Anxiety correlates to decreased blood and prefrontal cortex IGF-1 levels in streptozotocin induced diabetes

Aksu, İlkay; Ateş, Mehmet; Baykara, Başak; Kıray, Müge; Şişman, Ali Rιza; Büyük, Erkan; Çetinkaya, Caner; Gümüş, Hikmet; Uysal, Nazan

doi:10.1016/j.neulet.2012.10.045

Cited by 63 publications

(34 citation statements)

References 41 publications

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“…In the present study, we used PDTC, an NF-κB inhibitor, to explore NF-κB mediated diabetic anxiety. It was found that diabetic mice after STZ-induced diabetic condition for 12 w exhibited a significant decrease in the percentage of open arm entries, which accorded with previous reports [29,45] . It was interesting that PDTC treatment for 10 w after STZ injection for 2 w reversed anxiety like behaviour induced by diabetic condition in mice as detected by EPM.…”

supporting

confidence: 90%

Pyrrolidine Dithiocarbamate Alleviated Anxiety in Diabetic Mice

Guang-pin¹

2017

ijps

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Chu, et al.: Antianxiety Potential of Pyrrolidine DithiocarbamateDiabetes is often associated with psychological complications such as anxiety. The aim of this study was to evaluate the effects of pyrrolidine dithiocarbamate on anxiety of streptozotocin-induced diabetic mouse using the open field and the elevated plus maze tests. Confirmed diabetic mice (>16.7 mM/l of blood glucose) were treated with pyrrolidine dithiocarbamate or 0.9% saline for 10 w. After pyrrolidine dithiocarbamate treatment, mice showed a higher percent of time retention and entries in open arms than the diabetic group in the elevated plus maze. However, there were no differences between total distance and average speed in both groups in the open field test. In conclusion, pyrrolidine dithiocarbamate treatment in diabetic mice exerted anxiolytic-like effects. The present study might be suggestive of a novel treatment approach to diabetic anxiety.

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supporting

confidence: 90%

Pyrrolidine Dithiocarbamate Alleviated Anxiety in Diabetic Mice

Guang-pin¹

2017

ijps

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“…Indoleamine 2,3-dioxygenase (IDO) is the first and ratelimiting enzyme of tryptophan catabolism through the kynurenine pathway (KP) (54). The KP represents the major catabolic route of tryptophan and is a source of nicotinamide adenine nucleotide, a cofactor in cellular respiration and energy production that plays a central role in DNA repair and transcriptional regulation (1). In addition, IDO plays a key role in regulation of inflammation.…”

mentioning

confidence: 99%

“…In addition, IDO plays a key role in regulation of inflammation. IDO can regulate immune responses and create immune tolerance, acting as a protective feedback mechanism against a possible overshooting T cell response (1). IDO expression is low in normal CNS but increases greatly during inflammatory conditions (1).…”

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confidence: 99%

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Loss of survival factors and activation of inflammatory cascades in brain sympathetic centers in type 1 diabetic mice

Thinschmidt

Caballero

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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Hu P, Thinschmidt JS, Caballero S, Adamson S, Cole L, Chan-Ling T, Grant MB. Loss of survival factors and activation of inflammatory cascades in brain sympathetic centers in type 1 diabetic mice. Am J Physiol Endocrinol Metab 308: E688 -E698, 2015. First published February 24, 2015 doi:10.1152/ajpendo.00504.2014.-Neuroinflammation and neurodegeneration have been observed in the brain in type 1 diabetes (T1D). However, little is known about the mediators of these effects. In T1D mice with 12-and 35-wk duration of diabetes we examined two mechanisms of neurodegeneration, loss of the neuroprotective factors insulin-like growth factor I (IGF-I) and IGF-binding protein-3 (IGFBP-3) and changes in indoleamine 2,3-dioxygenase (IDO) expression in the brain, and compared the response to age-matched controls. Furthermore, levels of matrix metalloproteinase-2 (MMP-2), nucleoside triphosphate diphosphohydrolase-1 (CD39), and ionized calcium-binding adaptor molecule 1 (Iba-1) were utilized to assess inflammatory changes in astrocytes, microglia, and blood vessels. In the diabetic hypothalamus (HYPO), we observed 20% reduction in neuronal soma diameter (P Ͻ 0.05) and reduced neuronal expression of IGFBP-3 (Ϫ32%, P Ͻ 0.05) and IGF-I (Ϫ15%, P Ͻ 0.05) compared with controls at 35 wk. In diabetic HYPO, MMP-2 expression was increased in astrocytes (46%, P Ͻ 0.01), and IDO ϩ cell density rose by (62%, P Ͻ 0.05). CD39 expression dropped by 30% (P Ͻ 0.05) in microglia and blood vessels. With 10 wk of systemic treatment using minocycline, an anti-inflammatory agent that crosses the blood-brain barrier, MMP-2, IDO, and CD39 levels normalized (P Ͻ 0.05). Our results suggest that increased IDO and early loss of CD39 ϩ protective cells lead to activation of inflammation in sympathetic centers of the CNS. As a downstream effect, the loss of the neuronal survival factors IGFBP-3 and IGF-I and the neurotoxic products of the kynurenine pathway contribute to the loss of neuronal density observed in the HYPO in T1D.

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“…During chronic neurodegenerative disorders that involve Alzheimer’s disease with DM (22, 56), insulin resistance has been reported in patients with Alzheimer’s disease that links impaired cellular metabolism with cognitive loss (57–59). DM also leads to neuropsychiatric disorders (60, 61), peripheral nerve disorders (27), and retinal disease (62–64). At the vascular cell level, elevated glucose levels reflective of those that occur during DM can result in endothelial cell senescence (25), impaired mobilization of endothelial progenitor cells from the bone marrow (65), neuroglialvascular unit compromise (62), inhibition of angiogenesis (26), and loss of endothelial cells (14, 30, 66–70).…”

Section: Dm Involvement Of Multiple Organ Systems and Oxidative mentioning

confidence: 99%

Programming Apoptosis and Autophagy with Novel Approaches for Diabetes Mellitus

Maiese¹

2015

CNR

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According to the World Health Organization, diabetes mellitus (DM) in the year 2030 will be ranked the seventh leading cause of death in the world. DM impacts all systems of the body with oxidant stress controlling cell fate through endoplasmic reticulum stress, mitochondrial dysfunction, alterations in uncoupling proteins, and the induction of apoptosis and autophagy. Multiple treatment approaches are being entertained for DM with Wnt1 inducible signaling pathway protein 1 (WISP1), mechanistic target of rapamycin (mTOR), and silent mating type information regulation 2 homolog) 1 (S. cerevisiae) (SIRT1) generating significant interest as target pathways that can address maintenance of glucose homeostasis as well as prevention of cellular pathology by controlling insulin resistance, stem cell proliferation, and the programmed cell death pathways of apoptosis and autophagy. WISP1, mTOR, and SIRT1 can rely upon similar pathways such as AMP activated protein kinase as well as govern cellular metabolism through cytokines such as EPO and oral hypoglycemics such as metformin. Yet, these pathways require precise biological control to exclude potentially detrimental clinical outcomes. Further elucidation of the ability to translate the roles of WISP1, mTOR, and SIRT1 into effective clinical avenues offers compelling prospects for new therapies against DM that can benefit hundreds of millions of individuals throughout the globe.

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Anxiety correlates to decreased blood and prefrontal cortex IGF-1 levels in streptozotocin induced diabetes

Cited by 63 publications

References 41 publications

Pyrrolidine Dithiocarbamate Alleviated Anxiety in Diabetic Mice

Pyrrolidine Dithiocarbamate Alleviated Anxiety in Diabetic Mice

Loss of survival factors and activation of inflammatory cascades in brain sympathetic centers in type 1 diabetic mice

Programming Apoptosis and Autophagy with Novel Approaches for Diabetes Mellitus

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