<i>Polysiphonia japonica</i> Extract Attenuates Palmitate‐Induced Toxicity and Enhances Insulin Secretion in Pancreatic Beta‐Cells

Cha, Seon-Heui; Kim, Hyunsoo; Hwang, Yongha; Jeon, You‐Jin; Jun, Hee-Sook

doi:10.1155/2018/4973851

Cited by 10 publications

(12 citation statements)

References 53 publications

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“…It has been demonstrated that chronic hyperglycemia and higher levels of circulating FFAs are commonly associated with the beta cell function deterioration [2]. Hyperglycemia could aggravate lipotoxicity-induced beta cell dysfunction (glucolipotoxicity) [5, 6]. Recently, transcriptomics and proteomics have been successfully adopted to discover major changes of protein-coding genes and proteins in pancreatic INS-1 cells exposed to glucolipotoxicity [18, 19].…”

Section: Discussionmentioning

confidence: 99%

“…Chronic elevation of hyperglycemia causes beta cell failure characterized by impaired insulin secretion and enhanced islet beta cell apoptosis (glucotoxicity) [3, 4]. Furthermore, long-term exposure of beta cells to FFA triggers apoptosis (lipotoxicity) and the elevated glucose augments fatty acid-induced beta cell death (glucolipotoxicity) [5–7]. The glucolipotoxicity plays a pivotal role in the worsening of beta cell function over time, which has been implicated in the development of T2DM [8].…”

Section: Introductionmentioning

confidence: 99%

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LncRNA LEGLTBC Functions as a ceRNA to Antagonize the Effects of miR-34a on the Downregulation of SIRT1 in Glucolipotoxicity-Induced INS-1 Beta Cell Oxidative Stress and Apoptosis

Xiang

Liu

Wang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Type 2 diabetes mellitus is a chronic metabolic disorder characterized by elevated blood glucose and/or high serum free fatty acids. Chronic hyperlipidemia causes the dysfunction of pancreatic beta cells, which is aggravated in the presence of hyperglycemia (glucolipotoxicity). Long noncoding RNAs (lncRNAs) have been suggested to play key roles in type 1 diabetes mellitus development. However, their roles in glucolipotoxicity-induced beta cell dysfunction are not fully understood. In the present study, we identified the differentially expressed lncRNAs in INS-1 cells exposed to high glucose and palmitate (HG/PA). Among the dysregulated lncRNAs, NONRATT003679.2 (low expression in glucolipotoxicity-treated beta cells (LEGLTBC)) was involved in glucolipotoxicity-evoked rat islet beta cell damage. LEGLTBC functioned as a molecular sponge of miR-34a in INS-1 cells. Additionally, SIRT1 was identified as a target of miR-34a and LEGLTBC promoted SIRT1 expression by sponging miR-34a. The upregulation of LEGLTBC attenuated HG/PA-induced INS-1 cell injury through the promotion of SIRT1-mediated suppression of ROS accumulation and apoptosis. This is the first study to comprehensively identify the lncRNA expression profiling of HG/PA-treated INS-1 beta cells and to demonstrate that LEGLTBC functions as a competing endogenous RNA and regulates miR-34a/SIRT1-mediated oxidative stress and apoptosis in INS-1 cells undergoing glucolipotoxicity.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

LncRNA LEGLTBC Functions as a ceRNA to Antagonize the Effects of miR-34a on the Downregulation of SIRT1 in Glucolipotoxicity-Induced INS-1 Beta Cell Oxidative Stress and Apoptosis

Xiang

Liu

Wang

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…Dieckol also reduced overexpression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) [ 182 ]. A recent study addressed the efficacy of an extract of the red seaweed Polysiphinia japonica on preserving cell viability and glucose-induced insulin secretion in a pancreatic β-cell line, Ins-1, treated with palmitate [ 183 ]. However, the tested extract contained, in addition to polyphenols, other components such as carbohydrates, lipid and proteins; hence, the described bioactivities may not be due only to polyphenols.…”

Section: Bioactive Properties Of Marine Phenolicsmentioning

confidence: 99%

Bioactive Properties of Marine Phenolics

2020

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Phenolic compounds from marine organisms are far less studied than those from terrestrial sources since their structural diversity and variability require powerful analytical tools. However, both their biological relevance and potential properties make them an attractive group deserving increasing scientific interest. The use of efficient extraction and, in some cases, purification techniques can provide novel bioactives useful for food, nutraceutical, cosmeceutical and pharmaceutical applications. The bioactivity of marine phenolics is the consequence of their enzyme inhibitory effect and antimicrobial, antiviral, anticancer, antidiabetic, antioxidant, or anti-inflammatory activities. This review presents a survey of the major types of phenolic compounds found in marine sources, as well as their reputed effect in relation to the occurrence of dietary and lifestyle-related diseases, notably type 2 diabetes mellitus, obesity, metabolic syndrome, cancer and Alzheimer’s disease. In addition, the influence of marine phenolics on gut microbiota and other pathologies is also addressed.

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“…Evidence has suggested that continuous exposure to high concentrations of free fatty acids (FFAs) and glucose may damage islet β-cells, activate apoptosis, and in turn, generate glucotoxicity and lipotoxicity (31)(32)(33)(34). To test whether TG could have a protective role against glucotoxicity and lipotoxicity by increasing the expression of PDX1, we established a glucotoxicity (35,36) and lipotoxicity (32,37) models in islet β-cell lines. We observed that 200 μM palmitic acid (PA) or 33mM glucose (Glu) significantly decreased cell viability of INS-1 cells, which indicated that both lipotoxic and glucotoxic models were successfully established ( Fig.…”

Section: Tg Protects Ins-1 Cells From Apoptosis Induced By High-fat Amentioning

confidence: 99%

Tectorigenin enhances PDX1 expression and protects pancreatic β-cells by activating ERK and reducing ER stress

Yao

Chen

et al. 2020

Journal of Biological Chemistry

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Pancreas/duodenum homeobox protein 1 (PDX1) is an important transcription factor that regulates islet β-cell proliferation, differentiation, and function. Reduced expression of PDX1 is thought to contribute to β-cell loss and dysfunction in diabetes. Thus, promoting PDX1 expression can be an effective strategy to preserve β-cell mass and function. Previously, we established a PDX1 promoter-dependent luciferase system to screen agents that can promote PDX1 expression. Natural compound tectorigenin (TG) was identified as a promising candidate that could enhance the activity of the promoter for PDX1 gene. In this study, we first demonstrated that TG could promote the expression of PDX1 in β-cells via activating extracellular signal-related kinase (ERK), as indicated by increased phosphorylation of ERK; this effect was observed under either normal or glucotoxic/lipotoxic conditions. We then found that TG could suppress induced apoptosis and improved the viability of β-cells under glucotoxicity and lipotoxicity by activation of ERK and reduction of reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress. These effects held true in vivo as well: prophylactic or therapeutic use of TG could obviously inhibit ER stress and decrease islet β-cell apoptosis in the pancreas of mice given a high-fat/high-sucrose diet (HFHSD), thus dramatically maintaining or restoring β-cell mass and islet size respectively. Accordingly, both prophylactic and therapeutic use of TG improved HFHSD impaired glucose metabolism in mice, as evidenced by ameliorating hyperglycemia and glucose intolerance. Taken together, TG, as an agent promoting PDX1 expression exhibits strong protective effects on islet β-cells both in vitro and in vivo.

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Polysiphonia japonica Extract Attenuates Palmitate‐Induced Toxicity and Enhances Insulin Secretion in Pancreatic Beta‐Cells

Cited by 10 publications

References 53 publications

LncRNA LEGLTBC Functions as a ceRNA to Antagonize the Effects of miR-34a on the Downregulation of SIRT1 in Glucolipotoxicity-Induced INS-1 Beta Cell Oxidative Stress and Apoptosis

LncRNA LEGLTBC Functions as a ceRNA to Antagonize the Effects of miR-34a on the Downregulation of SIRT1 in Glucolipotoxicity-Induced INS-1 Beta Cell Oxidative Stress and Apoptosis

Bioactive Properties of Marine Phenolics

Tectorigenin enhances PDX1 expression and protects pancreatic β-cells by activating ERK and reducing ER stress

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