Coupling of insulin‐responsive glucose transport to receptors for insulin‐like growth factor 1 in primary human fibroblasts

Maassen, J. A.; Zon, G.C.M. van der

doi:10.1111/j.1432-1033.1990.tb15609.x

Cited by 7 publications

(4 citation statements)

References 19 publications

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“…IGF-I was shown to enhance glucose uptake in BCC with maximal effect at 10-100 nM and a n EC,, of approximately 1 nM. Although these values seem higher than expected from the in vivo physiological potency of IGF-I, similar results have been reported for a great variety of cells in culture (Maher et al, 1989;Maassen et al, 1990;Bilan et al, 1991). I t has previously been reported that insulin in nM concentrations enhances glucose uptake in BCC reaching maximum at 8 nM insulin (Delicado and Miras Portugal, 1987).…”

Section: Discussionsupporting

confidence: 68%

GLUT1-mediated glucose transport and its regulation by IGF-I in cultured bovine chromaffin cells

1996

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Regulation of glucose transport was studied in primary cultures of bovine chromaffin cells (BCC) using the glucose analogue 2-deoxyglucose (DOG) as a model substrate. The glucose transporter in freshly isolated and cultured BCC was identified as GLUT1 by Western immunoblots. The level of GLUT1 increased by time in culture and was followed by an enhancement in uptake of DOG. The DOG uptake was stimulated by insulin-like growth factor I (IGF-I) with an EC50 of 1 nM and a maximal response (approximately 2-fold) was obtained at 10-100 nM IGF-I. Insulin was at least 100-fold less potent than IGF-I. Exposure to 10(-8) M IGF-I also caused a redistribution of GLUT1 from an intracellular compartment to a plasma membrane-enriched fraction. Our results demonstrate a GLUT1-mediated glucose uptake in adrenomedullary cells. An enhanced glucose transport in response to IGF-I appears to be coupled to activation of IGF receptor type 1 and GLUT1 translocation.

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Section: Discussionsupporting

confidence: 68%

GLUT1-mediated glucose transport and its regulation by IGF-I in cultured bovine chromaffin cells

1996

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“…IGF-1 receptor occupation by insulin most likely occurs with an excess of this hormone. Insulin has a lower IGF-1 receptor affinity compared to IGF-1 [24,25]. Our results show that insulin stimulates VSMC to produce collagen even when the homologous receptor is blocked.…”

Section: Discussionmentioning

confidence: 66%

“…It has been suggested that insulin, rather than IGF-1, acts as an effector on VSMC using the IGF-1 receptor. This type of interaction has been described in several types of cells [23][24][25]. IGF-1 receptor occupation by insulin most likely occurs with an excess of this hormone.…”

Section: Discussionmentioning

confidence: 99%

Insulin Stimulates Collagen Synthesis in Vascular Smooth Muscle Cells from Elderly Patients

Ruíz-Torres¹,

Melón²,

Muñoz³

1998

Gerontology

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The process of aging results in an increase in collagen in arterial walls, but the blood levels of insulin-like growth factor 1 (IGF-1) decrease remarkably as adults age. There is an almost simultaneous increase in insulin secretion, particularly in obese individuals. It is not known if, under these hormonal conditions, the enrichment of collagen in the arterial wall is due to insulin. We studied the effect of insulin on the production of collagen in vascular smooth muscle cells (VSMC) from elderly persons with high levels of insulin secretion after blocking the insulin receptors with a monoclonal antibody. Results were compared to those without insulin receptor blockage and to those with IGF-1. Despite the inhibition of ¹⁴C-glucose uptake, insulin clearly stimulated the release of procollagen III, and increased the collagen synthesis. The hydroxyproline labelling rate from ³H-proline increased to more than twice the control values. IGF-1 is a more potent effector than insulin, but the effect of insulin on the rate of collagen production became similar to IGF-1 when the specific receptors were blocked. The results indicate that under special conditions that occur with aging, insulin interacts with nonspecific receptors in VSMC, especially IGF-1, stimulating these cells to produce collagen.

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“…Very recently, it has been shown that IGF-I receptors in primary human fibroblasts can mediate a stimulation of glucose transport (Maassen and van der Zon, 1990). In contrast, another recent study has demonstrated that IGF-I stimulates glucose transport in human adipocytes via insulin receptors in spite of the presence of IGF-I receptors (Sinha et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

The signaling potential of the receptors for insulin and insulin‐like growth factor I (IGF‐I) in 3t3‐l1 adipocytes: Comparison of glucose transport activity, induction of oncogene c‐fos, glucose transporter mRNA, and DNA‐synthesis

Weiland

Bahr

Höhne

et al. 1991

Journal Cellular Physiology

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The receptors for insulin and insulin-like growth factor I (IGF-I) have in common a high sequence homology and diverse overlapping functions, (e.g., the stimulation of acute metabolic events and the induction of cell growth.). In the present study, we have compared the potential of insulin and IGF-I receptors in stimulating glucose transport activity, glucose transporter gene expression, DNA-synthesis, and expression of proto-oncogene c-fos in 3T3-L1 adipocytes which express high levels of both receptors. Binding of both hormones to their own receptors was highly specific as compared with binding to the respective other receptor (insulin receptor: KD = 3.6 nM, KI of IGF-I greater than 500 nM; IGF-I receptor, KD = 1.1 nM, KI of insulin = 191 nM). Induction of proto-oncogene c-fos mRNA by insulin and IGF-I paralleled their respective receptor occupancy and was thus induced by both hormones via their own receptor (EC50 of insulin, 3.7; IGF-I, 3.9 nM). Similarly, both insulin and IGF-I increased DNA synthesis (EC50 of insulin, 5.8 nM; IGF-I, 4.0 nM), glucose transport activity (EC50 of insulin, 1.7 nM; IGF-I, 1.4 nM), and glucose transporter (GLUT4) mRNA levels in concentrations corresponding with their respective receptor occupancy. These data indicate that in 3T3-L1 cells the alpha-subunits of insulin and IGF-I receptors have an equal potential to stimulate a metabolic and a mitogenic response.

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Coupling of insulin‐responsive glucose transport to receptors for insulin‐like growth factor 1 in primary human fibroblasts

Cited by 7 publications

References 19 publications

GLUT1-mediated glucose transport and its regulation by IGF-I in cultured bovine chromaffin cells

GLUT1-mediated glucose transport and its regulation by IGF-I in cultured bovine chromaffin cells

Insulin Stimulates Collagen Synthesis in Vascular Smooth Muscle Cells from Elderly Patients

The signaling potential of the receptors for insulin and insulin‐like growth factor I (IGF‐I) in 3t3‐l1 adipocytes: Comparison of glucose transport activity, induction of oncogene c‐fos, glucose transporter mRNA, and DNA‐synthesis

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