The role of phospholipase A2-derived mediators in obesity

Abbott, Marcia J.; Tang, Tsung-Ta; Sul, Hei Sook

doi:10.1016/j.ddmec.2011.01.003

Cited by 25 publications

(14 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the HFD group, the levels of lysoPC 14:0, 18:0, and 20:3, and lysoPC-P 18:0 were increased, while the lysoPC 16:1, 18:2, and 20:5, and PC 34:2 and 34:0 levels were decreased compared to the ND group. LysoPC is converted from PC by phospholipase A2, which is activated under inflammatory conditions such as with a HFD [ 41 , 42 ]. Many studies showed lysoPCs as significant biomarkers of mice fed a HFD [ 8 ], overweight/obesity humans [ 23 ], and obesity-resistant BALB/c mice [ 43 ].…”

Section: Resultsmentioning

confidence: 99%

Urine and Serum Metabolite Profiling of Rats Fed a High-Fat Diet and the Anti-Obesity Effects of Caffeine Consumption

et al. 2015

View full text Add to dashboard Cite

Abstract:In this study, we investigated the clinical changes induced by a high fat diet (HFD) and caffeine consumption in a rat model. The mean body weight of the HFD with caffeine (HFDC)-fed rat was decreased compared to that of the HFD-fed rat without caffeine. The levels of cholesterol, triglycerides (TGs), and free fatty acid, as well as the size of adipose tissue altered by HFD, were improved by caffeine consumption. To investigate the metabolites that affected the change of the clinical factors, the urine and serum of rats fed a normal diet (ND), HFD, and HFDC were analyzed using ultra performance liquid chromatography quadruple time-of-flight mass spectrometry (UPLC-Q-TOF-MS), gas chromatography (GC-TOF-MS), and linear trap quadruple mass spectrometry (LTQ-XL-MS) combined with multivariate analysis. A total of 68 and 52 metabolites were found to be different in urine and serum, respectively. After being fed caffeine, some glucuronide-conjugated compounds, lysoPCs, CEs, DGs, TGs, taurine, and hippuric acid were altered compared to the HFD group. In this study, caffeine might potentially inhibit OPEN ACCESSMolecules 2015, 20 3108 HFD-induced obesity and we suggest possible biomarker candidates using MS-based metabolite profiling.

show abstract

Section: Resultsmentioning

confidence: 99%

Urine and Serum Metabolite Profiling of Rats Fed a High-Fat Diet and the Anti-Obesity Effects of Caffeine Consumption

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Recently, adipose-specific PLA2 have received attention for potential anti-obesity and anti-diabetic roles. Both genetic and pharmacological inhibition of particular PLA2s has resulted in obesity-resistant mouse models, suggesting a potential to develop new drugs [39]. In addition, COX-2 has long been believed to play a role in the inflammatory process as a result of obesity with an HF diet [9,40].…”

Section: Discussionmentioning

confidence: 99%

Targeting ROS and cPLA2/COX2 Expressions Ameliorated Renal Damage in Obese Mice with Endotoxemia

Chang

Yeh

Ho³

et al. 2019

IJMS

View full text Add to dashboard Cite

Obesity is associated with metabolic endotoxemia, reactive oxygen species (ROS), chronic inflammation, and obese kidney fibrosis. Although the fat–intestine–kidney axis has been documented, the pathomechanism and therapeutic targets of obese kidney fibrosis remain unelucidated. To mimic obese humans with metabolic endotoxemia, high-fat-diet-fed mice (HF group) were injected with lipopolysaccharide (LPS) to yield the obese kidney fibrosis–metabolic endotoxemia mouse model (HL group). Therapeutic effects of ROS, cytosolic phospholipases A2 (cPLA2) and cyclooxygenase-2 (COX-2) inhibitors were analyzed with a quantitative comparison of immunohistochemistry stains and morphometric approach in the tubulointerstitium of different groups. Compared with basal and HF groups, the HL group exhibited the most prominent obese kidney fibrosis, tubular epithelial lipid vacuoles, and lymphocyte infiltration in the tubulointerstitium. Furthermore, inhibitors of nonspecific ROS, cPLA2 and COX-2 ameliorated the above renal damages. Notably, the ROS-inhibitor-treated group ameliorated not only oxidative injury but also the expression of cPLA2 and COX-2, indicating that ROS functions as the upstream signaling molecule in the inflammatory cascade of obese kidney fibrosis. ROS acts as a key messenger in the signaling transduction of obese kidney fibrosis, activating downstream cPLA2 and COX-2. The given antioxidant treatment ameliorates obese kidney fibrosis resulting from a combined high-fat diet and LPS—ROS could serve as a potential therapeutic target of obese kidney fibrosis with metabolic endotoxemia.

show abstract

“…In the body, PLA2 hydrolyzes fatty acids (FA) from the sn-2 position of phospholipids to generate FA and lysophospholipids [26]. These products are tightly linked to obesity.…”

Section: Introductionmentioning

confidence: 99%

Peptide Fraction pOh2 Exerts Antiadipogenic Activity through Inhibition of C/EBP-αand PPAR-γExpression in 3T3-L1 Adipocytes

Nguyen

et al. 2017

BioMed Research International

View full text Add to dashboard Cite

Many studies have comprehensively examined the venom of Ophiophagus hannah snake. Its venom comprises different compounds exhibiting a wide range of pharmacological activities. In this investigation, four peptide fractions (PFs), ranging from 3 kDa to 10 kDa, isolated from the Vietnamese snake venom of O. hannah were separated by HPLC and investigated for their inhibitory activity on adipogenesis in 3T3-L1 adipocytes. The most effective PF was then further purified, generating two peptides, pOh1 and pOh2. Upon investigation of these two peptides on 3T3-L1 adipocytes, it was revealed that, at 10 μg/mL, pOh2 was able to inhibit the lipid accumulation in 3T3-L1 adipocytes by up to 56%, without affecting cell viability. Furthermore, the pOh2 downregulated the gene expression of important transcription factors C/EBP-α and PPAR-γ. In addition, aP2 and GPDH adipocyte-specific markers were also significantly reduced compared to untreated differentiated cells. Taken together, pOh2 inhibited the expression of key transcription factors C/EBP-α and PPAR-γ and their target genes, aP2 and GPDH, thereby blocking the adipocyte differentiation. In conclusion, this novel class of peptide might have potential for in vivo antiobesity effects.

show abstract

The role of phospholipase A2-derived mediators in obesity

Cited by 25 publications

References 52 publications

Urine and Serum Metabolite Profiling of Rats Fed a High-Fat Diet and the Anti-Obesity Effects of Caffeine Consumption

Urine and Serum Metabolite Profiling of Rats Fed a High-Fat Diet and the Anti-Obesity Effects of Caffeine Consumption

Targeting ROS and cPLA2/COX2 Expressions Ameliorated Renal Damage in Obese Mice with Endotoxemia

Peptide Fraction pOh2 Exerts Antiadipogenic Activity through Inhibition of C/EBP-αand PPAR-γExpression in 3T3-L1 Adipocytes

Contact Info

Product

Resources

About