Evaluation of the components of insulin‐like growth factor (IGF)‐IGF binding protein (IGFBP) system in adolescents with type 1 diabetes and persistent microalbuminuria: relationship with increased urinary excretion of IGFBP‐3 18 kD N‐terminal fragment

Spagnoli, Anna; Chiarelli, Francesco; Vorwerk, Peter; Boscherini, B; Rosenfeld, Ron G.

doi:10.1046/j.1365-2265.1999.00842.x

Cited by 23 publications

(24 citation statements)

References 35 publications

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“…Another explanation for low IGF-I concentrations in patients with type 1 diabetes could be increased elimination as a result of proteolysis of IGFBP-3 or increased excretion of IGF-I by the kidneys as a result of diabetic nephropathy (34). However, in normoalbuminuric patients, IGFBP-3 proteolysis is not increased (34,35) and in our study we found no difference in IGF-I concentrations in patients with or without albuminuria. The available data thus suggest insuf®cient portal concentrations of insulin as the most probable cause of low plasma IGF-I in adult patients with type 1 diabetes of long duration.…”

Section: Discussioncontrasting

confidence: 55%

Circulating IGF-I concentrations are low and not correlated to glycaemic control in adults with type 1 diabetes

Ekman¹,

Nyström²,

Arnqvist

2000

European Journal of Endocrinology

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Objective: To study plasma concentrations of insulin-like growth factor-I (IGF-I) in adults with type 1 diabetes (IDDM) in comparison with a reference population, and the in¯uence of glycaemic control, dose of insulin, and sex on the concentration of circulating IGF-I in IDDM. Design and methods: Patients with type 1 diabetes were recruited consecutively from our outpatient diabetes unit. In all, 79 men and 55 women aged 20±60 years with a disease duration $6 years (range 6±51 years) took part in the study. A reference population of 80 men and 83 women aged 20±60 years was randomly obtained from the population registry. IGF-I was measured with radioimmunoassay after acid±ethanol extraction.

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Section: Discussioncontrasting

confidence: 55%

Circulating IGF-I concentrations are low and not correlated to glycaemic control in adults with type 1 diabetes

Ekman¹,

Nyström²,

Arnqvist

2000

European Journal of Endocrinology

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“…Doublier et al provided the first evidence that the lesions of glomerulosclerosis are related to a reduction in circulating IGF-I and an increase in IGFBP-1 levels (11). The same clinical picture (reduced circulating IGF-I and increased IGFBP-1 levels) has been found in human diabetics that develop microalbuminuria (12,13).…”

Section: Introductionmentioning

confidence: 88%

An IGF-I gene polymorphism modifies the risk of developing persistent microalbuminuria in type 1 diabetes

Hovind

Lamberts²,

Hop³

et al. 2007

eur j endocrinol

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Objective: Derangements of the GH-IGF-I axis have been associated with microalbuminuria (MA) in type 1 diabetes. The aim of this study was to investigate whether an IGF-I gene promoter polymorphism influenced the development of persistent MA in type 1 diabetes. Design: A prospective follow-up study of a cohort of 277 patients with newly diagnosed type 1 diabetes consecutively enrolled between September 1979 and August 1984. Methods: Urinary albumin excretion rate over 24 h was measured in each patient at least once a year. Persistent MA was defined as a urinary albumin excretion rate between 30 and 300 mg/24 h. Results: During a median follow-up of 18.0 years (range 1.0-21.5), 79 of 277 patients developed persistent MA. IGF-I gene genotype was available for 216 subjects; in 73% of the subjects, the wildtype genotype of this IGF-I gene polymorphism was present, while 27% had the variant type. At baseline, there were no differences in IGF-I levels and HbA 1c values between subjects with the wild type and subjects with variant type. By Kaplan-Meier analysis, subjects with the variant type of this polymorphism had during follow-up a higher risk of development of MA compared subjects with the wild type (PZ0.03). Conclusions: Subjects with the variant type of an IGF-I gene polymorphism had a significantly increased risk of developing MA. This risk was not mediated through changes in circulating IGF-I levels. Our study suggests that in type 1 diabetes, this IGF-I gene polymorphism is a risk factor of MA.European Journal of Endocrinology 156 83-90

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“…Uremic diabetic adults excrete IGFBP-3, as do type 1 diabetic adolescents with microalbuminuria, patients whose urinary levels of IGFBP-3 correlate directly to urinary albumin excretion [27]. Elevated levels of IGFBP fragments have been identified in urine from non-diabetic children with acute renal failure due to increased IGFBP-3 protease activity [28,29].…”

Section: Introductionmentioning

confidence: 99%

Insulin-like growth factor binding protein-3 mediates cytokine-induced mesangial cell apoptosis

Vasylyeva

Chen

Ferry

2005

Growth Hormone & IGF Research

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Mesangial cells are critical for glomerular filtration. Mesangial cell dysfunction, the hallmark of diabetic nephropathy, results from disordered mesangial growth induced by cytokines, abnormal hemodynamic influence, and metabolic factors associated with chronic hyperglycemia. Insulinlike growth factors (IGFs) and their high affinity binding proteins (IGFBPs) exert major actions on mesangial cell survival, but their underlying mechanisms remain unclear. In light of emerging IGF-independent roles for IGFBP-3, we investigated IGFBP-3 actions during mesangial cell apoptosis induced by cytokine or high glucose concentration.Quantified by DNA fragmentation ELISA and Annexin V flow cytometry, apoptosis occurred in rat mesangial cells (RMC) exposed to 2 μg/mL IGFBP-3 for 24 h under high ambient or standard glucose. Anti-sense IGFBP-3 oligo at 10 μg/mL significantly inhibited apoptosis induced by 100 ng/mL TNF-α, serum-free conditions, or high (25 mM) glucose. Increased IGFBP-3 release associated with high ambient glucose or TNF-α was inhibited by pre-treatment with anti-sense oligo. Under serum-free conditions, recombinant human IGFBP-3 blocked Akt phosphorylation at threonine 308 (pThr308), whereas anti-sense oligo treatment was associated with enhanced pThr308 activity. In summary, these data support a novel mechanism for TNF-α-induced mesangial cell apoptosis mediated by IGFBP-3 and present regulation of pThr308 activity as a novel mechanism underlying IGFBP-3 action.

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Evaluation of the components of insulin‐like growth factor (IGF)‐IGF binding protein (IGFBP) system in adolescents with type 1 diabetes and persistent microalbuminuria: relationship with increased urinary excretion of IGFBP‐3 18 kD N‐terminal fragment

Cited by 23 publications

References 35 publications

Circulating IGF-I concentrations are low and not correlated to glycaemic control in adults with type 1 diabetes

Circulating IGF-I concentrations are low and not correlated to glycaemic control in adults with type 1 diabetes

An IGF-I gene polymorphism modifies the risk of developing persistent microalbuminuria in type 1 diabetes

Insulin-like growth factor binding protein-3 mediates cytokine-induced mesangial cell apoptosis

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