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Mouse blastocysts respond metabolically to short‐term stimulation by insulin and IGF‐1 through the insulin receptor
Author(s) -
Harvey Mark B.,
Kaye Peter L.
Publication year - 1991
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.1080290307
Subject(s) - insulin , medicine , biology , endocrinology , insulin receptor , receptor , stimulation , blastocyst , antiserum , embryo , embryogenesis , insulin resistance , antibody , microbiology and biotechnology , biochemistry , immunology
Insulin specifically stimulates protein synthesis in compacted mouse embryos on days 3 and 4 after fertilization, with an EC 50 of 0.5 pM (Harvey and Kaye, 1988). The identity of the receptor mediating this short‐term effect of insulin was further examined by dose–response studies with IFG‐1 and by using a specific anti‐insulin receptor antiserum that has no appreciable cross‐reaction with IGF‐1 receptors. IGF‐1 caused a maximum 40% stimulation of protein synthesis after 4 h exposure (similar to the response to insulin) with an EC 50 of 150 pM IGF‐1. The insulin receptor‐specific antiserum, or IgGs isolated from it, also stimulated protein synthesis at dilutions as high as 1:1,000 to the same degree as insulin (∼40%). This agonistic action of the insulin receptor antiserum, the EC 50 of 150 pM for IGF‐1, and the previously established EC 50 of 0.5 pM for insulin, all with similar maximal stimulation, strongly support the conclusion that the short‐term metabolic stimulation of mouse blastocysts by insulin is mediated by insulin receptors. Immunosurgical isolation of inner cell masses before and after exposure to 1.7 pM insulin (sufficient to stimulate only the insulin receptor) showed that insulin stimulates protein synthesis in these cells as well as in the trophectoderm cells of the blastocyst. This finding suggests that in intact blastocysts, insulin may travel across the trophectoderm to the inner cell mass, acting anabolically on both tissues. Analysis of the agonistic effect of the B‐10 antiserum showed there was no evidence of an unresponsive subpopulation of embryos.