scholarly journals Effects of Phosphoethanolamine Supplementation on Mitochondrial Activity and Lipogenesis in a Caffeine Ingestion Caenorhabditis elegans Model

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3348
Author(s):  
Hyemin Min ◽  
Esther Youn ◽  
Jaehoon Kim ◽  
Su Young Son ◽  
Choong Hwan Lee ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Caenorhabditis Elegans ◽  
Regulatory Element ◽  
Caffeine Intake ◽  
Mitochondrial Activity ◽  
Mitochondrial Morphology ◽  
Caffeine Ingestion ◽  
C Elegans ◽  
Element Binding Protein ◽  
Amp Activated Protein Kinase

Caffeine intake is strongly linked to lipid metabolism. We previously reported the age-dependent physiological effects of caffeine intake in a Caenorhabditis elegans model. Since nutritional status can actively influence metabolism and overall health, in this study, we evaluated the effect of caffeine intake on lipid metabolism in adult-stage C. elegans. We found that, in C. elegans, fat storage and the level of phosphoethanolamine (PE) were significantly reduced with caffeine intake. In addition, mitochondrial activity decreased and mitochondrial morphology was disrupted, and the expression of oxidative stress response genes, hsp-6, gst-4, and daf-16, was induced by caffeine intake. Furthermore, the level of an energy metabolism sensor, phospho-AMP-activated protein kinase, was increased, whereas the expression of the sterol regulatory element binding protein gene and its target stearoyl-CoA desaturase genes, fat-5, -6, and -7, was decreased with caffeine intake. These findings suggest that caffeine intake causes mitochondrial dysfunction and reduces lipogenesis. Interestingly, these changes induced by caffeine intake were partially alleviated by PE supplementation, suggesting that the reduction in mitochondrial activity and lipogenesis is in part because of the low PE level, and proper dietary supplementation can improve organelle integrity.

Rubidium chloride increases lifespan through an AMPK/FOXO-dependent pathway in Caenorhabditis elegans

2021 ◽  
Author(s):  
Mengjiao Hao ◽  
Zhikang Zhang ◽  
Yijun Guo ◽  
Huihao Zhou ◽  
Qiong Gu ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Stress Responses ◽  
Aging Effect ◽  
Stress Effect ◽  
Neuroprotective Effects ◽  
C Elegans ◽  
Cycle Arrest ◽  
Age Related ◽  
Promising Target ◽  
Amp Activated Protein Kinase

Abstract AMP-activated protein kinase (AMPK) is involved in life span maintenance, stress responses, and germ cell cycle arrest upon dauer entry. AMPK is currently considered a promising target for preventing age-related diseases. Rubidium is one of the trace elements in human body. As early as the 1970s, RbCl has been was reported to have neuroprotective effects. In this work, we report the anti-aging effect of RbCl in Caenorhabditis elegans. Specifically, we reveal that (1) RbCl does increase the lifespan and enhance stress resistance in C. elegans without disturbing their fecundity. (2) RbCl induces superoxide dismutase (SOD) expression, which is essential for its anti-aging and anti-stress effect. (3) AAK-2 and DAF-16 are essential to the anti-aging efficacy of RbCl, and RbCl can promote DAF-16 translocating into the nucleus, suggesting that RbCl delays aging through regulating AMPK/FOXO pathway. RbCl can be a promising agent against aging related diseases.

scholarly journals Piceatannol, a Natural Stilbene, Extends the Lifespan of Caenorhabditis elegans Under Fasting Through Inhibition of Lipolysis

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 38-38
Author(s):  
Jang Miran ◽  
Zhang Yuan ◽  
Bai Juan ◽  
Jun-Bae An ◽  
Park Yeonhwa ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Caenorhabditis Elegans ◽  
Negative Energy ◽  
Hormone Sensitive Lipase ◽  
Pcr Analysis ◽  
Lifespan Extension ◽  
Mrna Levels ◽  
Free Glycerol ◽  
C Elegans ◽  
Glycerol Level

Abstract Objectives Lipolysis is the catabolic process that hydrolyzes triglyceride (TG) to free fatty acids (FFAs) and glycerol under negative energy balance such as fasting. In adipocytes, adipose TG lipase (ATGL), hormone-sensitive lipase (HSL), and monoglyceride lipase play key roles in a series of TG hydrolysis reactions in mammals. However, overly activated adipose lipolysis is believed to contribute to link between obesity and systemic inflammation and oxidative stress. We previously demonstrated that piceatannol (PIC), a natural resveratrol analogue, inhibits adipogenesis in cultured adipocytes and lipogenesis in Caenorhabditis elegans. Furthermore, we showed that PIC extends the lifespan of C. elegans via the insulin/IGF-1 signaling. However, the effects of PIC on lipid metabolism during fasting state is unknown. Methods We conducted Oil-Red-O assay, Enzyme assay (TG and Free glycerol contents), PCR analysis and lifespan assay. Results In this study, we demonstrated that PIC-treated C. elegans exhibited suppressed lipolysis under fasting as judged by increased lipid accumulation and TG levels with decreased free glycerol level. Consistent with these findings, PIC treatment resulted in decreased mRNA levels of genes involved lipolysis such as atgl-1, hosl-1 and aak-2 in fasted C. elegans. Also, PIC treatment augmented fasting-induced lifespan of C. elegans by an increased daf-16 gene expression. However, such effect was abolished when atgl-1, aak-2, and daf-16 mutants were treated with PIC. In addition, we also found that autophagy is required for PIC-induced lifespan in C. elegans during fasting since autophagy inhibitor treatments and autophagy gene deficient worms resulted in blunting the lifespan extension effect of PIC. Conclusions Collectively, our results indicate that PIC contributes to lifespan extension in C. elegans during fasting possibly through regulating lipolysis- and/or autophagy-dependent lipid metabolism. Funding Sources 1. The National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) (2019R1A2C1086146) and (2019R1A6A3A03033878) 2. The Rural Development Administration of the Republic of Korea.

scholarly journals Tissue-Specific Effects of Central Leptin on the Expression of Genes Involved in Lipid Metabolism in Liver and White Adipose Tissue

Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 5604-5610 ◽  
Author(s):  
Nilda Gallardo ◽  
Elena Bonzón-Kulichenko ◽  
Teresa Fernández-Agulló ◽  
Eduardo Moltó ◽  
Sergio Gómez-Alonso ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
White Adipose Tissue ◽  
Binding Protein ◽  
Regulatory Element ◽  
Epididymal Adipose Tissue ◽  
Key Enzymes ◽  
Specific Effects ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

Leptin reduces adiposity and exerts antisteatotic effects on nonadipose tissues. However, the mechanisms underlying leptin effects on lipid metabolism in liver and white adipose tissue have not been fully clarified. Here, we have studied the effects of central leptin administration on key enzymes and transcription factors involved in lipid metabolism in liver and epididymal adipose tissue. Intracerebroventricular leptin infusion for 7 d did not change leptin plasma levels but decreased triacylglyceride content in liver, epididymal adipose tissue, and plasma. In both tissues this treatment markedly decreased the expression of key enzymes of the de novo fatty acid (FA) synthesis such as acetyl-coenzyme A-carboxylase, FA synthase, and stearoyl-coenzyme A desaturase-1, in parallel with a reduction in mRNA expression of sterol regulatory element binding protein-1c in liver and carbohydrate regulatory element binding protein in adipose tissue. In addition, leptin also decreased phosphoenol-pyruvate carboxykinase-C expression in adipose tissue, an enzyme involved in glyceroneogenesis in this tissue. Central leptin administration down-regulates delta-6-desaturase expression in liver and adipose tissue, in parallel with the decrease of the expression of sterol regulatory element binding protein-1c in liver and peroxisome proliferator activated receptor α in adipose tissue. Finally, leptin treatment, by regulating adipose triglyceride lipase/hormone sensitive lipase/diacylglycerol transferase 1 expression, also established a new partitioning in the FA-triacylglyceride cycling in adipose tissue, increasing lipolysis and probably the FA efflux from this tissue, and favoring in parallel the FA uptake and oxidation in the liver. These results suggest that leptin, acting at central level, exerts tissue-specific effects in limiting fat tissue mass and lipid accumulation in nonadipose tissues, preventing the development of obesity and type 2 diabetes.

scholarly journals Estrogen Regulation of Adiposity and Fuel Partitioning

2005 ◽  
Vol 280 (43) ◽  
pp. 35983-35991 ◽  
Author(s):  
Tara M. D'Eon ◽  
Sandra C. Souza ◽  
Mark Aronovitz ◽  
Martin S. Obin ◽  
Susan K. Fried ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Energy Intake ◽  
Molecular Mechanisms ◽  
Ex Vivo ◽  
Regulatory Element ◽  
Estrogen Regulation ◽  
Lipogenic Genes ◽  
Element Binding Protein ◽  
Amp Activated Protein Kinase

Menopause is associated with increased adiposity and greater risk of metabolic disease. In the ovariectomized (OVX) rodent model of menopause, increased adiposity is prevented by estrogen (E2) replacement, reflecting both anorexigenic and potentially metabolic actions of E2. To elucidate metabolic and molecular mechanisms by which E2 regulates fat storage and fat mobilization independently of reduced energy intake, C57 BL/6 mice were ovariectomized, randomized to estrogen (OVX-E2) or control pellet implants (OVX-C), and pairfed for 40 days. E2 treatment was associated with reduced adipose mass and adipocyte size and down-regulation of lipogenic genes in adipocytes under the control of sterol-regulatory element-binding protein 1c. Adipocytes of OVX-E2 mice contained >3-fold more perilipin protein than adipocytes of pairfed control (OVX) mice, and this difference was associated with enhanced ex vivo lipolytic response to catecholamines and with greater levels of serum-free fatty acids following fasting. As in adipose tissue, E2 decreased the expression of lipogenic genes in liver and skeletal muscle. In the latter, E2 appears to promote the partitioning of free fatty acids toward oxidation and away from triglyceride storage by up-regulating the expression of peroxisome proliferation activator receptor-δ and its downstream targets and also by directly and rapidly activating AMP-activated protein kinase. Thus, novel genomic and non-genomic actions of E2 promote leanness in OVX mice independently of reduced energy intake.

scholarly journals The Hepatotoxicity of Alantolactone and Germacrone: Their Influence on Cholesterol and Lipid Metabolism in Differentiated HepaRG Cells

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1720
Author(s):  
Tomáš Zárybnický ◽  
Petra Matoušková ◽  
Lenka Skálová ◽  
Iva Boušová
Keyword(s):  
Lipid Metabolism ◽  
Mrna Expression ◽  
Anticancer Agents ◽  
Regulatory Element ◽  
Intercellular Adhesion Molecule ◽  
Functional Markers ◽  
Intercellular Adhesion Molecule 1 ◽  
Element Binding Protein ◽  
Coa Reductase ◽  
Toxic Concentrations

The sesquiterpenes alantolactone (ATL) and germacrone (GER) are potential anticancer agents of natural origin. Their toxicity and biological activity have been evaluated using the differentiated HepaRG (dHepaRG) cells, a hepatocyte-like model. The half-maximal inhibitory concentrations of cell viability after 24-h treatment of dHepaRG cells are approximately 60 M for ATL and 250 M for GER. However, both sesquiterpenes induce reactive oxygen species (ROS) formation in non-toxic concentrations and significantly dysregulate the mRNA expression of several functional markers of mature hepatocytes. They similarly decrease the protein level of signal transducer and activator of transcription 3 (STAT3), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-B) and their transcription target, intercellular adhesion molecule 1 (ICAM-1). Based on the results of a BATMAN-TCM analysis, the effects of sesquiterpenes on cholesterol and lipid metabolism were studied. Sesquiterpene-mediated dysregulation of both cholesterol and lipid metabolism was observed, during which these compounds influenced the protein expression of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and sterol regulatory element-binding protein 2 (SREBP-2), as well as the mRNA expression of HMGCR, CYP19A1, PLIN2, FASN, SCD, ACACB, and GPAM genes. In conclusion, the two sesquiterpenes caused ROS induction at non-toxic concentrations and alterations in cholesterol and lipid metabolism at slightly toxic and toxic concentrations, suggesting a risk of liver damage if administered to humans.

scholarly journals Hypolipidaemic and antioxidative effects of oligonol, a low-molecular-weight polyphenol derived from lychee fruit, on renal damage in type 2 diabetic mice

2010 ◽  
Vol 104 (8) ◽  
pp. 1120-1128 ◽  
Author(s):  
Jeong Sook Noh ◽  
Hyun Young Kim ◽  
Chan Hum Park ◽  
Hajime Fujii ◽  
Takako Yokozawa
Keyword(s):  
Type 2 Diabetes ◽  
Lipid Peroxidation ◽  
Lipid Metabolism ◽  
Regulatory Element ◽  
Advanced Glycation Endproducts ◽  
Receptor Expression ◽  
Diabetic Mice ◽  
Element Binding Protein ◽  
Abnormal Lipid Metabolism

Oligonol was orally administered at 10 or 20 mg/kg body weight per d for 8 weeks to db/db mice with type 2 diabetes, and its effects were compared with those of the vehicle in db/db and m/m (misty, non-diabetic) mice. Serum and renal biochemical factors, protein expressions related to lipid metabolism and inflammation, and advanced glycation endproducts were measured. There were significant reductions in the serum lipid concentration, reactive oxygen species (ROS) and lipid peroxidation, as well as improvements in renal function parameters. In addition, oligonol treatment significantly decreased ROS levels and lipid peroxidation in the kidney. In particular, the renal lipid contents such as TAG and total cholesterol were significantly reduced in the oligonol-administered groups through the up-regulation of PPARα and down-regulation of sterol regulatory element-binding protein-1 in db/db mice. Moreover, oligonol inhibited non-fluorescent AGE formation and their receptor expression, suggesting that it could effectively inhibit AGE development caused by oxidative stress and/or dyslipidaemia in the kidney of db/db mice. Furthermore, augmented expressions of NF-κBp65, cyclo-oxygenase-2 and inducible NO synthase were down-regulated to the levels of m/m mice in the group given oligonol at 20 mg/kg. This means that oligonol would act as a regulator in the inflammatory response of type 2 diabetes. The present results suggest that oligonol could have renoprotective effects against abnormal lipid metabolism and ROS-related AGE formation in type 2 diabetes.

scholarly journals Cafestol Increases Fat Oxidation and Energy Expenditure in Caenorhabditis Elegans via DAF-12-dependent Pathway (OR34-02-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Renalison Farias-Pereira ◽  
Yeonhwa Park
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Caenorhabditis Elegans ◽  
Energy Expenditure ◽  
Hormone Receptors ◽  
Cholesterol Homeostasis ◽  
Scientific Development ◽  
Gene Expressions ◽  
Fat Accumulation ◽  
C Elegans

Abstract Objectives Cafestol, a diterpene found in coffee beans, is reported to be an agonist of farnesoid X receptors (FXR), nuclear hormone receptors involved in cholesterol homeostasis. It is also known that FXR plays critical roles in other metabolic pathways, including lipid metabolism; however, little is known about cafestol's effects on lipid metabolism. The goal of the current study was to investigate the effects of cafestol on lipid metabolism using Caenorhabditis elegans as a model system. Methods C. elegans was treated for 2 days with cafestol or 0.2% dimethyl sulfoxide (vehicle control). Triglycerides, locomotor behavior (an indicator of energy expenditure) and lipid metabolism-related gene expressions were measured. Results Cafestol at 60 µM significantly reduced fat accumulation by 20% compared to the control. Cafestol increased locomotor activity by 38% compared to the control. The effects of cafestol on fat accumulation were dependent on daf-12 (a functional homolog of the human FXR) and further confirmed by the upregulation of a DAF-12-target gene, fard-1 (the homolog of the human fatty acid reductase 1). Cafestol's fat-lowering effects were also dependent on tub-1 (an ortholog of the human TUBBY), which is involved in the neurological regulation of energy expenditure. Cafestol upregulated the expression of ech-1.1, involved in fatty acid β-oxidation; however, no effects of cafestol were observed on lipogenesis, lipolysis or lipid uptake and transport. Conclusions In conclusion, cafestol regulates lipid metabolism in C. elegans by increasing fatty acid β-oxidation and energy expenditure dependent on daf-12/FXR. Funding Sources Brazilian National Counsel of Technological and Scientific Development (CNPq).

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