Nr2e1 Deficiency Augments Palmitate‐Induced Oxidative Stress in Beta Cells

Shi, Xiaoli; Deng, Huaxin; Dai, Zhijiang; Xu, Yancheng; Xiong, Xiaokan; Ma, Pei; Cheng, Jing

doi:10.1155/2016/9648769

Cited by 16 publications

(7 citation statements)

References 30 publications

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“…Knockdown of NE2E1 in another β cell line, the MIN6 cells, resulted in decreased proliferation with a partial G0/G1 cell-cycle arrest. Interestingly, NE2E1 deficiency also led to decreased antioxidant enzymes and an augmentation of palmitate-induced oxidative stress in β cells, suggesting a potential role of imbalanced oxidant/antioxidant system in the regulation of β cell proliferation [ 51 ].…”

Section: Oxidative Stress Influences Cell-cycle Regulators In mentioning

confidence: 99%

Oxidative Stress in Pancreatic Beta Cell Regeneration

Wang

2017

Oxidative Medicine and Cellular Longevity

170

132

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Pancreatic β cell neogenesis and proliferation during the neonatal period are critical for the generation of sufficient pancreatic β cell mass/reserve and have a profound impact on long-term protection against type 2 diabetes (T2D). Oxidative stress plays an important role in β cell neogenesis, proliferation, and survival under both physiological and pathophysiological conditions. Pancreatic β cells are extremely susceptible to oxidative stress due to a high endogenous production of reactive oxygen species (ROS) and a low expression of antioxidative enzymes. In this review, we summarize studies describing the critical roles and the mechanisms of how oxidative stress impacts β cell neogenesis and proliferation. In addition, the effects of antioxidant supplements on reduction of oxidative stress and increase of β cell proliferation are discussed. Exploring the roles and the potential therapeutic effects of antioxidants in the process of β cell regeneration would provide novel perspectives to preserve and/or expand pancreatic β cell mass for the treatment of T2D.

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Section: Oxidative Stress Influences Cell-cycle Regulators In mentioning

confidence: 99%

Oxidative Stress in Pancreatic Beta Cell Regeneration

Wang

2017

Oxidative Medicine and Cellular Longevity

170

132

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“…Mice with knockout of NR2E1 , the mammalian homologue of tailless , develop insulin resistance and non-alcoholic fatty liver disease, and reduced growth and adiposity, with the phenotype being aggravated on a high-fat diet 39 . Furthermore, knockdown of NR2E1 in mouse β-cells leads to decreased insulin secretion and proliferation, and increased apoptosis 40 . In humans, NR2E1 has also been found to correlate with inflammation as well as high-fasting glucose and insulin levels in T2D 41 .…”

Section: Discussionmentioning

confidence: 99%

Genetic variation of macronutrient tolerance in Drosophila melanogaster

et al. 2022

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Carbohydrates, proteins and lipids are essential nutrients to all animals; however, closely related species, populations, and individuals can display dramatic variation in diet. Here we explore the variation in macronutrient tolerance in Drosophila melanogaster using the Drosophila genetic reference panel, a collection of ~200 strains derived from a single natural population. Our study demonstrates that D. melanogaster, often considered a “dietary generalist”, displays marked genetic variation in survival on different diets, notably on high-sugar diet. Our genetic analysis and functional validation identify several regulators of macronutrient tolerance, including CG10960/GLUT8, Pkn and Eip75B. We also demonstrate a role for the JNK pathway in sugar tolerance and de novo lipogenesis. Finally, we report a role for tailless, a conserved orphan nuclear hormone receptor, in regulating sugar metabolism via insulin-like peptide secretion and sugar-responsive CCHamide-2 expression. Our study provides support for the use of nutrigenomics in the development of personalized nutrition.

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“…When the cells were growing well, the cells were rinsed with PBS once, then the standard medium without sugar was added and incubated for 30 min. Next HEPES balanced Krebs–Ringer bicarbonate buffer (KRBB) 13 containing 0.1% BSA solution with 2.5 mmol/L glucose was added and incubated for 1 h, and the supernatant was collected for detection of basal insulin secretion. Then 20 mmol/L glucose KRBB solution was added and incubated for 1 h, and the supernatant was collected to detect insulin secretion after glucose stimulation.…”

Section: Methodsmentioning

confidence: 99%

Sigma receptor knockdown augments dysfunction and apoptosis of beta cells induced by palmitate

Wang

et al. 2021

Exp Biol Med (Maywood)

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Sigma-1 receptor (Sig-1R) is located in the endoplasmic reticulum (ER) and clustered on the mitochondria related endoplasmic membranes, which are involved in the regulation of nervous system disease. Here, we designed Sig-1R silence MIN6 cells and studied the influence of Sig-1R silence on beta cells. We showed Sig-1R inactivation in MIN6 cells could not only decrease cell proliferation but also inhibit cell cycle, and this inhibitory effect on cell cycle might be achieved by regulating the FoxM1/Plk1/Cenpa pathway. Moreover, Sig-1R deficiency increased MIN6 cells sensitivity to lipotoxicity, exaggerated palmitate (PA)-induced apoptosis, and impaired insulin secretion. On the other hand, ER chaperone GRP78 and ER proapoptotic molecules CHOP increased in Sig-1R knockdown MIN6 cells. The ATP level decreased and reactive oxygen species (ROS) increased in this kind of cells. Furthermore not only GRP78 and CHOP levels, but also ATP and ROS levels changed more in Sig-1R silence cells after cultured with PA. Therefore, Sig-1R deficiency exaggerated PA induced beta cells apoptosis by aggravating ER stress and mitochondrial dysfunction. Together, our study showed that Sig-1R might influence the proliferation, apoptosis, and function of beta cells.

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Nr2e1 Deficiency Augments Palmitate‐Induced Oxidative Stress in Beta Cells

Cited by 16 publications

References 30 publications

Oxidative Stress in Pancreatic Beta Cell Regeneration

Oxidative Stress in Pancreatic Beta Cell Regeneration

Genetic variation of macronutrient tolerance in Drosophila melanogaster

Sigma receptor knockdown augments dysfunction and apoptosis of beta cells induced by palmitate

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