Effects of Antiinsulin Receptor Antibodies on Amino Acid Uptake by Cultured Rat Hepatocytes*

Shimoyama, Ryushi; Savage, C. Richard; Boden, Günther

doi:10.1210/jcem-60-5-928

Cited by 7 publications

(3 citation statements)

References 20 publications

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“…To clarify this situation, a specific human auto-antiserum that is highly reactive with insulin receptors and has no appreciable cross- reactivity with IGF-1 receptors (Jonas et al, 1982) was used. This B-10 antiserum has been similarly used to confirm that insulin stimulation of hepatocytes is mediated through insulin receptors (Shimoyama et al, 1985). Both the B-10 antiserum, and the IgGs purified from it, stimulated protein synthesis to the same degree as insulin (Figs.…”

Section: Discussionmentioning

confidence: 98%

Mouse blastocysts respond metabolically to short‐term stimulation by insulin and IGF‐1 through the insulin receptor

Harvey

Kaye

1991

Molecular Reproduction Devel

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Insulin specifically stimulates protein synthesis in compacted mouse embryos on days 3 and 4 after fertilization, with an EC50 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 EC50 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 (approximately 40%). This agonistic action of the insulin receptor antiserum, the EC50 of 150 pM for IGF-1, and the previously established EC50 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.

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Section: Discussionmentioning

confidence: 98%

Mouse blastocysts respond metabolically to short‐term stimulation by insulin and IGF‐1 through the insulin receptor

Harvey

Kaye

1991

Molecular Reproduction Devel

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“…This assay was performed in the same way as the IGF-l-receptor immunoprecipitation assay, except for the use of 125 l-labeled insulin receptor instead of IGF-I receptor. IgG was prepared by affinity chromatography with protein A-Sepharose as described (14). Placental membrane IGF-I binding-inhibition assay.…”

Section: Methodsmentioning

confidence: 99%

“…Diabetes 37:1708- 14,1988 E xistence of autoantibodies against the insulin receptor, causing a clinical syndrome characterized by severe insulin resistance, diabetes or glucose intolerance, and acanthosis nigricans, has been well established (1). In view of the close structural and immunological similarity between insulin and insulin-like growth factor I (IGF-I) receptors (2,3), we questioned whether similar antibodies also exist against the IGF-I receptor and if so, what their effects may be.…”

mentioning

confidence: 99%

Antibodies to Insulin-Like Growth Factor I Receptors in Diabetes and Other Disorders

Tappy

Fujita‐Yamaguchi²,

LeBon³

et al. 1988

Diabetes

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A newly developed immunoprecipitation assay, with 125I-labeled highly purified human placental insulin-like growth factor I (IGF-I) receptor, was used to search for IGF-I-receptor antibodies in human sera. Eleven of 141 patient sera tested (7.8%) immunoprecipitated labeled IGF-I receptor. Immunoprecipitation was comparable with sera and IgG prepared from these sera. Seven of the 11 sera (3 of 31 with rheumatic disorders, 3 of 48 with non-insulin-dependent diabetes, and 1 of 52 with insulin-dependent diabetes) failed to inhibit IGF-I binding to human placental membranes and thus contained non-binding-inhibitory IGF-I-receptor antibodies. Their pathophysiological function remained uncertain. The remaining 4 sera (2 of 3 with type B severe insulin resistance, 1 of 7 with polycystic ovary syndrome (PCO), and 1 of 31 with rheumatic disorders) inhibited IGF-I binding. Plasma IGF-I concentrations were elevated (663 and 802 ng/ml, respectively) in 2 patients (1 with PCO and another with systemic lupus erythematosus) with binding-inhibitory IGF-I-receptor antibodies, suggesting IGF-I resistance that was probably mediated by the IGF-I-receptor antibodies. In conclusion, we identified two species of human IGF-I-receptor antibodies. Sera from 7 of 141 patients tested contained IgG autoantibodies that bound to the IGF-I receptor at a locus different from the IGF-I binding site and did not inhibit IGF-I binding. Sera from 4 of 141 patients contained antibodies that bound to the IGF-I receptor at or near the IGF-I binding site, inhibited IGF-I binding, and probably caused IGF-I resistance.

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Amino Acid Transport in Liver

Kilberg

Häussinger

1992

Mammalian Amino Acid Transport

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Effects of Antiinsulin Receptor Antibodies on Amino Acid Uptake by Cultured Rat Hepatocytes*

Cited by 7 publications

References 20 publications

Mouse blastocysts respond metabolically to short‐term stimulation by insulin and IGF‐1 through the insulin receptor

Mouse blastocysts respond metabolically to short‐term stimulation by insulin and IGF‐1 through the insulin receptor

Antibodies to Insulin-Like Growth Factor I Receptors in Diabetes and Other Disorders

Amino Acid Transport in Liver

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