Lipid Accumulation In Adipocytes Research Articles

Exploring the multiple effects of butein on adipogenic differentiation, inflammatory responses, and glucose metabolism in cellular models

Obesity is a significant risk factor for the development of type 2 diabetes due to its association with increased oxidative stress and inflammation. This study investigates the potential therapeutic effects of butein, a plant-derived polyphenol used as a dietary supplement, on adipogenic differentiation in 3T3-L1 cells, as well as its effects on inflammation and glucose metabolism in co-cultured 3T3-L1 and RAW264 cells treated with lipopolysaccharide (LPS). While butein did not significantly affect lipid accumulation in adipocytes, it significantly upregulated the mRNA expression of genes involved in adipogenic differentiation. In addition, butein demonstrated the ability to reduce reactive oxygen species levels in adipocytes. In co-culture with LPS-stimulated cells, butein exhibited anti-inflammatory properties by suppressing the expression of pro-inflammatory cytokines. Although its efficacy in reversing LPS-induced glucose metabolism in 3T3-L1 adipocytes was limited, butein significantly inhibited GLUT1 expression in LPS-stimulated RAW264 cells. The effects of butein on adipogenic differentiation, inflammation and glucose metabolism were found to be concentration dependent, suggesting potential protective benefits in co-cultured cell models under LPS stimulation.

Ablation of LKB1 gene changes the lipid profiles of goat intramuscular fat and enhances polyunsaturated fatty acids deposition

The content and composition of intramuscular fat (IMF) affect the cooked meat palatability such as tenderness and juiciness. Thus, elucidation of lipid deposition and its composition in goat IMF is necessary. Here, Jianzhou big-ear goats with higher IMF content is associated with lower mRNA level of LKB1 gene, compared with those of Chuannan black goats. Functionally, knockdown of LKB1 promoted intramuscular adipocyte lipid accumulation. Next, LC-MS/MS based pseudo target analysis found that 409 lipids existed in goat intramuscular adipocytes, of which polyunsaturated fatty acids accounted for most lipids. Compared with the control, 78 differential lipids were screened in the siLKB1 group, enriched in the triacylglycerols and fatty acids subclasses. The combined analysis between lipidomic and published transcriptomic data showed that siLKB1 enhanced polyunsaturated fatty acids synthesis through upregulation expression of HACD4. Finally, the promotion of lipid accumulation and polyunsaturated fatty acids synthesis in the LKB1 knockdown cells were partly rescued by ablation of HACD4. Collectively, these data provide a genetic target to produce PUFA enriched functional goat meat and expand new insights into improvement of meat quality.

YAP and ECM Stiffness: Key Drivers of Adipocyte Differentiation and Lipid Accumulation.

ECM stiffness significantly influences the differentiation of adipose-derived stem cells (ADSCs), with YAP-a key transcription factor in the Hippo signaling pathway-playing a pivotal role. This study investigates the effects of ECM stiffness on ADSC differentiation and its relationship with YAP signaling. Various hydrogel concentrations were employed to simulate different levels of ECM stiffness, and their impact on ADSC differentiation was assessed through material properties, adipocyte-specific gene expression, lipid droplet staining, YAP localization, and protein levels. Our results demonstrated that increasing hydrogel stiffness enhanced adipocyte differentiation in a gradient manner. Notably, inhibiting YAP signaling further increased lipid droplet accumulation, suggesting that ECM stiffness influences adipogenesis by modulating YAP signaling and its cytoplasmic phosphorylation. This study elucidates the molecular mechanisms underlying ECM stiffness-dependent lipid deposition, highlighting YAP's regulatory role in adipogenesis. These findings provide valuable insights into the regulation of cell differentiation and have important implications for tissue engineering and obesity treatment strategies.

Resveratrol and Its Derivatives Diminish Lipid Accumulation in Adipocytes In Vitro-Mechanism of Action and Structure-Activity Relationship.

Expansion of white adipose tissue causes systemic inflammation and increased risk of metabolic diseases due to its endocrine function. Resveratrol was suggested to be able to prevent obesity-related disorders by mimicking caloric restriction; however, its structure-activity relationships and molecular targets are still unknown. We aimed to compare the effects of resveratrol and its analogues on adipocyte metabolism and lipid accumulation in vitro. Mouse embryonic fibroblasts were differentiated to adipocytes in the absence or presence of resveratrol or its derivatives (oxyresveratrol, monomethylated resveratrol, or trimethylated resveratrol). Intracellular lipid content was assessed by Oil Red O staining. Glucose uptake and its response to insulin were estimated by 2-NBDG, and mitochondrial activity was assayed via resazurin reduction. Involvement of potential molecular pathways was investigated by concurrent treatment with their inhibitors. Although lipid accumulation was significantly reduced by all analogues without altering protein content, oxyresveratrol was the most potent (IC50 = 4.2 μM), while the lowest potency was observed with trimethylated resveratrol (IC50 = 27.4 μM). Increased insulin-stimulated glucose uptake was restored by each analogue with comparable efficiency. The enhanced mitochondrial activity was normalized by resveratrol and its methylated derivatives, while oxyresveratrol had a minor impact on it. Among the examined pathways, inhibition of SIRT1, PGC-1α, and JNK diminished the lipid-reducing effect of the compounds. Autophagy appeared to play a key role in the effect of all compounds but oxyresveratrol. Resveratrol and its analogues can mimic caloric restriction with complex mechanisms, including activation of SIRT1, PGC-1α, and JNK, making them possible drug candidates to treat obesity-related diseases.

Vine Tea Extract (VTE) Inhibits High-Fat Diet-Induced Adiposity: Evidence of VTE's Anti-Obesity Effects In Vitro and In Vivo.

This study focused on evaluating the anti-obesity effects of an extract from Ampelopsis grossedentata (Hand.-Mazz.) W. T. Wang, also known as vine tea, in mature adipocytes and high-fat diet-induced obese mice. Vine tea extract (VTE) effectively decreased lipid accumulation in mature adipocytes without cytotoxicity, as confirmed by the regulation of several factors associated with adipogenesis, lipogenesis, or lipolysis. Subsequently, in a 12-week experiment with obese mice, oral VTE administration significantly reduced body weight gain induced with high-fat diet intake. Au-topsy findings showed reduced fat accumulation in various areas without liver damage. The VTE-administered group showed lower serum LDL levels, while increasing HDL, than the high-fat diet-administered group. Analysis of adipose tissue biomarkers indicated VTE's ability to inhibit adipogenesis and lipogenesis, promote lipolysis, and regulate energy metabolism, contributing to reduced adiposity induced by the consumption of a high-fat diet.

Effects of Flavanone Derivatives on Adipocyte Differentiation and Lipid Accumulation in 3T3-L1 Cells.

Flavanones, a class of flavonoids, are abundant in fruits, vegetables, and herbs. They are known to have several biological activities, such as anti-inflammatory and anti-cancer activities, but their effects on obesity remain unclear. Obesity is closely associated with adipocyte differentiation and lipid accumulation in adipose tissue. Therefore, in this study, we examined the effects of flavanone derivatives on adipocyte differentiation and lipid accumulation by using 3T3-L1 cells. Among the 15 flavanone derivatives studied, 4'-phenylflavanone (4PF), with a biphenyl structure, significantly inhibited adipocyte differentiation-related lipid accumulation in 3T3-L1 cells; this inhibition of lipid accumulation was dose-dependent. Gene expression analysis showed that 4PF suppressed the expression of adipogenic marker genes. Although the induction of peroxisome proliferator activator γ2 (Pparγ2), a master regulator of adipocyte differentiation, and its target genes during adipocyte differentiation was attenuated in 4PF-treated cells, 4PF did not directly regulate Pparγ2 gene expression and its activation. In contrast, 4PF suppressed mitotic clonal expansion (MCE), which is associated with changes in the expression of proliferation-related genes at the early stages of adipocyte differentiation. Taken together, these results suggest that 4PF inhibits lipid accumulation because it suppresses MCE during adipocyte differentiation. Thus, our findings may help in the development of anti-obesity drugs.

Liubao tea extract restrains obesity-related hyperlipidemia via regulation of AMPK/p38/NF-κB pathway and intestinal microbiota

Liubao tea, a traditional dark tea, has gained widespread recognition for various health benefits. In this study, the effects of Liubao tea extract (LTE) on obesity-related hyperlipidemia and the potential mechanism involved were explored. Anti-obesity compounds such as tricetin, isovitexin, tiliroside, etc. in LTE were identified. In high-fat diet mouse models, LTE effectively reduced tissues, organs, and body weight growth, and restored abnormal serum lipid levels. LTE could reverse adipocyte enlargement, lipid accumulation, and hepatic microstructure abnormalities. Notably, LTE reshaped gut microbiota by boosting beneficial bacteria (e.g., Bacteroides, Akkermansia, Psychrobacter) and suppressing harmful bacteria (e.g., Dubosiella, Faecalibaculum). Spearman correlation analysis unveiled significant associations between serum lipid levels, weight gain, LTE dosage, and gut microbiota, underlining the modulatory effects of LTE on metabolic disorders via the regulation of intestinal microbiota. Collectively, LTE could serve as a potential therapy for obesity-related hyperlipidemia prevention.

Curcuma longa rhizome extract activates brown adipocytes and inhibits lipogenesis in high-fat diet-fed mice

Interactions between the gut, adipose, and liver tissues play important roles in metabolic endotoxemia and gut dysbiosis. This study explored the effectiveness of Curcuma longa rhizome extract (CRE) in improving high-fat diet (HFD)-induced metabolic disorders and modulating gut environments. CRE treatment inhibited lipid accumulation in 3T3-L1 white adipocytes and activated thermogenesis-related genes in T37i brown adipocytes. CRE was administered to HFD-fed mice for 8 weeks, and serum, feces, colon, white adipose, and liver tissue were analyzed. CRE ameliorated the symptoms of metabolic disorders in mice with HFD-induced obesity by suppressing body weight and fat mass gain, adipocyte size, insulin resistance, and hepatic steatosis. CRE regulated gut axis-based mechanisms by inhibiting gut permeability, metabolic endotoxemia, and de novo lipogenesis, and promoting gut barrier integrity. Serum metabolites were negatively correlated with most biomarkers for metabolic disorders. Therefore, CRE could alleviate metabolic disorders by improving the intestinal environment and modulating the gut axis.

Swertiamarin ameliorates type 2 diabetes by activating ADRB3/UCP1 thermogenic signals in adipose tissue

Background and purposeSwertiamarin (STM), a secoiridoid glycoside from Swertia chirayita (Roxb.) H. Karst, has been shown to decrease body weight, blood glucose, and blood lipids by inhibiting adipose tissue hypertrophy. However, the underlying mechanisms remain unclear. In particular, adipose thermogenesis is a novel avenue for exploring the pharmacological effects of STM. We aim to investigate the efficacy of STM on type 2 diabetes mellitus (T2DM), with a focus on underlying mechanisms, particularly the activation of ADRB3/UCP1 thermogenic signaling pathways. MethodsT2DM model was established by a high-fat diet (HFD) and streptozotocin (STZ) in C57BL/6 J male mice. Mice were given to either 100 or 200 mg kg-1/day of STM, or 200 mg kg-1/day of metformin (Glucophage) via intragastric administration for 7 weeks. In vitro, 3T3-L1 cells were differentiated into adipocytes. Molecular markers related to ADRB3-UCP1 signals, lipolysis, and mitochondrial function were detected. ResultsSTM-treated diabetic mice showed a reduction of body weight, fat mass, and blood glucose/lipids and an improvement in insulin sensitivity. Bioinformatics analysis indicated STM promoted lipid metabolism and mitochondrial function, features by closely associated with adipose thermogenesis. STM upregulated the lipolysis-related genes and p-HSL protein in inguinal subcutaneous white adipose tissue (igSWAT) and brown adipose tissue (BAT). STM-treated mice processed a more active energy metabolism. Additionally, the ADRB3-UCP1 signals, mitochondrial-related genes, and oxidative phosphorylation were improved in igSWAT and BAT. In vitro, we found STM interacted with ADRB3, increasing glucose uptake, glycerol release, ADRB3-UCP1 signals, p-HSL expression, mitochondrial content, oxidative phosphorylation complex expression with improved mitochondrial Δψm, as well as reduced lipid accumulation in adipocytes. All these effects were reversed upon ADRB3 inhibition. ConclusionThis study identifies a previously unknown role of STM activating ADRB3/UCP1 signals in adipose tissue, suggesting a potential strategy for treating T2DM.

Whole transcriptome sequencing analysis reveals the effect of circZFYVE9/miR-378a-3p/IMMT axis on mitochondrial function in adipocytes

Recent research highlights the complex regulation of lipid accumulation and mitochondrial function in adipocytes via non-coding RNAs like microRNAs and circular non-coding RNAs. Circular non-coding RNAs act as endogenous regulators, impacting lipid metabolism and mitochondrial function by interacting with miRNAs. Sequencing white and brown adipose tissues in mice revealed significant variations in 1936 mRNAs, 127 miRNAs, and 171 circRNAs. Analyses showed these RNAs' involvement in vital processes like mitochondrial biogenesis, oxidative phosphorylation, and the citric acid cycle, crucial for lipid metabolism. Focus on top differentially regulated miRNAs led to the construction of a regulatory network involving circRNAs, miRNAs, and mRNAs, illuminating the role of endogenous RNAs in lipid metabolism and mitochondrial function. The circZFYVE9/miR-378a-3p/IMMT axis was identified as influential in adipogenic differentiation of 3T3-L1 preadipocytes by regulating mitochondrial function. This study expands the understanding of non-coding RNAs in adipose tissue, particularly their connection to mitochondrial function and metabolism.

Tributyltin Enhances Macrophage Inflammation and Lipolysis, Contributing to Adipose Tissue Dysfunction.

Tributyltin (TBT) is a synthetic chemical widely used in industrial and commercial applications. TBT exposure has been proven to elicit obesogenic effects. Gestational exposure led to increased white adipose tissue depot size in exposed (F1, F2) animals and in unexposed generations (F3, F4), an example of transgenerational inheritance. TBT exerts these effects in part by increasing the number and size of white adipocytes, altering the fate of multipotent mesenchymal stromal stem cells to favor the adipocyte lineage, altering adipokine secretion, and modulating chromatin structure. Adipose tissue resident macrophages are critical regulators in adipose tissue; however, the effects of TBT on adipose tissue macrophages remained unclear. Here we investigated the effects of TBT on macrophages and consequent impacts on adipocyte function. TBT significantly enhanced palmitate-induced inflammatory gene expression in mouse bone marrow derived macrophages and this effect was attenuated by the antagonizing action of the nuclear receptor peroxisome proliferator activated receptor gamma. TBT-treated macrophages decreased lipid accumulation in white adipocytes differentiated from mesenchymal stromal stem cells accompanied by increased expression of lipolysis genes. Lastly, ancestral TBT exposure increased Tnf expression in adipose tissue resident macrophages in both exposed (F2) and unexposed (F3) generations, suggesting that TBT exposure led to an inherited predisposition toward inflammatory adipose tissue macrophages that can manipulate adipose tissue function. These findings provide new insights into the interplay between adipocytes and adipose tissue macrophages in obesity, further establishing a role for obesogens such as TBT in the development of obesity-related metabolic disorders.

Overexpression of ALDOC Promotes Porcine Intramuscular and Intermuscular Fat Deposition by Activating the AKT-mTORC1 Signaling Pathway.

Skeletal muscle fat accumulation, a common complication of obesity, has garnered increasing attention. For livestock animals, intramuscular fat content is a key determinant of meat quality and directly influences consumer preferences for different meat products. However, genes effectively regulating intramuscular and intermuscular fat (IIMF) deposition remain largely unexplored. To address this gap, we employed transcriptome sequencing of muscle from pigs with high and low IIMF contents, uncovering Aldolase C (ALDOC) as a novel key gene controlling IIMF. ALDOC overexpression significantly enhanced the IIMF content both in vivo and in vitro. Mechanistic investigations revealed that ALDOC activates the AKT-mTORC1 axis to promote lipid accumulation in myotubes and intramuscular adipocytes. Notably, the mTORC1 inhibitor rapamycin abrogated ALDOC's proadipogenic effect. Our findings establish ALDOC as a novel key gene regulating IIMF deposition and identify the ALDOC-AKT-mTORC1 signaling pathway as a promising therapeutic target for treating skeletal muscle fat infiltration and improving pork quality.

Effects of the Fungicide Prothioconazole on Lipid Metabolism in Mice: Whitening Alterations of Brown Adipose Tissue.

With considerable concerns about the associations between metabolic disorders and agricultural biocides, there are scattered data suggesting that the triazole fungicide prothioconazole (PTC) at lower doses than the no observed adverse effect level of 5000 μg/kg/d possibly has the potential to disrupt glycolipid metabolism in mammals. Here, we investigated the effects of 50, 500, and 5000 μg/kg/d of PTC on glycolipid metabolism in mice following 8 weeks of administration via drinking water, with specific attention on brown adipose tissue (BAT) and white adipose tissue (WAT) in addition to the liver. We found that along with the increased serum triglyceride level in the 5000 μg/kg/d group, small fatty vacuoles occurred in livers in all treatment groups, indicating lipid accumulation. No change in WAT was observed, but PTC caused BAT whitening, characterized by adipocyte hypertrophy, more unilocular adipocytes with enlarged lipid droplets, reduced UCP1 levels, and down-regulated Doi2 expression, and even the dose of 50 μg/kg/d was effective. Transcriptomic analysis revealed immune inhibition and circadian rhythm disturbance in BAT from the 5000 μg/kg/d group, which are in agreement with BAT whitening and inactivation. On employing the C3H10T1/2 cells in vitro, we found that PTC treatment concentration-dependently promoted lipid accumulation in brown adipocytes, along with altered expression of thermogenesis-related and circadian genes. Taken together, our study shows that low doses of PTC caused BAT whitening, calling for much attention to the new target by pollutants.

Plasma C24:0 ceramide impairs adipose tissue remodeling and promotes liver steatosis and glucose imbalance in offspring of rats

Fetal programming by exposure to high-energy diets increases the susceptibility to type 2 diabetes mellitus (T2DM2) in the offspring. Glucose imbalance during fetal programming might be associated to still unknown selective lipid species and their characterization might be beneficial for T2DM diagnosis and treatment. We aim to characterize the effect of the lipid specie, C24:0 ceramide, on glucose imbalance and metabolic impairment in cellular and murine models. A lipidomic analysis identified accumulation of C24:0 ceramide in plasma of offspring rats exposed to high-energy diets during fetal programing, as well as in obese-T2DM subjects. In vitro experiments in 3T3L-1, hMSC and HUH7 cells and in in vivo models of Wistar rats and C57BL/6 mice demonstrated that C24:0 ceramide disrupted glucose balance, and differentiation and lipid accumulation in adipocytes, whereas promoted liver steatosis. Mechanistically, C24:0 ceramide impaired mitochondrial fatty acid oxidation in adipocytes and hepatic cells, tentatively by favoring reactive oxygen species accumulation and calcium overload in the mitochondria; and also, activates endoplasmic reticulum (ER) stress in hepatocytes. We propose that C24:0 ceramide accumulation in the offspring followed a prenatal diet exposure, impair lipid allocation into adipocytes and enhances liver steatosis associated to mitochondrial dysfunction and ER stress, leading to glucose imbalance.

Rosehip Extract Decreases Reactive Oxygen Species Production and Lipid Accumulation in Hypertrophic 3T3-L1 Adipocytes with the Modulation of Inflammatory State.

Rosa canina L. (rosehip) is used worldwide in traditional medicine as a plant with medicinal properties. However, its anti-obesity effects are not fully explained on a transcriptional level. In the present work, the 3T3-L preadipocytes were utilized to explore the impact of R. canina fruit extract (RCE) on the cellular and molecular pathways involved in adipocyte hypertrophy. Obtained results showed the ability of RCE to reduce lipid overloads in hypertrophic adipocytes associated with the down-regulation of mRNA expressions of adipogenic transcription factors such as PPARγ, C/EBPα, and SREBP-1c as well as genes involved in lipid biosyntheses such as FAS, LPL, and aP2. Moreover, obesity-associated oxidative stress (antioxidant enzyme activities and ROS generation) and inflammation were ameliorated in RCE-treated hypertrophic adipocytes. The mRNA and protein levels of adipokines such as leptin, resistin, and adiponectin were restored to more favorable levels. Rosa canina fruit might be a valuable source of phytochemicals in preventing obesity and obesity-related metabolic complications.

Bioprospection of rattlesnake venom peptide fractions with anti-adipose and anti-insulin resistance activity in vitro

Animal venoms are natural products that have served as a source of novel molecules that have inspired novel drugs for several diseases, including for metabolic diseases such as type-2 diabetes and obesity. From venoms, toxins such as exendin-4 (Heloderma suspectum) and crotamine (Crotalus durissus terrificus) have demonstrated their potential as treatments for obesity. Moreover, other toxins such as Phospholipases A2 and Disintegrins have shown their potential to modulate insulin secretion in vitro. This suggests an unexplored diversity of venom peptides with a potential anti-obesogenic in Mexican rattlesnake venoms. For that reason, this study explored the in vitro effect of Crotalus venom peptide-rich fractions on models for insulin resistance, adipocyte lipid accumulation, antioxidant activity, and inflammation process through nitric oxide production inhibition. Our results demonstrated that the peptide-rich fractions of C. aquilus, C. ravus, and C. scutulatus scutulatus were capable of reverting insulin resistance, enhancing glucose consumption to normal control; C. culminatus, C. molossus oaxacus, and C. polystictus diminished the lipid accumulation on adipocytes by 20%; C. aquilus, C. ravus, and C. s. salvini had the most significant cellular antioxidant activity, having nearly 80% of ROS inhibition. C. aquilus, C. pyrrhus, and C. s. salvini inhibited nitric oxide production by about 85%. We demonstrated the potential of these peptides from Crotalus venoms to develop novel drugs to treat type-2 diabetes and obesity. Moreover, we described for the first time that Crotalus venom peptide fractions have antioxidant and inflammatory properties in vitro models.

Vanillin, ferulic acid and their 1:1 combination inhibit lipid accumulation in 3T3 L1 adipocytes and 3D spheroids

BackgroundObesity is poised to be a major healthcare crisis worldwide. Genetic predisposition, inadequate activity, changing lifestyle and dietary patterns are cited as major causes for obesity. Even as a number of anti-obesity medications hit the market, there is still an ongoing quest to explore natural compounds, which are perceived as safer alternatives, for their anti-obesity activity. This study explores the anti-obesity potential of dietary polyphenols vanillin, ferulic acid and their combination using 3T3 L1 adipocytes and their 3D spheroids. MethodsStudies were conducted on differentiated 3T3 L1 adipocytes and their 3D spheroids. Assays conducted on 3T3 L1 adipocytes include Oil red O, fluorescent Nile Red staining and triglyceride quantification to assess effect on lipid droplet accumulation. 2 NBDG was used to assess glucose uptake following drug treatment. 3D spheroid cultures were generated and triglyceride content was quantified. Effect of drug treatment on gene expression was analysed using qRT-PCR. Results of monolayer culture were compared with 3D spheroid models. ResultsVanillin, ferulic acid and their combination lower intracellular triglyceride content and lipid droplet accumulation, inhibiting glucose uptake and conversion to triglycerides in 3T3 L1 adipocytes and their 3D spheroids. Compounds and their combination downregulated mRNA expression of C/EBP α and PPAR ɣ, FAS, ACC1, GLUT4, LPL, aP2. Vanillin treatment upregulated leptin mRNA expression. ConclusionVanillin, ferulic acid and their combination lower lipid accumulation and glucose uptake in 3T3 L1 adipocytes and 3D spheroids.

Identification of novel anti-obesity saponins from the ovary of sea cucumber (Stichopus japonicus)

The potential anti-obesity effects of sea cucumber extract have been reported. However, the individual saponins responsible for these effects are yet to be isolated and characterized. This study aimed to identify the most effective sea cucumber body part for inhibiting lipid accumulation in adipocytes and to elucidate the compounds responsible for this effect using nuclear magnetic resonance (NMR) techniques. Sea cucumber ovary 80 % ethanol extract (SCOE) demonstrated remarkable efficacy in inhibiting adipocyte differentiation compared to other sea cucumber body parts with 50 % or 80 % ethanol extracts. SCOE anti-obesity effect was evaluated in C57BL/6 mice fed a high-fat diet, which revealed significant reductions in body weight, serum lipids, adipose tissue, and liver weight. Using column chromatography, eight saponins were isolated from the SCOE, four of which exhibited potent inhibitory effects on adipocyte differentiation. Of these, three active saponins, holotoxins A, B, and D1, were newly identified. These findings highlight the potential of SCOE and its saponins as effective anti-obesity agents.

Lipid-Lowering and Anti-Inflammatory Effects of Campomanesia adamantium Leaves in Adipocytes and Caenorhabditis elegans.

Obesity is a pandemic disease characterized by lipid accumulation, increased proinflammatory cytokines, and reactive oxygen species. It is associated with the development of comorbidities that lead to death. Additionally, drug treatments developed to control obesity are insufficient and have a variety of adverse effects. Thus, the search for new anti-obesity therapies is necessary. Campomanesia adamantium is a species from the Brazilian Cerrado that has the potential to treat obesity, as described by the antihyperlipidemic activity of its roots. Therefore, this study aimed to investigate the activity of the aqueous extract of C. adamantium leaves (AECa) on the control of reactive species in vitro, on lipid accumulation in adipocytes and Caenorhabditis elegans, and on the production of proinflammatory cytokines in adipocytes. The antioxidant capacity of AECa was observed by its action in scavenging DPPH• free radical, iron-reducing power, and inhibition of β-carotene bleaching. AECa reduced lipid accumulation in preadipocytes and in C. elegans. Moreover, AECa reduced the production of the proinflammatory cytokines MCP-1, TNF-α, and IL-6 in adipocytes. In summary, the antioxidant activity and the ability of AECa to reduce the accumulation of lipids and proinflammatory cytokines indicate, for the first time, the anti-obesity potential of C. adamantium leaves.

Anti-obesity effects of Beta vulgaris and Eruca sativa-based extracts.

Obesity is a major source of morbidity worldwide with more than 2 billion adults being overweight or obese. The incidence of obesity has tripled in the last 50 years, leading to an increased risk for a variety of noncommunicable diseases. Previous studies have demonstrated the positive effects of green leafy vegetables on weight gain and obesity and have attributed these beneficial properties, at least in part, to nitrates and isothiocyanates. Nitrates are converted to nitric oxide (NO) and isothiocyanates are known to release hydrogen sulfide (H2S). Herein, we investigated the effect of extracts and fractions produced from Beta vulgaris and Eruca sativa for their ability to limit lipid accumulation, regulate glucose homeostasis, and reduce body weight. Extracts from the different vegetables were screened for their ability to limit lipid accumulation in adipocytes and hepatocytes and for their ability to promote glucose uptake in skeletal muscle cultures; the most effective extracts were next tested in vivo. Wild type mice were placed on high-fat diet for 8 weeks to promote weight gain; animals receiving the selected B. vulgaris and E. sativa extracts exhibited attenuated body weight. Treatment with extracts also led to reduced white adipose tissue depot mass, attenuated adipocyte size, reduced expression of Dgat2 and PPARγ expression, and improved liver steatosis. In contrast, the extracts failed to improve glucose tolerance in obese animals and did not affect blood pressure. Taken together, our data indicate that extracts produced from B. vulgaris and E. sativa exhibit anti-obesity effects, suggesting that dietary supplements containing nitrates and sulfide-releasing compounds might be useful in limiting weight gain.