Selenoprotein SelK increases the secretion of insulin from MIN6 β cells

Meng, Xianmin; Zhang, Huiling; Feng, Linlin; Chen, Manling; Liu, Yingying; Yu, Xia; Huan, Feng-Ning; Lu, Jin‐Jian; Wang, Dan; Liu, Hongsheng; Chen, Chang-Lan

doi:10.1039/c7ra05379g

Cited by 11 publications

(5 citation statements)

References 51 publications

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“…This is in line with data showing that selenite induced insulin expression in vitro and release in islets of Langerhans [22]. Mechanistic insights are missing but this might relate to altered SelenoK expression, which regulates insulin secretion in Min6 cells [35]. Alternatively, increased pancreatic but unchanged circulating insulin levels might suggest increased insulin degradation via insulindegrading enzyme (IDE).…”

Section: Discussionsupporting

confidence: 83%

Obesity Hinders the Protective Effect of Selenite Supplementation on Insulin Signaling

et al. 2022

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The intake of high-fat diets (HFDs) containing large amounts of saturated long-chain fatty acids leads to obesity, oxidative stress, inflammation, and insulin resistance. The trace element selenium, as a crucial part of antioxidative selenoproteins, can protect against the development of diet-induced insulin resistance in white adipose tissue (WAT) by increasing glutathione peroxidase 3 (GPx3) and insulin receptor (IR) expression. Whether selenite (Se) can attenuate insulin resistance in established lipotoxic and obese conditions is unclear. We confirm that GPX3 mRNA expression in adipose tissue correlates with BMI in humans. Cultivating 3T3-L1 pre-adipocytes in palmitate-containing medium followed by Se treatment attenuates insulin resistance with enhanced GPx3 and IR expression and adipocyte differentiation. However, feeding obese mice a selenium-enriched high-fat diet (SRHFD) only resulted in a modest increase in overall selenoprotein gene expression in WAT in mice with unaltered body weight development, glucose tolerance, and insulin resistance. While Se supplementation improved adipocyte morphology, it did not alter WAT insulin sensitivity. However, mice fed a SRHFD exhibited increased insulin content in the pancreas. Overall, while selenite protects against palmitate-induced insulin resistance in vitro, obesity impedes the effect of selenite on insulin action and adipose tissue metabolism in vivo.

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Section: Discussionsupporting

confidence: 83%

Obesity Hinders the Protective Effect of Selenite Supplementation on Insulin Signaling

et al. 2022

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“…Meng et al . have found that selenoprotein K modulates the expression of inositol trisphosphate receptor type 3, thereby influencing intracellular Ca 2+ levels and insulin release . Recently, Se has been found to have potential for improving insulin resistance and increasing insulin sensitivity .…”

Section: Discussionmentioning

confidence: 99%

Selenium affects the activity of black tea in preventing metabolic syndrome in high‐fat diet‐fed Sprague–Dawley rats

Gao

Ruan

et al. 2019

J Sci Food Agric

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BACKGROUND: Metabolic syndrome, a group of factors that increase the risk of health problems, is becoming increasingly common. Strategies to prevent metabolic syndrome have received substantial attention. Black tea consumption and selenium (Se) intake have been reported to be associated negatively with the prevalence of metabolic syndrome. We therefore sought to investigate whether Se-rich black tea might have a stronger effect than Se-deficient black tea in the prevention of metabolic syndrome.RESULTS: Sprague-Dawley rats were divided into four groups and fed a normal rodent diet, high-fat diet, high-fat diet containing 3% Se-rich black tea, or a high-fat diet containing 3% Se-deficient black tea for 4 weeks. Blood and tissue samples were tested at the end of the experiment. The results suggested that both types of black tea ameliorated high-fat diet-induced body-weight gain, lowered serum triglycerides and attenuated intestinal barrier dysfunction. Selenium-rich black tea showed stronger activity in decreasing fasting serum glucose and increasing insulin sensitivity, as well as stronger hepatoprotection, owing to higher total antioxidant capacity and activated hepatic antioxidant enzymes. However, it did not exhibit better effects in preventing fat accumulation. The different effects of Se-rich and Se-deficient black tea on the gut microbiota might have been partially responsible for the results. CONCLUSION: Compared with Se-deficient black tea, Se-rich black tea displayed stronger activity in preventing high-fat diet-induced hyperglycemia and liver damage but was not better at preventing fat accumulation and attenuating dysbiosis. More experiments are needed to understand the underlying mechanisms further. Effects on intestinal barrier functionPrevious studies have implicated a causal relationship between the pathophysiological changes in the gut epithelium and altered gut J Sci Food Agric 2020; 100: 225-234

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“…Selk, which is located in ER and plasma membrane, is a newly identified selenoprotein, which may be required for normal development but does not reveal changes in the total antioxidant status of embryos and cells [61]. Furthermore, a recent study suggested that the expression of Selk may increase the secretion of insulin in the endoplasmic reticulum (ER) [62]. Selk might increase lipid consumption in the liver and then suppress NAFLD and NASH.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Endoplasmic-Reticulum-Resident Selenoproteins in a Nonalcoholic Fatty Liver Disease Pig Model Induced by a High-Fat Diet

Wang

Meng

et al. 2020

Nutrients

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The present study aimed to investigate the intervention of selenium in the oxidative stress and apoptosis of pig livers, which were induced by a high-fat diet, and the effects of four endoplasmic reticulum (ER)-resident selenoproteins in the process. A 2 × 4 design trial was conducted that included two dietary fat levels (BD = basal diet and HFD = high-fat diet) and four dietary Se supplementation levels (0, 0.3, 1.0, and 3.0 mg/kg of the diet, in the form of sodium selenite (Na2SeO3)). Our results indicated that the HFD significantly increased the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the serum, as well as the degree of steatosis, the content of malondialdehyde (MDA), the apoptotic rate, and the level of mRNA caspase-3 in the liver compared to their BD counterparts (p < 0.05). Moreover, these parameters in the HFD groups were more significantly reduced (p < 0.05) for a Se concentration of 1.0 mg/kg than for the other concentrations. Further, for both the BD and HFD, the groups supplemented with 1.0 mg/kg Se showed the highest mRNA level of selenoprotein S. In conclusion, the consumption of an HFD can induce oxidative damage and apoptosis in the liver. This shows that the supplementation of Se at 1.0 mg/kg may be the optimum concentration against damage induced by HFD, and Sels may play a key role in this process.

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Selenoprotein SelK increases the secretion of insulin from MIN6 β cells

Abstract: The expression of selenoprotein SelK triggers the secretion of insulin from MIN6 β cells by increasing the cytosolic free Ca2+ level, resulting from the up-regulated IP3R3 expression.

Cited by 11 publications

References 51 publications

Obesity Hinders the Protective Effect of Selenite Supplementation on Insulin Signaling

Obesity Hinders the Protective Effect of Selenite Supplementation on Insulin Signaling

Selenium affects the activity of black tea in preventing metabolic syndrome in high‐fat diet‐fed Sprague–Dawley rats

The Effects of Endoplasmic-Reticulum-Resident Selenoproteins in a Nonalcoholic Fatty Liver Disease Pig Model Induced by a High-Fat Diet

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