Antioxidant and reducing lipid accumulation effects of rutin in Caenorhabditis elegans

BioFactors ◽  
2021 ◽  
Author(s):  
Xianjin Qin ◽  
Wenqian Wang ◽  
Weihua Chu
Keyword(s):  
Caenorhabditis Elegans ◽  
Lipid Accumulation

scholarly journals Salvia hispanica L. (chia) seeds oil extracts reduce lipid accumulation and produce stress resistance in Caenorhabditis elegans

2018 ◽  
Vol 15 (1) ◽  
Author(s):  
Cristiane Freitas Rodrigues ◽  
Willian Salgueiro ◽  
Matheus Bianchini ◽  
Juliana Cristina Veit ◽  
Robson Luiz Puntel ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Stress Resistance ◽  
Lipid Accumulation ◽  
Salvia Hispanica ◽  
Salvia Hispanica L

scholarly journals Autophagy-dependent gut-to-yolk biomass conversion generates visceral polymorbidity in aging C. elegans

2017 ◽  
Author(s):  
Marina Ezcurra ◽  
Alexandre Benedetto ◽  
Thanet Sornda ◽  
Ann F. Gilliat ◽  
Catherine Au ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Lipid Accumulation ◽  
Damage Accumulation ◽  
Biomass Conversion ◽  
Late Life ◽  
Unknown Etiology ◽  
Wild Type ◽  
Type Function ◽  
C Elegans ◽  
Theory Of Aging

Aging (senescence) is characterized by the development of numerous pathologies, some of which limit lifespan. Key to understanding aging is discovery of the mechanisms (etiologies) that cause senescent pathology. In Caenorhabditis elegans a major senescent pathology of unknown etiology is atrophy of its principal metabolic organ, the intestine. Here we identify a cause of not only this pathology, but also of yolky lipid accumulation and redistribution (a form of senescent obesity): autophagy-mediated conversion of intestinal biomass into yolk. Inhibiting intestinal autophagy or vitellogenesis rescues both visceral pathologies, and can also extend lifespan. This defines a disease syndrome leading to polymorbidity and contributing to late-life mortality. Activation of gut-to-yolk biomass conversion by insulin/IGF-1 signaling (IIS) promotes reproduction and senescence. This illustrates how major, IIS-promoted senescent pathologies in C. elegans can originate not from damage accumulation, but from continued action of a wild-type function (vitellogenesis), consistent with the recently proposed hyperfunction theory of aging.

scholarly journals NHR-80 senses the mitochondrial UPR to rewire citrate metabolism for lipid accumulation in Caenorhabditis elegans

Cell Reports ◽  
2022 ◽  
Vol 38 (2) ◽  
pp. 110206
Author(s):  
Rendan Yang ◽  
Yamei Li ◽  
Yanli Wang ◽  
Jingjing Zhang ◽  
Qijing Fan ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Lipid Accumulation ◽  
Citrate Metabolism

scholarly journals The Role of Cation Diffusion Facilitator CDF-1 in Lipid Metabolism in Caenorhabditis elegans

2021 ◽  
Author(s):  
Ying Hu ◽  
Yanli Wang ◽  
Xuanjun Wang ◽  
Xiaoyun Wu ◽  
Lin Fu ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Caenorhabditis Elegans ◽  
Lipid Accumulation ◽  
Unsaturated Fatty Acids ◽  
Metabolic Diseases ◽  
Regulatory Element ◽  
Zinc Level ◽  
Zinc Homeostasis ◽  
Cation Diffusion ◽  
Cation Diffusion Facilitator

Abstract Zinc is one of the most important trace elements as it plays a vital role in many biological processes. As well, aberrant zinc metabolism has been implicated in lipid-related metabolic diseases. Previously, we showed that zinc antagonizes iron to regulate sterol regulatory element-binding proteins and the stearoyl-CoA desaturase (SREBP-SCD) pathway in lipid metabolism in the model organism Caenorhabditis elegans. In this study we present the identification of another cation diffusion facilitator, CDF-1, which regulates lipid metabolism along with SUR-7 in response to zinc. Inactivation of SBP-1, the only homolog of SREBPs, leads to an increased zinc level but decreased lipid accumulation. However, either the cdf-1(n2527) or sur-7(tm6523) mutation could successfully restore the altered fatty acid profile, fat content, and zinc level of the sbp-1(ep79) mutant. Furthermore, we found that CDF-1/SUR-7 may functionally bypass SBP-1 to directly affect the conversion activity of SCD in the biosynthesis of unsaturated fatty acids and lipid accumulation. Collectively, these results consistently support the link between zinc homeostasis and lipid metabolism via the SREBP-SCD axis by the cation diffusion facilitators CDF-1 and SUR-7.

scholarly journals PHA-4/FoxA senses nucleolar stress to regulate lipid accumulation in Caenorhabditis elegans

2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Jieyu Wu ◽  
Xue Jiang ◽  
Yamei Li ◽  
Tingting Zhu ◽  
Jingjing Zhang ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Lipid Accumulation ◽  
Nucleolar Stress

scholarly journals The role of cation diffusion facilitator CDF-1 in lipid metabolism in Caenorhabditis elegans

2020 ◽  
Author(s):  
Ying Hu ◽  
Yanli Wang ◽  
Xuanjun Wang ◽  
Xiaoyun Wu ◽  
Lin Fu ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Caenorhabditis Elegans ◽  
Lipid Accumulation ◽  
Unsaturated Fatty Acids ◽  
Metabolic Diseases ◽  
Regulatory Element ◽  
Zinc Level ◽  
Zinc Homeostasis ◽  
Cation Diffusion ◽  
Cation Diffusion Facilitator

AbstractZinc is one of the most important trace elements that plays a vital role in many biological processes, and aberrant zinc metabolism has been implicated in lipid-related metabolic diseases. Previously, we showed that zinc antagonizes iron to regulate sterol regulatory element-binding proteins and stearoyl-CoA desaturase (SREBP-SCD) pathway in lipid metabolism in model organism Caenorhabditis elegans. Here, we further identified another cation diffusion facilitator CDF-1 in addition to SUR-7 in response to zinc to regulate lipid metabolism. Inactivation of SBP-1, the only homolog of SREBPs, leads to increased zinc level but decreased lipid accumulation reversely. However, either cdf-1(n2527) or sur-7(tm6523) mutation could successfully restore the altered fatty acid profile, fat content and zinc level of sbp-1(ep79) mutant. Furthermore, we found that CDF-1/SUR-7 may function bypass SBP-1 to directly affect the conversion activity of SCD in the biosynthesis of unsaturated fatty acids and lipid accumulation. Collectively, these results consistently support the link between zinc homeostasis and lipid metabolism via SREBP-SCD axis by cation diffusion facilitators CDF-1 and SUR-7.

scholarly journals Aqueous Bark Extract of Ceiba speciosa (A. St.-Hill) Ravenna Protects against Glucose Toxicity in Caenorhabditis elegans

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Fabrine Bianchin dos Santos ◽  
Caroline Brandão Quines ◽  
Luiz Eduardo Ben Pilissão ◽  
Ana Helena de Castro Dal Forno ◽  
Cristiane Freitas Rodrigues ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Lipid Accumulation ◽  
Biological Activities ◽  
Folk Medicine ◽  
Stem Bark ◽  
Bark Extract ◽  
C Elegans ◽  
Glucose Levels ◽  
Exogenous Glucose ◽  
Pharyngeal Pumping

Plants are widely used in folk medicine because of their pharmacological properties. Ceiba speciosa, popularly known as paineira-rosa or tree-of-wool, is a species found in the Northwest of Rio Grande do Sul, being native of the upper Uruguay River, Brazil. The tea obtained from the stem bark is employed in folk medicine to reduce cholesterol, triacylglycerides, and glucose levels. However, there are no studies in the literature proving its efficacy or the safety of its use. For this study, we used Caenorhabditis elegans as an animal model considering its advantages for risk assessment and pharmacological screenings. For the toxicological tests, C. elegans N2 (wild type) was treated with the aqueous extract of the stem bark of C. speciosa (ECE) at the first larval stage (L1) at concentrations of 5, 25, 50, and 250 μg/mL. To evaluate biological activities, we challenged the extract for oxidative stress resistance in the presence of paraquat (0.5 mM), H2O2 (1 mM), and against glucose-induced toxicity. Our results demonstrated that ECE did not alter survival rate, pharyngeal pumping, and reproduction of the nematodes. The extract was not able to protect the nematodes against the toxicity induced by prooxidants. Notably, ECE protected against glucotoxicity by increasing worms’ life span and by reducing glucose levels. On the other hand, ECE treatment did not reduce lipid accumulation induced by exogenous glucose feeding, as observed in worms which lipid droplets were tagged with GFP. Based on our results, we believe that the extract is indeed promising for further studies focusing on carbohydrates metabolism; however, it needs to be carefully evaluated since the extract does not seem to modulate lipid accumulation.

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