Insulin-like growth factor-I and diabetes. A review

Simpson, Helen; Umpleby, AM; Russell-Jones, DL

doi:10.1016/s1096-6374(98)80098-1

Cited by 51 publications

(38 citation statements)

References 77 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, the IGF also mimic some of the metabolic actions of insulin and act as insulin sensitizers (2). IGF-I has approximately 1/12th the glucose-lowering capacity of insulin (3), in vivo and an equipotent effect on ex vivo muscle strips (4), as well as being an insulin sensitizer, and has been considered as a putative treatment agent for both type-1 and type-2 diabetes (5,6). The IGFBP are a family of six binding proteins that bind to IGF with high affinity and specificity.…”

mentioning

confidence: 99%

Insulin-Like Growth Factor Binding Protein-3 Induces Insulin Resistance in Adipocytes In Vitro and in Rats In Vivo

et al. 2007

View full text Add to dashboard Cite

Insulin-like growth factor binding protein (IGFBP)-3 binds to IGF and modulates their actions and also possesses intrinsic activities. We investigated its effects on insulin action and found that when IGFBP-3 was added to fully differentiated 3T3-L1 adipocytes in culture, insulin-stimulated glucose transport was significantly inhibited to 60% of control in a time-and dose-dependent manner. Tumor necrosis factor (TNF)-␣ treatment also inhibited glucose transport to the same degree as IGFBP-3 and, in addition, increased IGFBP-3 levels 3-fold. Co-treatment with TNF-␣ and IGFBP-3 antisense partially prevented the inhibitory effect of TNF-␣ on glucose transport, indicating a role for IGFBP-3 in cytokine-induced insulin resistance. Insulin-stimulated phosphorylation of the insulin receptor was markedly decreased by IGFBP-3 treatment. IGFBP-3 treatment suppressed adiponectin expression in 3T3-L1 adipocytes. Infusion of IGFBP-3 to Sprague-Dawley rats for 3 h decreased peripheral glucose uptake by 15% compared with controls as well as inhibiting glycogen synthesis. Systemic administration of IGFBP-3 to rats for 7 d resulted in a dramatic 40% decrease in peripheral glucose utilization and glycogen synthesis. These in vitro and in vivo findings demonstrate that IGFBP-3 has potent insulin-antagonizing capability and suggest a role for IGFBP-3 in cytokine-induced insulin resistance and other mechanisms involved in the development of type-2 diabetes. (Pediatr Res 61: 159-164, 2007)

show abstract

mentioning

confidence: 99%

Insulin-Like Growth Factor Binding Protein-3 Induces Insulin Resistance in Adipocytes In Vitro and in Rats In Vivo

et al. 2007

View full text Add to dashboard Cite

show abstract

“…31 Importantly, recombinant IGF-I exacerbated diabetic retinopathy, when administered to diabetic patients in an attempt to suppress growth hormone secretion and reverse insulin resistance. 32,33 Despite these indications, however, direct proof of the precise role of IGF-I in the development and progression of diabetic retinopathy is lacking, and the signaling pathway(s) mediating its actions have not been delineated. We have previously demonstrated that IGF-I potently increases VEGF expression in retinal pigment epithelial (RPE) cells in vitro and has an additive effect with hypoxia in vivo.…”

mentioning

confidence: 99%

Insulin-Like Growth Factor-I Plays a Pathogenetic Role in Diabetic Retinopathy

Poulaki

Joussen

Mitsiades

et al. 2004

The American Journal of Pathology

138

View full text Add to dashboard Cite

Although the molecular pathophysiology of diabetic retinopathy, the current leading cause of blindness in Western societies, 1 is not fully elucidated, studies have documented a pivotal role for leukocyte adherence within the retinal vasculature. The adhesion of leukocytes to the retinal endothelium is a process that depends on ␤ 2 integrin-intercellular adhesion molecule (ICAM)-1 interactions and leads to breakdown of the blood-retinal barrier. 2 These data, in combination with our previous findings that aggressive anti-inflammatory therapy suppressed leukocyte adhesion and blood retinal breakdown in a relevant animal model, 3 support the hypothesis that a chronic subclinical inflammation may underlie much of the vascular pathology of diabetic retinopathy. 4 These vascular pathological findings are orchestrated by vascular endothelial growth factor (VEGF), a factor that potently promotes the growth and maintenance of endothelial cells and the formation of new vessels, and is implicated in both background and proliferative diabetic retinopathy. 5-11 Intraocular VEGF levels are increased in diabetic patients with blood-retinal barrier breakdown and neovascularization, 5,10,12,13 whereas the specific inhibition of VEGF prevents these complications in animal models. 7,11,14 Therefore, regulation of VEGF expression could conceivably be both a mediator for converging local and systemic stimuli modulating vessel pathophysiology, as well as a target for therapeutic intervention. Within a constellation of known modulators of VEGF expression that can possibly function at the transcriptional [through AP-1, AP-2, steroid hormone receptors, p53, and nuclear factor (NF-B)] or posttranscriptional level, [15][16][17][18] hypoxia is the most potent inducer of VEGF transcription in vivo; its effects are mainly mediated by the helix-loop helix (bHLH)-PAS transcription factor HIF-1␣, which heterodimerizes with the bHLH-PAS protein ARNT or HIF-1␤, 19 -22 and binds to consensus and ancillary hypoxia-response elements (HREs) in the VEGF promoter. 21,[23][24][25]

show abstract

“…Clinically, IGF-I has been used as a replacement for insulin to facilitate glucose transport and metabolism in diabetes, especially under insulin-resistant conditions (1,27). Combined treatment with IGF-I and insulin in diabetic patients was reported to correct growth hormone hy-persecretion, improve insulin sensitivity and glucose control, and decrease the requirement for insulin (39). Our laboratory has recently shown that diabetic cardiomyopathy may be prevented with insulin-sensitizing antidiabetics such as metformin (34).…”

mentioning

confidence: 99%

IGF-I attenuates diabetes-induced cardiac contractile dysfunction in ventricular myocytes

Norby

Wold

Duan

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

Diabetic cardiomyopathy is characterized by impaired ventricular contraction and altered function of insulin-like growth factor I (IGF-I), a key factor for cardiac growth and function. Endogenous IGF-I has been shown to alleviate diabetic cardiomyopathy. This study was designed to evaluate exogenous IGF-I treatment on the development of diabetic cardiomyopathy. Adult rats were divided into four groups: control, control + IGF-I, diabetic, and diabetic + IGF-I. Streptozotocin (STZ; 55 mg/kg) was used to induce experimental diabetes immediately followed by a 7-wk IGF-I (3 mg · kg−1 · day−1 ip) treatment. Mechanical properties were assessed in ventricular myocytes including peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR90) and maximal velocities of shortening/relengthening (±dL/d t). Intracellular Ca2+ transients were evaluated as Ca2+-induced Ca2+ release and Ca2+ clearing constant. Levels of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA), phospholamban (PLB), and glucose transporter (GLUT4) were assessed by Western blot. STZ caused significant weight loss and elevated blood glucose, demonstrating the diabetic status. The diabetic state is associated with reduced serum IGF-I levels, which were restored by IGF-I treatment. Diabetic myocytes showed reduced PS and ±dL/d t as well as prolonged TPS, TR90, and intracellular Ca2+ clearing compared with control. IGF-I treatment prevented the diabetes-induced abnormalities in PS, ±dL/d t, TR90, and Ca2+ clearing but not TPS. The levels of SERCA and GLUT4, but not PLB, were significantly reduced in diabetic hearts compared with controls. IGF-I treatment restored the diabetes-induced decline in SERCA, whereas it had no effect on GLUT4 and PLB levels. These results suggest that exogenous IGF-I treatment may ameliorate contractile disturbances in cardiomyocytes from diabetic animals and could provide therapeutic potential in the treatment of diabetic cardiomyopathy.

show abstract

Insulin-like growth factor-I and diabetes. A review

Cited by 51 publications

References 77 publications

Insulin-Like Growth Factor Binding Protein-3 Induces Insulin Resistance in Adipocytes In Vitro and in Rats In Vivo

Insulin-Like Growth Factor Binding Protein-3 Induces Insulin Resistance in Adipocytes In Vitro and in Rats In Vivo

Insulin-Like Growth Factor-I Plays a Pathogenetic Role in Diabetic Retinopathy

IGF-I attenuates diabetes-induced cardiac contractile dysfunction in ventricular myocytes

Contact Info

Product

Resources

About