Nerve Growth Factor Increases in Pancreatic β Cells After Streptozotocin-Induced Damage in Rats

Larrieta, M. E.; Vital, Paz; Mendoza-Rodríguez, Adriana; Cerbón, Marco; Hiriart, Marcia

doi:10.1177/153537020623100405

Cited by 39 publications

(23 citation statements)

References 24 publications

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“…Diabetes was confirmed in the treated rats by measuring the fasting blood glucose concentration 48 h after injection. Rats with fasting blood glucose of more than 200 mg/dl was considered diabetic and included in the study (Larrieta et al 2006) Animal experiments To study the effect of CKP feeding on carbohydrate metabolism and the expression of NFkB and iNOS, the rats were divided into 3 groups of six animals each: Group I-Normal control, Group-II-Diabetic control, Group III-Diabetic administered 8 % CKP. All the animals received a normal laboratory diet.…”

Section: Methodsmentioning

confidence: 99%

Dietary coconut kernel protein beneficially modulates NFκB and RAGE expression in streptozotocin induced diabetes in rats

et al. 2012

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Previous studies showed that arginine rich coconut kernel protein (CKP) maintains glucose homeostasis in experimental diabetic rats. But the mechanism of this effect was not clear. This study investigated the effect of CKP on the expression of liver receptor for advance glycated end products (RAGE), inducible nitric oxide synthase (iNOS) and NFkB. Diabetes was induced by injecting a single dose of streptozotocin (75 mg/kg body weight) intraperitoneally. After inducing diabetes, CKP was administered to rats orally for 45 days. After the experimental period, serum glucose, insulin, liver glycogen, glucose metabolizing enzyme activities and the expression of liver RAGE, iNOS and NFkB was evaluated. The results showed that CKP beneficially modulated the levels of glucose and insulin as well as the metabolizing enzyme activities. Expression of RAGE and NFkB was found to be over expressed in diabetic rats but was found to be down regulated in CKP fed diabetic rats. iNOS expression was down regulated in diabetic rats, which was expressed normally in CKP fed diabetic rats.These results clearly demonstrated that anti diabetic activity of CKP is mediated through NFkB pathway.

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Section: Methodsmentioning

confidence: 99%

Dietary coconut kernel protein beneficially modulates NFκB and RAGE expression in streptozotocin induced diabetes in rats

et al. 2012

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“…Recent studies reveal that NGF exerts various non-neuronal effects including stimulation of insulin secretion by pancreatic b-cells, and these cells synthesize and release NGF [28]. Furthermore, NGF and BDNF are implicated in the pathogenesis of cardiometabolic diseases including MS [16,29,30].…”

Section: Discussionmentioning

confidence: 99%

Metabolic Syndrome and Neurotrophins: Effects of Metformin and Non-Steroidal Antiinflammatory Drug Treatment

Hristova¹

2011

EAJM

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Objective: Metabolic syndrome (MS) presents with central obesity, impaired glucose metabolism, dyslipidemia and hypertension. Our aim was to examine the effect of metformin treatment either alone or in combination with non-steroidal anti-inflammatory drugs (NSAID) on plasma levels of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) in patients with early stage MS (MS-es) and generalized MS (MS-ge). Materials and Methods:The study compared 35 female patients with MS-es (mean age of 43.39±1.54 years) and 40 patients with MSge (mean age of 45.69±2.18 years) to 10 age-matched controls each. Patients with MS-es were administered 850 mg metformin twice daily. The patients with MS-ge were divided into two groups of 20 patients per group. One group received metformin alone, while the other group received metformin in combination with 500 mg aspirin and 150 mg Diclac daily. Plasma NGF and BDNF levels were measured by ELISA. Statistical data analysis was performed using ANOVA.Results: Plasma NGF and BDNF levels were significantly higher in MS-es patients and lower in MS-ge patients than in controls. NGF levels were decreased in both groups after treatment with metformin. NGF levels were significantly higher in MS-ge patients on combined therapy than in those on metformin only. Conclusion:The combination of metformin and NSAID treatment is more effective than metformin alone on NGF and BDNF production as well as on metabolism-related anthropometric and laboratory features. This represents a pathogenetic therapeutic mechanism in MS due to its strong anti-inflammatory effect and improves MS-ge symptoms.Key Words: Brain-derived neurotrophic factor, Early stage metabolic syndrome, Generalized metabolic syndrome, Inflammation, Nerve growth factor Özet Amaç: Metabolik sendrom (MS), santral obezite, bozulmuş glukoz metabolizması, dislipidemi ve hipertansiyon ile kendini göstermek-tedir. Hedefimiz, tek başına metformin tedavisinin ve erken evre MS'li hastalarda (MS -es) ve generalize MS (MS-ge) sinir büyüme faktörü (NGF) ve beyin kaynaklı nörotrofik faktör (BDNF) plazma düzeyleri üzerine non-steroid antienflamatuar ilaçlar (NSAID) ile birlikte etkisini araştırmaktır. Gereç ve Yöntem:Çalışma, MS-es'li 35 kadın hasta (yaş ortalaması 43.39±1.54 yıl) ve 40 MS-ge'li kadın hasta (yaş ortalaması 45.69±2.18 yıl) ve her biri ile yaş olarak eşleştirilmiş 10 hastadan oluşan kontrol grubu ile yapılmıştır. MS-es ile hastalar günde iki kez 850 mg dozda metformin verilmiştir. MS-ge ile hastalar, her biri 20 hasta iki gruba ayrıldı. Bunlar, 150 mg günlük doz 500 mg ve Diclac (Diklofenak Na) bir doz aspirin ile ya tek başına veya kombine olarak metformin almıştır. Plazma NGF ve BDNF düzeyleri ELISA yöntemi ile ölçüldü. İsta-tistik veri işleme, ANOVA yöntemi ile yapıldı. Bulgular: Plazma NGF ve BDNF MS-es hastalarda önemli ölçüde daha yüksek ve MS-ge olanlar kontrollere göre daha düşüktü. NGF düzeyleri metformin ile tedavi sonrasında her iki grupta da azalmıştır. NGF seviyeleri sadece bu on metformin kombine tedavi MS-...

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“…23 NGF exerts both stimulatory and inhibitory effects on PanCa cells, depending on the NGF expression level and ratio of TrkA to p75. 24,25 Overexpression of NGF may contribute to PNI of PanCa cells by inducing hyperplasia of nerves, which reduces apoptosis of PanCa cells due to the combined signaling effects of NGF and TrkA in PanCa.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemic tumor microenvironment induces perineural invasion in pancreatic cancer

Ma²,

Han

et al. 2015

Cancer Biology & Therapy

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Glucose intolerance and frank diabetes mellitus (DM) can increase the risk of cancer death for pancreatic cancer (PanCa). However, the mechanism by which these factors influence cancer deaths is not clear. In this study, we established a model system to mimic the pancreatic tumor microenvironment in patients with DM to examine the biological behavior of PanCa cells and nerves in cell culture and in animals. Our in vitro studies demonstrated that hyperglycemia promoted the proliferation and invasion of PanCa cell lines and upregulated the expression of nerve growth factor in these cells. Also, the migration of Schwann cells (SCs) was inhibited by hyperglycemia and neurites exerted pathological regeneration. Furthermore, the interaction between the PanCa cells and nerves was enhanced in the tumor microenvironment. We further showed that hyperglycemia promoted the perineural invasion (PNI) of PanCa in vivo. These data suggest that DM worsens the prognosis of PanCa because of aggravated PNI. Thus, our study illustrates a novel mechanism by which hyperglycemia decreases survival in patients with PanCa.

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Nerve Growth Factor Increases in Pancreatic β Cells After Streptozotocin-Induced Damage in Rats

Cited by 39 publications

References 24 publications

Dietary coconut kernel protein beneficially modulates NFκB and RAGE expression in streptozotocin induced diabetes in rats

Dietary coconut kernel protein beneficially modulates NFκB and RAGE expression in streptozotocin induced diabetes in rats

Metabolic Syndrome and Neurotrophins: Effects of Metformin and Non-Steroidal Antiinflammatory Drug Treatment

Hyperglycemic tumor microenvironment induces perineural invasion in pancreatic cancer

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