Insulin-like growth factors I and II, also known as somatomedin C and somatomedin A, respectively, are
single chain polypeptides which share an amino acid sequence homology of about 47% with insulin and
about 31% with relaxin and with them comprise the insulin family of polypeptide growth factors. Their
functions include mediation of growth hormone action, stimulation of growth of cultured cells, stimulation of the action
of insulin, and involvement in development and growth. They appear to be autocrine regulators of cell proliferation.
Ligand, Growth factor
IGF2 is a mitogen for many cell types and an important modulator of muscle growth and differentiation. The gene is
widely expressed during prenatal development and its activity is regulated by genomic imprinting, the gene being
inactive on the chromosome inherited from the mother in most normal tissues.
Poretsky L, et al. reviewed the insulin-related ovarian regulatory system in health and disease.
Giudice LC. reviewed the growth factor action on ovarian function in polycystic ovary syndrome.
Yuan W, et al. reported that insulin-like growth factor-II mediates the steroidogenic and growth promoting actions of follicle
stimulating hormone on human ovarian pre-antral follicles cultured in vitro.
Expression regulated by
Granulosa, Theca, Luteal cells
el-Roeiy A, et al. reported the expression of the genes encoding the insulin-like growth factors (IGF-I and II), the IGF and insulin
receptors, and IGF-binding proteins-1-6 and the localization of their gene products in normal and
polycystic ovary syndrome ovaries.
Secondary, Antral, Preovulatory, Corpus luteum
Mutation name: None
type: null mutation fertility: subfertile Comment:DeChiara et al. (1991) produced targeted disruption of the Igf2 gene in mice by homologous recombination in ES cells.
Transmission of this mutation through the male germline resulted in heterozygous progeny that were growth deficient. In
contrast, when the disrupted gene was transmitted maternally, the heterozygous offspring were phenotypically normal.
Homozygous mutants were indistinguishable in appearance from growth-deficient heterozygous sibs.
Mutation name: None
type: targeted overexpression fertility: embryonic lethal Comment:Sun et al. (1997) introduced Igf2 transgenes into
the mouse genome by using embryonic stem (ES) cells and thereby caused transactivation of the endogenous Igf2 gene.
The consequent overexpression of Igf2 resulted in most of the symptoms of Beckwith-Wiedemann syndrome (BWS), including
prenatal overgrowth, polyhydramnios, fetal and neonatal lethality, disproportionate organ overgrowth including tongue
enlargement, and skeletal abnormalities. This was presented as evidence that IGF2 overexpression is a key determinant