Differential gene expression in pancreatic tissues of streptozocin-induced diabetic rats and genetically-diabetic mice in response to hypoglycemic dipeptide cyclo (His-Pro) treatment

Choi, Song Ah; Suh, Hyung Joo; Yun, Jong Won; Choi, Jang Won

doi:10.1007/s11033-012-1746-1

Cited by 5 publications

(3 citation statements)

References 42 publications

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“…This can lead to localized synthesis of cytokines, resulting in recruitment of immune cells to the site of production (Donath and Shoelson, 2011) which will trigger beta cell dysfunction and exacerbate insulin resistance. Nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) has a central regulatory role in FFA-induced inflammation and beta cell death (Choi et al, 2012). The saturated FFA, palmitate, induces beta cell dysfunction in vivo by activating inflammatory processes within mouse islets (Eguchi et al, 2012).…”

Section: Beta Cell Demise and Dysfunctionmentioning

confidence: 99%

“…The saturated FFA, palmitate, induces beta cell dysfunction in vivo by activating inflammatory processes within mouse islets (Eguchi et al, 2012). Palmitate treatment increased expression of major cytokines implicated in beta cell dysfunction (Choi et al, 2012), viz., interleukin (IL) 6, IL8 (CXCL1), IP10 [chemokine (C-X-C motif) ligand 10 (CXCL10)], MCP1 (CCL2), and MIP1A (CCL3) (Donath et al, 2010), where they may influence beta cells in an autocrine manner (Choi et al, 2012). Insulin sensitivity is impaired by saturated FFA and improved by polyunsaturated FFA (Siri-Tarino et al, 2010).…”

Section: Beta Cell Demise and Dysfunctionmentioning

confidence: 99%

See 1 more Smart Citation

Beta Cell Dysfunction and Insulin Resistance

Cerf¹

2013

Front. Endocrinol.

739

471

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Beta cell dysfunction and insulin resistance are inherently complex with their interrelation for triggering the pathogenesis of diabetes also somewhat undefined. Both pathogenic states induce hyperglycemia and therefore increase insulin demand. Beta cell dysfunction results from inadequate glucose sensing to stimulate insulin secretion therefore elevated glucose concentrations prevail. Persistently elevated glucose concentrations above the physiological range result in the manifestation of hyperglycemia. With systemic insulin resistance, insulin signaling within glucose recipient tissues is defective therefore hyperglycemia perseveres. Beta cell dysfunction supersedes insulin resistance in inducing diabetes. Both pathological states influence each other and presumably synergistically exacerbate diabetes. Preserving beta cell function and insulin signaling in beta cells and insulin signaling in the glucose recipient tissues will maintain glucose homeostasis.

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Section: Beta Cell Demise and Dysfunctionmentioning

confidence: 99%

Section: Beta Cell Demise and Dysfunctionmentioning

confidence: 99%

Beta Cell Dysfunction and Insulin Resistance

Cerf¹

2013

Front. Endocrinol.

739

471

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“…Microarray analysis revealed that the expression of PTDSS was increased in diabetic model rats. Downregulation of PTDSS induced the levels of PC (Choi et al, 2012). Linoleic acid and alpha-linolenic acid metabolisms are associated with metabolic syndrome.…”

Section: Discussionmentioning

confidence: 96%

Untargeted Metabolomic Analysis of the Effects and Mechanism of Nuciferine Treatment on Rats With Nonalcoholic Fatty Liver Disease

Cui

Cao

et al. 2020

Front. Pharmacol.

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Metabolomic analysis has been used to characterize the effects and mechanisms of drugs for nonalcoholic fatty liver disease (NAFLD) at the metabolic level. Nuciferine is an active component derived from folium nelumbinis and has been demonstrated to have beneficial effects on a highfat diet (HFD) induced hepatic steatosis model. However, the effect of the altered metabolites of nuciferine on NAFLD has not yet been elucidated. In this study, we established a NAFLD rat model using HFD and treated with nuciferine. The lipid content levels, pro-inflammatory cytokines, and oxidative stress were investigated to access the therapeutic effects of nuciferine. Additionally, the metabolic regulatory mechanisms of nuciferine on NAFLD were analyzed using untargeted metabolomics. Gene expression of the key enzymes related to the changed metabolic pathways following nuciferine intervention was also investigated. The results showed that nuciferine treatment significantly reduced the body weight, levels of lipids, and liver enzymes in the blood and improved the hepatic steatosis in the NAFLD rat model. Nuciferine treatment also increased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decreased the levels of methane dicarboxylic aldehyde (MDA) in the liver. Nuciferine treatment decreased the serum levels of interleukin (IL)-6, IL-1b, and tumor necrosis factor-alpha (TNF-a) and upregulated the gene expression of IL-6, IL-1b, and TNF-a in the liver. Metabolomic analysis indicated a metabolism disorder in the NAFLD rat model reflected in a dysfunction of the glycerophospholipid, linoleic acid, alpha-linolenic acid, arginine and proline metabolism. Conversely, treatment with nuciferine improved the metabolic disorder in the NAFLD rat model. Nuciferine treatment also regulated the gene expression of key enzymes related to the glycerophospholipid, linoleic acid, and alpha-linolenic acid metabolism pathways in the liver. In conclusion, our study demonstrated an amelioration of the metabolic disorders following nuciferine treatment in NAFLD rat model. Our study contributes to the understanding of the effects and mechanisms of drugs for complex diseases using metabolomic analysis and experimental approaches.

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