Thyroxine treatment increases circulating levels of insulin‐like growth factor binding protein‐1: a placebo‐controlled study

Angervo, Maarit; Tiihonen, Mikko; Leinonen, Pekka; Välimäki, Matti; Seppälä, Matti

doi:10.1111/j.1365-2265.1993.tb00352.x

Cited by 13 publications

(15 citation statements)

References 24 publications

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“…There have been a number of studies examining the effects of thyroid status on serum concentrations of IGF-I and its binding proteins in patients with thyroid dysfunction [8][9][10][11][12][13][14][15][16]. Main results of these in vivo investigations suggest that there is an increase in serum levels of IGF-I in patients with hyperthyroidism [8,13,15,17,18], and a decrease of these values in patients with hypothyroidism [8][9][10]12].…”

Section: Introductionmentioning

confidence: 99%

Growth hormone/insulin-like growth factor axis in patients with subclinical thyroid dysfunction

Akın

Yaylalı

Turgut

et al. 2009

Growth Hormone & IGF Research

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Section: Introductionmentioning

confidence: 99%

Growth hormone/insulin-like growth factor axis in patients with subclinical thyroid dysfunction

Akın

Yaylalı

Turgut

et al. 2009

Growth Hormone & IGF Research

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“…Body height was adjusted for the possible confounders age and sex. Participants who were taking medications for type 2 diabetes or hormone conditions were excluded from the analyses of serum IGF-I, because these types of medication are known to influence IGF-I concentrations (27)(28)(29). Furthermore, serum IGF-I was adjusted for the possible confounders age, sex, and BMI.…”

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confidence: 99%

A Polymorphism in the Gene for IGF-I

Heutink²,

et al. 2001

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Evidence is accumulating that low levels of IGF-I play a role in the pathogenesis of type 2 diabetes and cardiovascular diseases. We examined the role of a genetic polymorphism in the promoter region of the IGF-I gene in relation to circulating IGF-I levels and growth measured as body height, and we studied the relationship of this polymorphism with type 2 diabetes and myocardial infarction. The relation between the IGF-I polymorphism and body height was assessed in a populationbased sample of 900 subjects from the Rotterdam Study. Within each genotype stratum, 50 subjects were randomly selected for a study of the relation of this polymorphism with serum IGF-I levels. To assess the risk for type 2 diabetes, we studied 220 patients and 596 normoglycemic control subjects. For myocardial infarction, 477 patients with evidence of myocardial infarction on electrocardiogram and 808 control subjects were studied. A 192-bp allele was present in 88% of the population, suggesting that this is the wild-type allele from which all other alleles originated. Body height was, on average, 2.7 cm lower (95% CI for difference -4.6 to -0.8 cm, P ‫؍‬ 0.004), and serum IGF-I concentrations were 18% lower (95% CI for difference -6.0 to -1.3 mmol/l, P ‫؍‬ 0.003) in subjects who did not carry the 192-bp allele. In noncarriers of the 192-bp allele, an increased relative risk for type 2 diabetes (1.7 [95% CI 1.1-2.7]) and for myocardial infarction (1.7 [95% CI 1.1-2.5]) was found. In patients with type 2 diabetes, the relative risk for myocardial infarction in subjects without the 192-bp allele was 3.4 (95% CI 1.1-11.3). Our study suggests that a genetically determined exposure to relatively low IGF-I levels is associated with an increased risk for type 2 diabetes and myocardial infarction. Diabetes 50:637-642, 2001

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“…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.…”

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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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Thyroxine treatment increases circulating levels of insulin‐like growth factor binding protein‐1: a placebo‐controlled study

Abstract: Oral thyroxine produces a rise in serum IGFBP-1 levels without a change in serum IGF-I concentration.

Cited by 13 publications

References 24 publications

Growth hormone/insulin-like growth factor axis in patients with subclinical thyroid dysfunction

Growth hormone/insulin-like growth factor axis in patients with subclinical thyroid dysfunction

A Polymorphism in the Gene for IGF-I

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

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