Reduced insulin-like growth factor-I mRNA content in liver, adrenal glands and spinal cord of diabetic rats

Ishii, Douglas N.; Guertin, D. M.; Whalen, L. R.

doi:10.1007/s001250050219

Cited by 3 publications

(6 citation statements)

References 49 publications

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Section: Discussionmentioning

confidence: 99%

“…A key mediator for the prevention of diabetic neuropathy is IGF‐1 (Ishii et al, 1994; Zhuang et al, 1997). In diabetes situations, the IGF‐1 signaling is, however, reduced (Ishii et al, 1994; Zhuang et al, 1997), which results in impaired neurotrophic support and increased susceptibility to hyperglycemia‐induced damage. IGF‐1 protects neuronal cells from both oxidative stress and apoptosis induced by various stimuli, such as high concentrations of glucose (Cheng and Feldman, 1998; Tanii et al, 2000; Vestling et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…In conclusion, this study implicates that UCP3 may be involved in IGF‐1‐mediated protection from hyperglycemia‐induced oxidative stress and neuronal injuries by controlling MMP. Defective UCP3 expression (Argyropoulos et al, 1998; Krook et al, 1998; Otabe et al, 1999; Schrauwen et al, 2001), along with reduced IGF‐1 signaling in diabetic patients (Ishii et al, 1994; Zhuang et al, 1997), may increase the disposition to develop diabetic neuronal injuries.…”

Section: Discussionmentioning

confidence: 99%

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Insulin‐like growth factor type 1 prevents hyperglycemia‐induced uncoupling protein 3 down‐regulation and oxidative stress

Gustafsson

Söderdahl

Jönsson

et al. 2004

J of Neuroscience Research

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Uncoupling proteins (UCPs) have been reported to decrease the mitochondrial production of reactive oxygen species (ROS) by lowering the mitochondrial inner membrane potential (MMP). We have previously shown that UCP3 expression is positively regulated by insulin-like growth factor-1 (IGF-1). The aim of this study was to investigate the role of UCPs in IGF-1-mediated protection from hyperglycemia-induced oxidative stress and neurodegeneration. Human neuroblastoma SH-SY5Y cells were differentiated with retinoic acid for 6 days, after which exposure to 8, 30, or 60 mM glucose with or without 10 nM IGF-1 was started. After 48-72 hr, the number of neurites per cell, UCP3 protein expression, MMP, and intracellular levels of ROS and total glutathione were examined. These studies showed that glucose concentration-dependently reduced the number of neurites per cell, with a 50% reduction at 60 mM. In parallel, the UCP3 protein expression was down-regulated, and the MMP was raised 3.5-fold, compared with those in cells incubated with 8 mM glucose. Also, the ROS levels were increased, showing a twofold maximum at 60 mM glucose. This was accompanied by a twofold elevation of total glutathione levels, confirming an altered cellular redox state. IGF-1 treatment prevented the glucose-induced neurite degeneration and UCP3 down-regulation. Furthermore, the MMP and the intracellular levels of ROS and glutathione were normalized to those of control cells. These data indicate that IGF-1 may protect from hyperglycemia-induced oxidative stress and neuronal injuries by regulating MMP, possibly by the involvement of UCP3.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Insulin‐like growth factor type 1 prevents hyperglycemia‐induced uncoupling protein 3 down‐regulation and oxidative stress

Gustafsson

Söderdahl

Jönsson

et al. 2004

J of Neuroscience Research

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“…Reduction in systemic IGF‐I levels and increased IGF‐I binding protein levels contribute to impaired IGF‐I activity in Type 1 diabetic patients210. In the STZ rat, the IGF‐I mRNA expression is dramatically reduced in the liver and adrenal glands as well as in the spinal cord, which correlates with significantly decreased conduction velocities in both spinal cord and peripheral nerves211. Both IGF‐I and IGF‐II mRNA expressions are significantly decreased in sciatic nerve 5–7 days after the induction of STZ diabetes212 and well established in the BB/Wor rat after 6 weeks of diabetes213.…”

Section: Pathogenesis Of Dpnmentioning

confidence: 99%

Diabetic neuropathy - a continuing enigma

Sugimoto

Murakawa

Sima

2000

Diabetes Metab. Res. Rev.

161

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In this article we will review the clinical signs and symptoms of diabetic somatic polyneuropathy (DPN), its prevalence and clinical management. Staging and classification of DPN will be exemplified by various staging paradigms of varied sophistication. The results of therapeutic clinical trials will be summarized. The pathogenesis of diabetic neuropathy reviews an extremely complex issue that is still not fully understood. Various recent advances in the understanding of the disease will be discussed, particularly with respect to the differences between neuropathy in the two major types of diabetes. The neuropathology and natural history of diabetic neuropathy will be discussed pointing out the heterogeneities of the disease. Finally, the various prospective therapeutic avenues will be dealt with and discussed.

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“…Reduction in systemic IGF-I levels and increased IGF-I-binding proteins contribute to impaired IGF-I activity in type 1 diabetic patients (Crosby et al, 1992). In the STZ-diabetic rat, the IGF-I mRNA expression is dramatically reduced in the liver and in the spinal cord, which correlates with significantly decreased conduction velocities in both spinal cord and peripheral nerves (Ishii et al, 1994;Wuarin et al, 1994). Both IGF-I and IGF-II mRNA expressions are significantly decreased in sciatic nerve of STZ diabetes (Wuarin et al, 1994) and well established in both peripheral nerve and the brain in the type 1 BB/Wor rat after 8 weeks of diabetes (Xu et al, 2002;Li et al, 2002a;Pierson et al, 2002Pierson et al, , 2003a.…”

Section: Perturbed Neurotropismmentioning

confidence: 99%

Type 1 Diabetic Neuropathy and C‐peptide

Sima

Zhang

Grunberger

2003

Journal of Diabetes Research

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The most common microvascular diabetic complication, diabetic peripheral polyneuropathy (DPN), affects type 1 diabetic patients more often and more severely. In recent decades, it has become increasingly clear that perpetuating pathogenetic mechanisms, molecular, functional, and structural changes and ultimately the clinical expression of DPN differ between the two major types of diabetes. Impaired insulin/C-peptide action has emerged as a crucial factor to account for the disproportionate burden affecting type 1 patients. C-peptide was long believed to be biologically inactive. However, it has now been shown to have a number of insulin-like glucoseindependent effects. Preclinical studies have demonstrated dose-dependent effects on Na+,K+-ATPase activity, endothelial nitric oxide synthase (eNOS), and endoneurial blood flow. Furthermore, it has regulatory effects on neurotrophic factors and molecules pivotal to the integrity of the nodal and paranodal apparatus and modulatory effects on apoptotic phenomena affecting the diabetic nervous system. In animal studies, C-peptide improves nerve conduction abnormalities, prevents nodal degenerative changes, characteristic of type 1 DPN, promotes nerve fiber regeneration, and prevents apoptosis of central and peripheral nerve cell constituents. Limited clinical trials have confirmed the beneficial effects of C-peptide on autonomic and somatic nerve function in patients with type 1 DPN. Therefore, evidence accumulates that replacement of C-peptide in type 1 diabetes prevents and even improves DPN. Large-scale food and drug administration (FDA)-approved clinical trials are necessary to make this natural substance available to the globally increasing type 1 diabetic population.

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Reduced insulin-like growth factor-I mRNA content in liver, adrenal glands and spinal cord of diabetic rats

Cited by 3 publications

References 49 publications

Insulin‐like growth factor type 1 prevents hyperglycemia‐induced uncoupling protein 3 down‐regulation and oxidative stress

Insulin‐like growth factor type 1 prevents hyperglycemia‐induced uncoupling protein 3 down‐regulation and oxidative stress

Diabetic neuropathy - a continuing enigma

Type 1 Diabetic Neuropathy and C‐peptide

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