We examined the effects of lysophosphatidic acid (LPA) on in vitro proliferation and differentiation of a porcine preadipocyte cell line, DFAT-P, and a mouse preadipocyte cell line, 3T3-L1. During the proliferation and differentiation phases, DFAT-P and 3T3-L1 cells expressed only the endothelial differentiation gene (EDG)-2 receptor and not EDG-4 and EDG-7 receptors. LPA promoted the proliferation of DFAT-P cells more extensively than that of 3T3-L1 cells. After adipogenic induction, LPA inhibited glycerol-3-phosphate dehydrogenase activity and lipid droplet accumulation, and suppressed peroxisome proliferator-activated receptor γ (PPARγ) protein expression, this inhibitory effect in DFAT-P cells was twice as high as that in 3T3-L1 cells. Furthermore, treatments with low LPA concentrations significantly inhibited adipocyte differentiation in DFAT-P cells but not in 3T3-L1 cells. We conclude that LPA promotes the proliferation of porcine preadipocytes through the EDG-2 receptor but inhibits their differentiation, and these effects depend on the down-regulation of PPARγ expression via the EDG-2 receptor. Furthermore, DFAT-P cells are more sensitive to LPA than 3T3-L1 cells. These findings in a porcine model will contribute to the understanding of LPA action mechanisms on in vitro proliferation and differentiation of preadipocytes in domestic animals and/or humans.
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http://dx.doi.org/10.1016/j.cbpb.2010.08.010 | DOI Listing |
Eur J Pharmacol
January 2025
College of Korean Medicine, Gachon University, Seongnam, 13120, South Korea. Electronic address:
Obesity due to excessive body fat accumulation remains a global problem. Patients with obesity have high cortisol levels, and its dysregulation is caused by increased 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) levels. The effects and mechanism of J2H-1702, an 11β-HSD1 inhibitor, on nonalcoholic steatohepatitis (NASH) were explored.
View Article and Find Full Text PDFJ Taibah Univ Med Sci
December 2024
Department of Veterinary Pre-Clinical Science, Faculty of Veterinary Medicine, Universiti Putra Malaysia, Serdang, Selangor, Malaysia.
Objective: Concerns over the increasing number of obese individuals and the associated health risks have prompted therapeutic option explorations. Similarly, this study aimed to establish fruit extract (SCFE) anti-adipogenic attributes in 3T3-L1 cells.
Methods: The polyphenolic compounds in SCFE were identified with Reverse phase-high performance liquid chromatography (RP-HPLC).
Zhejiang Da Xue Xue Bao Yi Xue Ban
January 2025
School of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, China.
Objectives: To investigate the effect of pachymic acid on brown/beige adipocyte differentiation and lipid metabolism in preadipocytes 3T3-L1 MBX.
Methods: The brown cocktail method was employed to induce 3T3-L1 MBX cells to differentiate into beige adipocytes. The impact of pachymic acid on the viability of 3T3-L1 MBX preadipocytes was evaluated using the CCK-8 assay.
Adipocyte
December 2025
Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Obesity is a global health concern that promotes chronic low-grade inflammation, leading to insulin resistance, a key factor in many metabolic diseases. Angiotensin 1-7 (Ang 1-7), a component of the renin-angiotensin system (RAS), exhibits anti-inflammatory effects in obesity and related disorders, though its mechanisms remain unclear. In this study, we examined the effect of Ang 1-7 on inflammation of white adipose tissue (WAT) in dietary-induced obese mice.
View Article and Find Full Text PDFJ Diabetes Metab Disord
June 2025
Department of Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Objectives: MicroRNAs (miRNAs) play a crucial role in the onset and progress of obesity. The inflammation of adipose tissue is deemed causative of the complications associated with obesity. This study delved into the potential mechanisms of miRNA-mediated SIRT1 regulation and inflammatory factors modulation in 3T3-L1 cells.
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