The IGF Binding Protein Superfamily

Hwa, Vivian; Oh, Youngman; Burren, Christine; Choi, Woo Sung; Graham, Donna L.; Ingermann, Angela R.; Kim, Ho-Seong; López‐Bermejo, Abel; Minniti, Giuseppe; Nagalla, Srinivasa R.; Pai, Ki-Soo; Spagnoli, Anna; Vorwerk, Peter; Wanek, Don; Wilson, Elizabeth M.; Yamanaka, Yoshitaka; Yang, Doo Hyun; Rosenfeld, Ron G.

doi:10.1007/978-1-59259-712-3_14

Cited by 7 publications

(11 citation statements)

References 37 publications

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“…This is in line with reports by Cotterill et al (11) and Frystyk et al (29). Moreover, there is evidence that IGFBP1 may bind insulin, although with lower affinity than for IGF-I (30). This would suggest a possibility that high IGFBP1 concentrations could directly counteract insulin effects.…”

Section: Discussionsupporting

confidence: 91%

Profound changes in the GH-IGF-I system in adolescent girls with IDDM: can IGFBP1 be used to reflect overall glucose regulation?

Halldin

Hagenäs²,

Tuvemo

et al. 2000

Pediatric Diabetes

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Disturbances in the relations between insulin, growth hormone (GH) and insulin-like growth factor I (IGF-I) may be a major cause behind deteriorated metabolic control in adolescent girls with type I diabetes. These patients have increased GH secretion and low IGF-I concentrations. The aim of this study was to identify possible endocrine mechanisms behind good and poor glycaemic control in such girls, focusing on the insulin-GH-IGF-I axis. Ten girls with well-controlled insulin-dependent diabetes mellitus (IDDM), hemoglobin A1c (HbA1c) 6.5+/-0.4% (normal range 3.9-5.2%) and nine healthy controls were investigated and compared with 11 girls with poor glucose regulation, HbA1c 10.9+/-0.4%, and their corresponding controls. Serum profiles of glucose, insulin, GH and IGF-binding protein 1 (IGFBP1) were analysed in addition to IGF-I and HbA1c. Two interesting observations were made. GH concentrations were equally elevated in the two diabetic groups regardless of metabolic control (mean 24 h GH - girls with poorly controlled diabetes 10.0+/-1.0 mU/L vs 9.8+/-1.7 - girls with well-controlled diabetes; p=ns). Likewise, the IGF-I concentrations were reduced to the same extent (233+/-19 vs 242+/-23 microg/L; p=0.75). Secondly, despite similar insulin concentrations (mean 24 h insulin - girls with poorly controlled diabetes 22.9+/-2.6 and girls with well-controlled diabetes 27.3+/-2.9 mU/L, respectively; p=0.26), there was a marked difference in IGFBP1 concentrations between the two groups with IDDM (mean IGFBP1 - girls with poorly controlled diabetes 70.5+/-9.1 microg/L vs girls with well-controlled diabetes 28.6+/-3.3; p<0.001). Despite equally elevated GH concentrations that may induce insulin resistance, the markedly lower concentrations of IGFBP1 in the well-controlled group indicate a higher hepatic insulin sensitivity in these girls compared with those with a poor control. Furthermore, in spite of similar total IGF-I concentrations, the lower IGFBP1 concentrations may result in higher IGF-I bioactivity in the well-controlled group. This may be reflected in better growth of the well-controlled group whose height of 168.7+/-0.9 vs 163.6+/-1.2 cm was significantly different (p<0.004). IGFBP1 may be a marker of overall insulinization in adolescents with type 1 diabetes, independent of the absolute insulin dose used for therapy.

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Section: Discussionsupporting

confidence: 91%

Profound changes in the GH-IGF-I system in adolescent girls with IDDM: can IGFBP1 be used to reflect overall glucose regulation?

Halldin

Hagenäs²,

Tuvemo

et al. 2000

Pediatric Diabetes

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“…IGF actions are regulated by IGF-binding proteins (IGFBPs), which act as transporters of IGFs, protect them from degradation, limit their binding to receptors and maintain a`reservoir' of biologically inactive IGF (Jones and Clemmons, 1995;Hwa et al, 1999;Martin and Baxter, 1999;Khandwala et al, 2000). IGF actions are regulated by IGF-binding proteins (IGFBPs), which act as transporters of IGFs, protect them from degradation, limit their binding to receptors and maintain a`reservoir' of biologically inactive IGF (Jones and Clemmons, 1995;Hwa et al, 1999;Martin and Baxter, 1999;Khandwala et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

The interaction of insulin-like growth factor-I with the N-terminal domain of IGFBP-5

et al. 2001

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Insulin-like growth factors (IGFs) are key regulators of cell proliferation, differentiation and transformation, and are thus pivotal in cancer, especially breast, prostate and colon neoplasms. They are also important in many neurological and bone disorders. Their potent mitogenic and anti-apoptotic actions depend primarily on their availability to bind to the cell surface IGF-I receptor. In circulation and interstitial fluids, IGFs are largely unavailable as they are tightly associated with IGF-binding proteins (IGFBPs) and are released after IGFBP proteolysis. Here we report the 2.1 A crystal structure of the complex of IGF-I bound to the N-terminal IGF-binding domain of IGFBP-5 (mini-IGFBP-5), a prototype interaction for all N-terminal domains of the IGFBP family. The principal interactions in the complex comprise interlaced hydrophobic side chains that protrude from both IGF-I and the IGFBP-5 fragment and a surrounding network of polar interactions. A solvent-exposed hydrophobic patch is located on the IGF-I pole opposite to the mini-IGFBP-5 binding region and marks the IGF-I receptor binding site.

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“…The cellular actions of IGF-I are regulated in part by circulating and tissue levels of IGFBPs (10,11). Although not exam- ined in the present study, the significance of this finding may be that the increased intestinal levels of IGFBP-3 can decrease the local amounts of bioactive IGF-I.…”

Section: Discussionmentioning

confidence: 48%

“…Systemic CCK participates in the regulation of gallbladder contraction, pancreatic secretion, stomach emptying, and intestinal motility (6). In vivo, IGF-I activity is modulated in part by IGF-binding proteins (IGFBPs) (10,11). Our laboratory and others have shown that the insulin-like growth factor (IGF) system may play a major role in the regulation of intestinal hormone gene expression, including CCK (8,9).…”

mentioning

confidence: 99%

Endocrine Disruptive Effects of Polychlorinated Aromatic Hydrocarbons on Intestinal Cholecystokinin in Rats*

Lee

Englander

et al. 2000

Endocrinology

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The ubiquitous and persistent nature of polychlorinated aromatic hydrocarbons (PCAHs) in our environment and the risk of exposure to PCAHs have provoked concern over their potential toxicity. In humans, exposure to PCAHs is aimed chiefly at epithelial cells residing in the intestinal mucosa, because oral intake of contaminated food is a major source of PCAHs. The purpose of this study, therefore, was to examine the effects of chronic exposure to various PCAHs [i.e. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), 3,3',4,4',5-pentachlorobiphenyl (PCB-126), and 2,2'4,4'5,5'-hexachlorobiphenyl (PCB-153)], given alone or as mixtures, on intestinal cholecystokinin (CCK) peptide and messenger RNA levels. We show that chronic PCAH treatment significantly lowers intestinal levels of stored CCK peptide. Intestinal CCK messenger RNA levels are not affected. In addition, 3,3',4,4',5-pentachlorobiphenyl treatment increased intestinal insulin-like growth factor-binding protein-3 levels in a dose-related manner. Acute 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment of intestinal CCK cells lowered levels of CCK-processing enzymes (i.e. prohormone convertase-1 and -2). Together, these data indicate that PCAHs may decrease intestinal levels of stored CCK peptide by affecting the intestinal insulin-like growth factor system and CCK processing.

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The IGF Binding Protein Superfamily

Cited by 7 publications

References 37 publications

Profound changes in the GH-IGF-I system in adolescent girls with IDDM: can IGFBP1 be used to reflect overall glucose regulation?

Profound changes in the GH-IGF-I system in adolescent girls with IDDM: can IGFBP1 be used to reflect overall glucose regulation?

The interaction of insulin-like growth factor-I with the N-terminal domain of IGFBP-5

Endocrine Disruptive Effects of Polychlorinated Aromatic Hydrocarbons on Intestinal Cholecystokinin in Rats*

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