Pretreatment of cultured preadipocytes with arachidonic acid during the differentiation phase without a cAMP-elevating agent enhances fat storage after the maturation phase

Khan, Ferdous; Syeda, Pinky Karim; Nartey, Michael N. N.; Rahman, Md. Saidur; Islam, Mohammad Safiqul; Nishimura, Kohji; Jisaka, Mitsuo; Shono, Fumiaki; Yokota, Kazushige

doi:10.1016/j.prostaglandins.2016.02.003

Cited by 7 publications

(8 citation statements)

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“…Because IBMX is a cAMP-elevating agent, incubation of 3T3-L1 cells with this compound during the differentiation phase may mimic the high protein/carbohydrate ratio in the diet. Indeed, adipogenesis is promoted when 3T3-L1 cells are incubated during the differentiation phase with AA, dexamethasone, and insulin, except IBMX [ 28 , 29 , 30 ]. The biosynthesis of PGE 2 and PGF 2α is decreased, whereas that of PGI 2 is increased under these culture conditions [ 30 ].…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, adipogenesis is promoted when 3T3-L1 cells are incubated during the differentiation phase with AA, dexamethasone, and insulin, except IBMX [ 28 , 29 , 30 ]. The biosynthesis of PGE 2 and PGF 2α is decreased, whereas that of PGI 2 is increased under these culture conditions [ 30 ]. In contrast, adding MDI and AA during the differentiation phase of 3T3-L1 cells increases the biosynthesis of PGE 2 and PGF 2α [ 28 , 31 ], and suppresses MDI-induced adipogenesis [ 28 , 29 , 31 ].…”

Section: Introductionmentioning

confidence: 99%

“…However, because there are no reports on which prostaglandins other than PGE 2 and PGF 2α are produced by AA added during the differentiation phase, nor on how the crosstalk between PGs produced and AA during the differentiation phase affects adipogenesis, the present study thus aimed to analyze these points. Furthermore, since LA has pro-adipogenic effects in the absence of IBMX during the differentiation phase of 3T3-L1 cells [ 30 ], we examined the effect of LA in the presence of IBMX.…”

Section: Introductionmentioning

confidence: 99%

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Arachidonic Acid Added during the Differentiation Phase of 3T3-L1 Cells Exerts Anti-Adipogenic Effect by Reducing the Effects of Pro-Adipogenic Prostaglandins

Nartey

Jisaka

Syeda

et al. 2023

Life

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A linoleic acid (LA) metabolite arachidonic acid (AA) added to 3T3-L1 cells is reported to suppress adipogenesis. The purpose of the present study aimed to clarify the effects of AA added during the differentiation phase, including adipogenesis, the types of prostaglandins (PG)s produced, and the crosstalk between AA and the PGs produced. Adipogenesis was inhibited by AA added, while LA did not. When AA was added, increased PGE2 and PGF2α production, unchanged Δ12-PGJ2 production, and reduced PGI2 production were observed. Since the decreased PGI2 production was reflected in decreased CCAAT/enhancer-binding protein-β (C/EBPβ) and C/EBPδ expression, we expected that the coexistence of PGI2 with AA would suppress the anti-adipogenic effects of AA. However, the coexistence of PGI2 with AA did not attenuate the anti-adipogenic effects of AA. In addition, the results were similar when Δ12-PGJ2 coexisted with AA. Taken together, these results indicated that the metabolism of ingested LA to AA is necessary to inhibit adipogenesis and that exposure of AA to adipocytes during only the differentiation phase is sufficient. As further mechanisms for suppressing adipogenesis, AA was found not only to increase PGE2 and PGF2α and decrease PGI2 production but also to abrogate the pro-adipogenic effects of PGI2 and Δ12-PGJ2.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Arachidonic Acid Added during the Differentiation Phase of 3T3-L1 Cells Exerts Anti-Adipogenic Effect by Reducing the Effects of Pro-Adipogenic Prostaglandins

Nartey

Jisaka

Syeda

et al. 2023

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“…We further confirmed whether the reduced level of intracellular TAG accumulation during the maturation phase was reflected in the expression levels of PPARγ, known as one of the master regulators of adipogenesis [ 39 ], and the adiponectin and LPL regulated downstream of PPARγ [ 15 , 16 ]. We found that the gene expression levels of PPARγ, adiponectin, and LPL in the 3T3-L1 cells peaked by day six in the maturation phase [ 40 ] ( Figure 2 A). In the maturation phase, the expression level of PPARγ in the 3T3-L1 cells was significantly reduced on day six after the addition of PGD 2 or 11d-11m-PGD 2 during the differentiation phase ( Figure 2 B).…”

Section: Resultsmentioning

confidence: 99%

Prostaglandin D2 Added during the Differentiation of 3T3-L1 Cells Suppresses Adipogenesis via Dysfunction of D-Prostanoid Receptor P1 and P2

Nartey

Jisaka

Syeda

et al. 2023

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We previously reported that the addition of prostaglandin, (PG)D2, and its chemically stable analog, 11-deoxy-11-methylene-PGD2 (11d-11m-PGD2), during the maturation phase of 3T3-L1 cells promotes adipogenesis. In the present study, we aimed to elucidate the effects of the addition of PGD2 or 11d-11m-PGD2 to 3T3-L1 cells during the differentiation phase on adipogenesis. We found that both PGD2 and 11d-11m-PGD2 suppressed adipogenesis through the downregulation of peroxisome proliferator-activated receptor gamma (PPARγ) expression. However, the latter suppressed adipogenesis more potently than PGD2, most likely because of its higher resistance to spontaneous transformation into PGJ2 derivatives. In addition, this anti-adipogenic effect was attenuated by the coexistence of an IP receptor agonist, suggesting that the effect depends on the intensity of the signaling from the IP receptor. The D-prostanoid receptors 1 (DP1) and 2 (DP2, also known as a chemoattractant receptor-homologous molecule expressed on Th2 cells) are receptors for PGD2. The inhibitory effects of PGD2 and 11d-11m-PGD2 on adipogenesis were slightly attenuated by a DP2 agonist. Furthermore, the addition of PGD2 and 11d-11m-PGD2 during the differentiation phase reduced the DP1 and DP2 expression during the maturation phase. Overall, these results indicated that the addition of PGD2 or 11d-11m-PGD2 during the differentiation phase suppresses adipogenesis via the dysfunction of DP1 and DP2. Therefore, unidentified receptor(s) for both molecules may be involved in the suppression of adipogenesis.

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“…The process was carried out in a CFX96C1000 Touch Real-Time PCR Detection System (Bio-Rad, USA) and data were analyzed by CFX Manager TM Software (CFX Manager TM Software) according to the manufacturer's protocol. Quantitative real-time PCR was conducted and according to a program followed by Khan et al [ 30 ], using forward and reverse primers designed by Primer 3 online software (Supplement Table 2 ). The mRNA levels for each of the target genes were measured in relative to the mRNA level of β-actin of the corresponding sample.…”

Section: Animals and Treatment Protocolsmentioning

confidence: 99%

Metformin treatment reverses high fat diet- induced non-alcoholic fatty liver diseases and dyslipidemia by stimulating multiple antioxidant and anti-inflammatory pathways

Pretreatment of cultured preadipocytes with arachidonic acid during the differentiation phase without a cAMP-elevating agent enhances fat storage after the maturation phase

Cited by 7 publications

References 50 publications

Arachidonic Acid Added during the Differentiation Phase of 3T3-L1 Cells Exerts Anti-Adipogenic Effect by Reducing the Effects of Pro-Adipogenic Prostaglandins

Arachidonic Acid Added during the Differentiation Phase of 3T3-L1 Cells Exerts Anti-Adipogenic Effect by Reducing the Effects of Pro-Adipogenic Prostaglandins

Prostaglandin D2 Added during the Differentiation of 3T3-L1 Cells Suppresses Adipogenesis via Dysfunction of D-Prostanoid Receptor P1 and P2

Metformin treatment reverses high fat diet- induced non-alcoholic fatty liver diseases and dyslipidemia by stimulating multiple antioxidant and anti-inflammatory pathways

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