 20 weeks compared with wild-type mice

endocrine/exocrine glands

increased insulin secretion ( J:184572 )

• in the pancreas compared with wild-type mice

liver/biliary system

decreased liver triglyceride level ( J:184572 )

• compared with Lepr^tm1Jke homozygotes

increased liver triglyceride level ( J:184572 )

• compared with wild-type mice

Allelic Composition	Gt(ROSA)26Sor^{tm1(CAG-Foxo1*)Jcbr}/Gt(ROSA)26Sor⁺ Pdpk1^tm1Jcbr/Pdpk1^tm1Jcbr Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm1(CAG-Foxo1*)Jcbr} mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Pdpk1^tm1Jcbr mutation (0 available); any Pdpk1 mutation (138 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:134336 )

N	• expression of the mutant foxo1 restores body weight, food consumption and blood glucose levels to normal

decreased circulating corticosterone level ( J:134336 )

• mutants have reduced basal and stress-induced corticosterone levels, similar to double Pdk1^tm1Jcbr Tg(Pomc1-cre)16Lowl mutants

endocrine/exocrine glands

decreased corticotroph cell number ( J:134336 )

• same reduction in corticotrophs as seen in double Pdk1^tm1Jcbr Tg(Pomc1-cre)16Lowl mutants

nervous system

decreased corticotroph cell number ( J:134336 )

• same reduction in corticotrophs as seen in double Pdk1^tm1Jcbr Tg(Pomc1-cre)16Lowl mutants

Allelic Composition	Pdpk1^tm1Jcbr/Pdpk1^tm1Jcbr Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdpk1^tm1Jcbr mutation (0 available); any Pdpk1 mutation (138 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

growth/size/body

increased body weight ( J:134336 )

• males and females fed either a normal chow diet or a high-fat chow diet display slightly but significantly increased body weight, although over time, weight normalizes

• corticosterone replacement in mutants increases food intake and body weight

homeostasis/metabolism

decreased circulating corticosterone level ( J:134336 )

• corticosterone replacement in mutants increases food intake and body weight

• reduction in plasma corticosterone concentrations is seen as early as 3 weeks of age, with levels continuing to decrease over time

• mutants show an impairment in stress-induced corticosterone production

• injection of ACTH analog does not increase plasma corticosterone to the level of control mice, consistent with adrenal insufficiency

abnormal circulating leptin level ( J:134336 )

• initially, mutants exhibit an elevation in serum leptin levels at 8 weeks of age, however by 18 weeks of age, they show lower serum leptin levels than controls but have an unchanged body weight

abnormal glucose homeostasis ( J:134336 )

decreased insulin secretion ( J:134336 )

• glucose-stimulated insulin secretion is lower than in controls

decreased circulating glucose level ( J:134336 )

• analysis of glucose-stimulated insulin secretion shows that although insulin secretion is lower, their blood glucose concentration is also lower than in controls

increased circulating glucose level ( J:134336 )

• initial elevation in serum glucose levels at 8 weeks of age

improved glucose tolerance ( J:134336 )

• old mutants perform better than controls during glucose tolerance tests

increased insulin sensitivity ( J:134336 )

• old mutants show significantly increased insulin sensitivity during insulin tolerance tests than controls

endocrine/exocrine glands

decreased corticotroph cell number ( J:134336 )

abnormal melanotroph morphology ( J:134336 )

• decrease in melanotroph numbers in the intermediate lobe of the pituitary, but do not see an obvious change in fur color or skin pigmentation

decreased insulin secretion ( J:134336 )

• glucose-stimulated insulin secretion is lower than in controls

adipose tissue

decreased gonadal fat pad weight ( J:134336 )

• at 18 weeks of age, mutants show reduced epigonadal fat-pad mass

behavior/neurological

polyphagia ( J:134336 )

• significant hyperphagia at 8 weeks of age but not at 10 weeks of age

• corticosterone replacement in mutants increases food intake and body weight

nervous system

decreased corticotroph cell number ( J:134336 )

abnormal melanotroph morphology ( J:134336 )

• decrease in melanotroph numbers in the intermediate lobe of the pituitary, but do not see an obvious change in fur color or skin pigmentation

Allelic Composition	Tg(CAG-PPARG*,-tdTomato)#Sig/0 Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: C57BL/6 * FVB/N * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-PPARG*,-tdTomato)#Sig mutation (0 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

behavior/neurological

behavior/neurological phenotype ( J:242422 )

N	• food intake

growth/size/body

growth/size/body region phenotype ( J:242422 )

N	• body water content

increased body fat mass ( J:242422 , J:242422 )

	• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)
	• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)

decreased lean body mass ( J:242422 , J:242422 )

	• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)
	• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)

decreased body weight ( J:242422 )

• 1 week after 4 days of leptin injections after 25 weeks on 10% fat isocaloric-matched control

increased body weight ( J:242422 , J:242422 )

	• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)
	• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)

adipose tissue

adipose tissue phenotype ( J:242422 )

N	• gonadal fat pad morphology 1 week after 4 days of leptin injections after 25 weeks on 10% fat isocaloric-matched control diet

increased subcutaneous adipose tissue amount ( J:242422 )

• 1 week after 4 days of leptin injections after 25 weeks on 10% fat isocaloric-matched control diet

increased body fat mass ( J:242422 , J:242422 )

	• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)
	• on 10% fat isocaloric-matched control diet or on regular laboratory chow diet containing 18% fat (J:242422)

increased brown adipose tissue mass ( J:242422 )

• 1 week after 4 days of leptin injections after 25 weeks on 10% fat isocaloric-matched control diet

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:242422 )

N	• fasted circulating glucose level

integument

increased subcutaneous adipose tissue amount ( J:242422 )

• 1 week after 4 days of leptin injections after 25 weeks on 10% fat isocaloric-matched control diet

Allelic Composition	Tg(CAG-PPARG,-tdTomato)#Sig/0 Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: C57BL/6 * FVB/N * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-PPARG,-tdTomato)#Sig mutation (0 available)
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

growth/size/body

increased body weight ( J:242422 )

• threefold larger increase in body weight than controls after intraperitoneal rosiglitazone injection on 45% HFD

Allelic Composition	Tg(Pomc1-cre)16Lowl/0
Genetic Background	involves: 129 * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Pomc1-cre)16Lowl mutation (1 available)

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

normal phenotype

no abnormal phenotype detected ( J:106354 )

• transgenic mice have identical body weights to wild-type littermates

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