Comparison of somatostatin distribution in pancreatic duct ligated rats and streptozotocin diabetic rats

Lee, Chang Kyu; Wakasugi, Hideyuki; Itoh, Hiroshi

doi:10.1007/bf02776585

Cited by 5 publications

(4 citation statements)

References 25 publications

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“…Streptozotocin (STZ) is a diabetogenic compound and is generally used to determine experimental animal models of diabetes due to its selective impairment activity of the insulin signal pathway (Lee et al, 1983 ). Previous studies have shown that intracerebroventricular (ICV) administration of low STZ doses into the brain induces disrupted homeostasis of brain insulin signaling and defect in cerebral glucose metabolism.…”

Section: Introductionmentioning

confidence: 99%

Streptozotocin Induces Alzheimer’s Disease-Like Pathology in Hippocampal Neuronal Cells via CDK5/Drp1-Mediated Mitochondrial Fragmentation

Park

Won

Seo

et al. 2020

Front. Cell. Neurosci.

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Aberrant brain insulin signaling plays a critical role in the pathology of Alzheimer's disease (AD). Mitochondrial dysfunction plays a role in the progression of AD, with excessive mitochondrial fission in the hippocampus being one of the pathological mechanisms of AD. However, the molecular mechanisms underlying the progression of AD and mitochondrial fragmentation induced by aberrant brain insulin signaling in the hippocampal neurons are poorly understood. Therefore, we investigated the molecular mechanistic signaling associated with mitochondrial dynamics using streptozotocin (STZ), a diabetogenic compound, in the hippocampus cell line, HT-22 cells. In this metabolic dysfunctional cellular model, hallmarks of AD such as neuronal apoptosis, synaptic loss, and tau hyper-phosphorylation are induced by STZ. We found that in the mitochondrial fission protein Drp1, phosphorylation is increased in STZ-treated HT-22 cells. We also determined that inhibition of mitochondrial fragmentation suppresses STZ-induced AD-like pathology. Furthermore, we found that phosphorylation of Drp1 was induced by CDK5, and inhibition of CDK5 suppresses STZ-induced mitochondrial fragmentation and AD-like pathology. Therefore, these findings indicate that mitochondrial morphology and functional regulation may be a strategy of potential therapeutic for treating abnormal metabolic functions associated with the pathogenesis of AD.

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Section: Introductionmentioning

confidence: 99%

Streptozotocin Induces Alzheimer’s Disease-Like Pathology in Hippocampal Neuronal Cells via CDK5/Drp1-Mediated Mitochondrial Fragmentation

Park

Won

Seo

et al. 2020

Front. Cell. Neurosci.

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“…Lee, Wakasugi & Ibayashi (1983) have shown a significant increase of somato¬ statin content in the duodenum after 3 weeks of ligation of the pancreatic duct compared with that in the sham-operated group, while Ballmann, Fölsch & Conlon (1985) observed no changes of somatostatin levels in the small intestine after 45 days of pancreatic acinar atrophy in the rat.…”

Section: Introductionmentioning

confidence: 93%

Somatostatin levels and binding in duodenal mucosa of rabbits with ligation of the pancreatic duct

Guijarro

Arilla²

1988

Journal of Endocrinology

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Atrophy of the exocrine pancreas was induced in rabbits by pancreatic duct ligation. Somatostatin concentration and binding in cytosol from rabbit duodenal mucosa were studied after 6 and 14 weeks of pancreatic duct ligation. Somatostatin-like immunoreactivity was significantly increased in the duodenal mucosa in both periods. Scatchard analysis showed a parallel increase in the number of binding sites rather than a change in their affinity. The physiological significance of these findings remains to be clarified.

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“…Additionally, anti-diabetic drugs exert protective effects on AD-related pathologies in the AD models of mice and monkeys 4 , 5 . Streptozotocin (STZ) is a diabetogenic and toxic compound for pancreatic β-cell generally used to establish animal models of diabetes owing to its ability to selectively disrupt the insulin signaling pathway 6 . The intracerebroventricular (ICV) injection of STZ into the brain is a well-established non-transgenic AD animal model showing behavioral, pathological, and molecular aspects of AD, including memory impairment, neuronal loss, and oxidative stress 7 , 8 .…”

Section: Introductionmentioning

confidence: 99%

Peroxiredoxin 1 inhibits streptozotocin-induced Alzheimer’s disease-like pathology in hippocampal neuronal cells via the blocking of Ca2+/Calpain/Cdk5-mediated mitochondrial fragmentation

Park,

Won,

Yang

et al. 2024

Sci Rep

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Oxidative stress plays an essential role in the progression of Alzheimer’s disease (AD), the most common age-related neurodegenerative disorder. Streptozotocin (STZ)-induced abnormal brain insulin signaling and oxidative stress play crucial roles in the progression of Alzheimer’s disease (AD)-like pathology. Peroxiredoxins (Prxs) are associated with protection from neuronal death induced by oxidative stress. However, the molecular mechanisms underlying Prxs on STZ-induced progression of AD in the hippocampal neurons are not yet fully understood. Here, we evaluated whether Peroxiredoxin 1 (Prx1) affects STZ-induced AD-like pathology and cellular toxicity. Prx1 expression was increased by STZ treatment in the hippocampus cell line, HT-22 cells. We evaluated whether Prx1 affects STZ-induced HT-22 cells using overexpression. Prx1 successfully protected the forms of STZ-induced AD-like pathology, such as neuronal apoptosis, synaptic loss, and tau phosphorylation. Moreover, Prx1 suppressed the STZ-induced increase of mitochondrial dysfunction and fragmentation by down-regulating Drp1 phosphorylation and mitochondrial location. Prx1 plays a role in an upstream signal pathway of Drp1 phosphorylation, cyclin-dependent kinase 5 (Cdk5) by inhibiting the STZ-induced conversion of p35 to p25. We found that STZ-induced of intracellular Ca2+ accumulation was an important modulator of AD-like pathology progression by regulating Ca2+-mediated Calpain activation, and Prx1 down-regulated STZ-induced intracellular Ca2+ accumulation and Ca2+-mediated Calpain activation. Finally, we identified that Prx1 antioxidant capacity affected Ca2+/Calpain/Cdk5-mediated AD-like pathology progress. Therefore, these findings demonstrated that Prx1 is a key factor in STZ-induced hippocampal neuronal death through inhibition of Ca2+/Calpain/Cdk5-mediated mitochondrial dysfunction by protecting against oxidative stress.

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Comparison of somatostatin distribution in pancreatic duct ligated rats and streptozotocin diabetic rats

Cited by 5 publications

References 25 publications

Streptozotocin Induces Alzheimer’s Disease-Like Pathology in Hippocampal Neuronal Cells via CDK5/Drp1-Mediated Mitochondrial Fragmentation

Streptozotocin Induces Alzheimer’s Disease-Like Pathology in Hippocampal Neuronal Cells via CDK5/Drp1-Mediated Mitochondrial Fragmentation

Somatostatin levels and binding in duodenal mucosa of rabbits with ligation of the pancreatic duct

Peroxiredoxin 1 inhibits streptozotocin-induced Alzheimer’s disease-like pathology in hippocampal neuronal cells via the blocking of Ca2+/Calpain/Cdk5-mediated mitochondrial fragmentation

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