Tg(IGFBP2)1Miel Transgene Detail MGI Mouse (MGI:3769995)

Tg(IGFBP2)1Miel
Transgene Detail

Nomenclature

Symbol:	Tg(IGFBP2)1Miel
Name:	transgene insertion 1, John Miell
MGI ID:	MGI:3769995
Synonyms:	line tg1
Transgene:	Tg(IGFBP2)1Miel Location: unknown

Transgene
origin

Strain of Origin:

FVB/N

Transgene
description

Transgene Type:	Transgenic (random, expressed)
Mutation:	Insertion
	The IGFBP-2 transgene (isolated from a human cosmid clone) contains the entire structural human IGFBP2 gene. This 39 kb transgene was microinjected into the pronucleus of FVB/N embryos. Two lines tg1 and tg2 were established and line tg1 was analyzed in detail. (J:121961)

Find Mice (IMSR)

Mouse strains and cell lines available from the International Mouse Strain Resource (IMSR)

Carrying this Mutation:

Mouse Strains: 1 strain available Cell Lines: 0 lines available

Phenotype
summary

Phenotype Summary by Mammalian Phenotype terms

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Genotypes are listed in the next section.

Key:

hm	homozygous	ht	heterozygous
cn	conditional genotype	cx	complex: > 1 genome feature
tg	involves transgenes	ot	other: hemizygous, indeterminate,...
N	normal phenotype		expected model not found

Affected Systems	Genotypes:	tg1
adipose tissue		√
decreased adipose tissue amount		√
abnormal fat cell morphology		√
abnormal abdominal fat pad morphology		√
		tg1
cardiovascular system		√
cardiovascular system phenotype		N
decreased systolic blood pressure		√
		tg1
growth/size		√
increased resistance to diet-induced obesity		√
weight gain		√
		tg1
homeostasis/metabolism		√
homeostasis/metabolism phenotype		N
increased resistance to diet-induced obesity		√
decreased circulating leptin level		√
decreased circulating triglyceride level		√
abnormal glucose homeostasis		√
decreased circulating glucose level		√
abnormal circulating insulin level		√
improved glucose tolerance		√
increased insulin sensitivity		√
		tg1
liver/biliary system		N
liver/biliary system phenotype		N

Phenotypic
data by
genotype

Phenotypic Data by Genotype

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Genotype

Allelic Composition

Genetic Background

tg1

Tg(IGFBP2)1Miel/0

FVB/N-Tg(IGFBP2)1Miel

growth/sizeincreased resistance to diet-induced obesity (J:121961)

on high-fat diet for 32 weeks, mutants remain lean with no significant increase in size of fat depots, whereas wild-type mice have markedly increased size of fat depots when examined at 40 weeks

weight gain (J:121961)

on a high-fat/high-calorie diet for 32 weeks from 8 weeks of age, mutants show attenuated weight gain relative to wild-type mice

adipose tissuedecreased adipose tissue amount (J:121961)

on high-fat diet for 32 weeks, mutants have smaller fat depots than wild-type mice on the same diet when examined at 40 weeks

abnormal fat cell morphology (J:121961)

adipocytes are smaller than in wild-type mice, on both regular (1390 vs. 2100 um² mean cell area) and high-fat chow diets (2800 vs. 5900 um² mean cell area)

abnormal abdominal fat pad morphology (J:121961)

transgenic mice on high-fat diet for 32 weeks have significant reduction intraabdominal fat than wild-type mice; similarly, regular chow-fed mutants have less abdominal fat than diet-matched controls

cardiovascular systemcardiovascular system phenotype (J:121961)

mutants are protected from age-related hypertension observed in aged wild-type mice

decreased systolic blood pressure (J:121961)

wild-type mice at 40 weeks show increased systolic blood pressure compared to transgenic mice on both regular chow and high-fat diets

liver/biliary systemliver/biliary system phenotype (J:121961)

on high-fat diet for 32 weeks, mutants exhibit lower liver weight relative to controls when examined at 40 weeks

on high-fat diet for 32 weeks, mutants do not exhibit steatosis, whereas wild-type livers have macroscopic appearance compatible with increased fat content

homeostasis/metabolismhomeostasis/metabolism phenotype (J:121961)

at 8 weeks of age, blood glucose and insulin levels are similar to wild-type mice

insulin levels are similar to wild-type at 4-6 months of age

on high-fat diet, total energy intake is not significantly different from wild-type

increased resistance to diet-induced obesity (J:121961)

on high-fat diet for 32 weeks, mutants remain lean with no significant increase in size of fat depots, whereas wild-type mice have markedly increased size of fat depots when examined at 40 weeks

decreased circulating leptin level (J:121961)

leptin level increase is blunted in transgenic mice on high-fat diet, compared to wild-type

decreased circulating triglyceride level (J:121961)

on high-fat diet, plasma triglyceride levels are significantly lower than in wild-type

abnormal glucose homeostasis (J:121961)

in response to IGF-I, transgenic mice show an attenuated hypoglycemic response; plasma glucose levels decrease by ~half the value exhibited by wild-type mice

decreased circulating glucose level (J:121961)

by 4-6 months of age, transgenic mice display lower nonfasted glucose levels than wild-type littermates

increase in blood glucose of transgenic mice on high-fat diet is significantly blunted relative to wild-type

abnormal circulating insulin level (J:121961)

in response to carbohydrate challenge, no siginificant increase in plasma insulin level is observed compared to elevated levels displayed by wild-type mice

improved glucose tolerance (J:121961)

mice are protected against the age-related decline in glucose tolerance displayed by wild-type mice between 8 and 40 weeks

on high-fat diet, transgenic mice are protected from development of glucose intolerance compared to wild-type

on both regular and high-fat diets, blood glucose of transgenic mice is significantly lower after glucose tolerance test than in wild-type

increased insulin sensitivity (J:121961)

hypoglycemic response to exogenous insulin is greater in 40-week old mice compared to controls

References

Original:	J:121961 Wheatcroft SB et al., "IGF-binding protein-2 protects against the development of obesity and insulin resistance." Diabetes 2007 Feb;56(2):285-94
All:	1 reference(s)

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