IL-6 Stimulation of Insulin-like Growth Factor Binding Protein (IGFBP)-1 Production

Samstein, Benjamin; Hoimes, Matthew L.; Fan, Jie; Frost, Robert A.; Gelato, Marie C.; Lang, Charles H.

doi:10.1006/bbrc.1996.1705

Cited by 76 publications

(53 citation statements)

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“…An upwards shift in the relationship between IGFBP-1 in relation to insulin is seen in other chronic conditions, such as those associated with low IGF-I levels, including growth hormone deficiency [40]. There are many other factors that have an impact on circulating IGFBP-1 and we can only speculate on the role of other counter-regulatory hormones [41] and of inflammatory cytokines [5,6], which might also have played a role in the relative increase in IGFBP-1 at 10 years in type 2 diabetes. It has been reported that, in patients with low fasting IGFBP-1, low IGF-I concentrations are associated with the development of IGT or type 2 diabetes 4.5 years later [17].…”

Section: Discussionmentioning

confidence: 90%

“…The suppression of IGFBP-1 production by insulin is achieved within the physiological range of insulin concentrations [1][2][3]. There are multiple stimulators, including glucagon [4] and inflammatory cytokines [5,6]. The pattern of regulation and its inhibitory effect on the insulin-like activity of the IGFs, suggest that IGFBP-1 has a role as a glucose counter-regulator [7].…”

Section: Introductionmentioning

confidence: 99%

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Insulin-like growth factor-binding protein-1 in the prediction and development of type 2 diabetes in middle-aged Swedish men

et al. 2008

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Aims/hypothesis Insulin-like growth factor-binding protein-1 (IGFBP-1) production in the liver is inhibited by insulin, and low circulating levels are associated with the metabolic syndrome. The aim of this study was to evaluate the predictive role and change in IGFBP-1 concentrations during development of abnormal glucose regulation. Methods IGFBP-1 levels were determined at baseline and at 10 years in an incident case-control prospective study of Swedish white men aged 35-56 years. Individuals with normal glucose tolerance at baseline who developed abnormal glucose tolerance during a 10 year period (n=355) according to WHO criteria were pair-matched to controls for age and family history of diabetes. Results Fasting IGFBP-1 concentrations were lower in individuals who later developed abnormal glucose regulation and correlated inversely with fasting proinsulin values (r =−0.48; p<0.0001), and both were significant predictors. Individuals in the highest quartile at baseline for an algorithm incorporating fasting IGFBP-1, blood glucose, proinsulin and waist and height had a 40-fold increased risk of developing type 2 diabetes compared with the lowest quartile (95% CI 7.7-214). IGFBP-1 increased 32% (95% CI 17-49%) during the 10 years in those developing diabetes and was increased in relation to insulin levels, suggesting the emergence of hepatic insulin resistance. Moreover, elevated IGFBP-1 levels at follow-up were associated with higher 2 h glucose values during an OGTT. Conclusions/interpretation Low IGFBP-1 predicts the development of abnormal glucose regulation and, as an inhibitor of the insulin-like actions of insulin-like growth factors, elevated levels of IGFBP-1 after the development of diabetes may also play a pathophysiological role.

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Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Insulin-like growth factor-binding protein-1 in the prediction and development of type 2 diabetes in middle-aged Swedish men

et al. 2008

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“…Glucagon increases IGFBP-1 levels when infused into healthy subjects (Hilding et al 1993) and hyperglucagonaemia is a common finding in chronic renal failure (Knochel 1983). Interleukin (IL)-1, IL-6 and tumour necrosis factor alpha (TNF-) stimulate IGFBP-1 release in vitro and administration of IL-6 to mice raises their IGFBP-1 levels (Samstein et al 1996). Increased TNFconcentration has been reported in patients dialysed with a complement-activating membrane (Canivet et al 1994).…”

Section: Discussionmentioning

confidence: 99%

Glutamate concentration in plasma, erythrocyte and muscle in relation to plasma levels of insulin-like growth factor (IGF)-I, IGF binding protein-1 and insulin in patients on haemodialysis

Filho

Hazel²,

Fürst³

et al. 1998

Journal of Endocrinology

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Elevated insulin-like growth factor binding protein (IGFBP) levels, including IGFBP-1, occur in renal failure, and may contribute towards reduced IGF bioactivity in uraemia. The reduced IGF bioactivity may, in turn, contribute towards the disturbances in protein metabolism present in renal failure. In this study, the relationships between intra-and extracellular amino acid (AA) levels and IGF-I and/or IGFBP-1 levels were studied in 30 adult patients (aged 24-70 years) on haemodialysis who had no clinical signs of malnutrition. Blood samples (n=30) and muscle biopsies (n=13) were collected for determination of free AA in erythrocytes (RBC), plasma and muscle by reverse-phase HPLC while IGFBP-1, IGF-I and insulin plasma levels were determined by radioimmunoassay.The patients on haemodialysis had elevated glutamate concentrations in RBC and plasma compared with healthy controls (524 26 vs 448 17 µmol/l, P<0·05 and 45 4 vs 32 4 µmol/l, P<0·01 respectively), although glutamate levels in muscle were within the normal range. The mean IGF-I level was slightly increased (.. score +0·74 0·30) but insulin levels were within the normal range. IGFBP-1 levels, which were inversely correlated to insulin (r= 0·40, P<0·02), were elevated threefold compared with controls. No plasma AA level displayed a significant correlation with IGF-I, IGFBP-1 or insulin levels. However, glutamate concentrations in RBC were positively correlated to IGFBP-1 (r=0·51, P<0·01) and inversely correlated to IGF-I (r= 0·46, P<0·01), although unrelated to insulin. Muscle glutamate, which was inversely related to RBC glutamate, displayed an opposite pattern with an inverse relation to IGFBP-1 levels (r= 0·73, P<0·01) and a positive correlation to IGF-I levels (r=0·64, P<0·02). Glutamate was the only AA to display an inverse correlation between RBC and muscle (r= 0·65, P<0·02, n=12).These findings lead us to propose that, in uraemia, the elevated IGFBP-1 levels, which reduce the bioavailability of IGFs, are linked to glutamate uptake in muscle, resulting in accumulation of RBC glutamate. Whether there is a causal relationship or the correlation is due to some common regulator is not clarified in the present study.

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“…However, during abdominal surgery, severe infection, trauma, and burn injury increased hepatic IGFBP-1 expression, and serum levels appear to be unrelated to insulin levels [27][28][29][30] and may be influenced instead by cytokines such as interleukin 6 (IL-6). 31 Likewise, despite high insulin levels, IGFBP-1 expression is also high during the perinatal period. 14,32,33 IGFBP-1 is one of the most highly induced immediate early genes transcribed in the remnant liver in the absence of protein synthesis by preexisting factors after partial hepatectomy.…”

mentioning

confidence: 99%

“…20,42 Other expression stimulants include thyroid hormone, epidermal growth factor, cytokines, and phorbol esters, the latter acting through protein kinase C inhibition. 31,[43][44][45] However, only IL-6 and phorbol esters have been shown to overcome the strong inhibition by insulin, at least in vitro.…”

mentioning

confidence: 99%

Liver-specific and proliferation-induced deoxyribonuclease I hypersensitive sites in the mouse insulin-like growth factor binding protein-1 gene

et al. 1999

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The insulin-like growth factor binding protein-1 (IGFBP-1) gene is highly expressed in fetal, perinatal, and regenerating liver. Up-regulation is transcriptionally mediated in regenerating liver and occurs in the first few minutes to hours after partial hepatectomy. In transgenic mice a 970-bp region from ؊776 to ؉151 of the IGFBP-1 promoter was sufficient for tissue-specific and induced expression of the gene in fetal and hepatectomized livers. However weak and/or poorly regulated expression in some transgenic lines suggested the existence of other regulatory regions. Here, genomic clones containing large regions 5Ј of the mouse IGFBP-1 gene sequence were isolated, subcloned, and sequenced. Deoxyribonuclease I (DNaseI) hypersensitivity analyses identified clusters of tissue-specific nucleasesensitive sites in the promoter region, ؊100 to ؊300, ؊2,300, ؊3,100, and ؊5,000 along with other weak sites. After partial hepatectomy, enhanced sensitivity and/or novel sites were detected in the ؊100/؊300, ؊5,000, and ؊3,100 regions, the promoter region remaining the most hypersensitive. A subset of these sites was present in fetal and perinatal livers. Novel tissue-specific sites that interacted with C/EBP and hepatic nuclear factor 3 (HNF3) transcription factors were identified in the ؊3,100 region. A hepatectomy-induced DNA binding complex containing the transcription factor USF1 was identified within the ؊100 to ؊300 region of the promoter. These results suggested that a complex array of tissue-specific and hepatic proliferationinduced transcription factors combine to regulate both the proximal promoter and more distal regulatory elements of the

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IL-6 Stimulation of Insulin-like Growth Factor Binding Protein (IGFBP)-1 Production

Cited by 76 publications

References 0 publications

Insulin-like growth factor-binding protein-1 in the prediction and development of type 2 diabetes in middle-aged Swedish men

Insulin-like growth factor-binding protein-1 in the prediction and development of type 2 diabetes in middle-aged Swedish men

Glutamate concentration in plasma, erythrocyte and muscle in relation to plasma levels of insulin-like growth factor (IGF)-I, IGF binding protein-1 and insulin in patients on haemodialysis

Liver-specific and proliferation-induced deoxyribonuclease I hypersensitive sites in the mouse insulin-like growth factor binding protein-1 gene

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