Cholecalciferol inhibits lipid accumulation by regulating early adipogenesis in cultured adipocytes and zebrafish

Kim, Joo Hyoun; Kang, Smee; Jung, Yu Na; Choi, Hyeon‐Son

doi:10.1016/j.bbrc.2015.12.049

Cited by 20 publications

(17 citation statements)

References 25 publications

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“…Thus, suppression of C/EBP␤ expression is an attractive target for diet-induced obesity. Food factors suppress the gene expression of C/EBP␤ through regulation of mitotic clonal expansion in 3T3-L1 adipocytes and zebrafish (38,39). In addition, direct treatment with caffeine also suppresses mitotic clonal expansion in 3T3-L1 adipocytes (40).…”

Section: Discussionmentioning

confidence: 99%

Caffeine-Stimulated Intestinal Epithelial Cells Suppress Lipid Accumulation in Adipocytes

Mitani

Nagano

Harada

et al. 2017

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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Summary Caffeine is a methylxanthine derived from plant foods such as coffee beans and tea leaves, and has multiple biological activities against physiological response and several diseases. Although there are some reports about the direct effect of caffeine against anti-lipid accumulation in vitro, the effect of caffeine on lipid accumulation in adipocytes through stimulating intestinal epithelial cells is unknown. Since direct treatment with caffeine to 3T3-L1 cells did not affect lipid accumulation, we determined whether caffeinestimulated intestinal epithelial Caco-2 cells influence the lipid accumulation in 3T3-L1 adipocytes. Caco-2 cells were cultured on a transwell insert with or without caffeine for 24 h. Subsequently, the basolateral component of the Caco-2 cell culture on the transwell was collected and termed caffeine-conditioning medium (CCM). When 3T3-L1 adipocytes were incubated with CCM, CCM decreased lipid accumulation and suppressed gene expression of proliferator activated receptor (PPAR) ␥ and CCAAT/enhancer binding protein (C/EBP) ␣ in 3T3-L1 adipocytes. Furthermore, CCM decreased the expression of C/EBP␤ and C/EBP␦ at the protein level, but not at the mRNA level. We observed that a proteasome inhibitor, MG132, inhibited CCM-caused down-expression of C/EBP␤ and C/EBP␦ proteins, and that CCM promoted the ubiquitination level of C/EBP␤ and C/EBP␦ proteins. Protein microarray analysis showed caffeine suppresses the secretion of inflammatory cytokines, interleukin-8 and plasminogen activator inhibitor-1 from Caco-2 cells. These results suggest that caffeine indirectly suppresses lipid accumulation in 3T3-L1 adipocytes through decreasing secretion of inflammatory cytokines from Caco-2 cells. Key Words caffeine, adipogenesis, 3T3-L1 adipocytes, Caco-2 cells Obesity is a risk factor for multiple lifestyle diseases such as apoplexy, heart disease and diabetes (1, 2). Adipocytes play a critical role in regulating lipid metabolism and energy balance, which are associated with adiposity (3). An increase in the number of differentiated mature adipocytes and excess accumulation of body fat leads to adiposity. Adipocytes accumulate intracellular lipids during differentiation. As an in vitro model system for adipogenesis, murine 3T3-L1 cells, which were originally derived from mouse embryos, are often used. Differentiation of 3T3-L1 cells is induced by exposure to the inducers, such as 3-isobutyl-1-methylxanthine (IBMX), dexamethasone and insulin, and is responsible for the accumulation of a large amount of intracellular lipid droplets during adipocyte differentiation. Adipogenesis, the differentiation process for producing adipocytes, is a complex process that is regulated by various transcription factors and their related genes. The expression levels of CCAAT/enhancer binding protein (C/EBP) ␤ and C/EBP␦, as transcriptional factors, are increased in the early phase of adipocyte differentiation (4). Subsequently, these transcription factors up-regulate proliferator activated receptor (PPAR) ␥ and C/EBP␣, a...

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Section: Discussionmentioning

confidence: 99%

Caffeine-Stimulated Intestinal Epithelial Cells Suppress Lipid Accumulation in Adipocytes

Mitani

Nagano

Harada

et al. 2017

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…The protocol consisted of a 15-day exposure to the compound on a high-fat diet background, starting at the first feeding period. For example, curcumin [50–53], indole-3-carbinol [54], baicalein [55], dieckol [56], ellagic acid [52], kaempferol [51], quercetin [56], seapolynol [57] and silibinin [58], have all been reported to inhibit lipid accumulation in these early, post-embryonic developmental stages, when the adipocyte lineage is just starting to be established [20,27]. In our work, we used the ZOT protocol at later larval developmental stages, when the animals had a well-established WAT [30].…”

Section: Discussionmentioning

confidence: 99%

Caffeic acid and hydroxytyrosol have anti-obesogenic properties in zebrafish and rainbow trout models

et al. 2017

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Some natural products, known sources of bioactive compounds with a wide range of properties, may have therapeutic values in human health and diseases, as well as agronomic applications. The effect of three compounds of plant origin with well-known dietary antioxidant properties, astaxanthin (ATX), caffeic acid (CA) and hydroxytyrosol (HT), on zebrafish (Danio rerio) larval adiposity and rainbow trout (Onchorynchus mykiss) adipocytes was assessed. The zebrafish obesogenic test (ZOT) demonstrated the anti-obesogenic activity of CA and HT. These compounds were able to counteract the obesogenic effect produced by the peroxisome proliferator-activated receptor gamma (PPARγ) agonist, rosiglitazone (RGZ). CA and HT suppressed RGZ-increased PPARγ protein expression and lipid accumulation in primary-cultured rainbow trout adipocytes. HT also significantly reduced plasma triacylglycerol concentrations, as well as mRNA levels of the fasn adipogenic gene in the adipose tissue of HT-injected rainbow trout. In conclusion, in vitro and in vivo approaches demonstrated the anti-obesogenic potential of CA and HT on teleost fish models that may be relevant for studying their molecular mode of action. Further studies are required to evaluate the effect of these bioactive components as food supplements for modulating adiposity in farmed fish.

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“…24) In addition, KLF members also control the adipogenic pathway 24) ; KLF2 is reported to suppress adipogenesis by inhibiting PPARγ. 25) In contrast, KLF4 regulates adipogenesis by promoting C/EBPβ expression. 24) Therefore, the regulation of early adipogenic factors is important to the overall adipogenic process.…”

Section: Discussionmentioning

confidence: 99%

“…A recent study showed that various early adipogenic factors are regulated by vitamin D precursors to reduce lipid accumulation during adipogenesis. 26) Excessive ROS, which induces oxidative stress, has been known to be closely involved in adipogenesis or obesogenic conditions. 27) A previous study indicated that both ROS production as well as nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4), a ROS generating enzyme, are markedly increased during the differentiation of 3T3-L1 cells into mature adipocytes.…”

Section: Discussionmentioning

confidence: 99%

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Dibenzoylmethane Suppresses Lipid Accumulation and Reactive Oxygen Species Production through Regulation of Nuclear Factor (Erythroid-Derived 2)-Like 2 and Insulin Signaling in Adipocytes

Kim

Kang

et al. 2018

Biological & Pharmaceutical Bulletin

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The aim of this study was to investigate the effects of dibenzoylmethane (1,3-diphenyl-1,3-propanedione, DBM) from licorice roots on lipid accumulation and reactive oxygen species (ROS) production in 3T3-L1 cells. DBM effectively inhibited lipid accumulation during adipogenesis, and its inhibitory effect was shown to be due to the down-regulation of adipogenic factors such as CCAAT-enhancer-binding protein-α (C/EBPα), peroxisome proliferator-activated receptor γ (PPARγ), and fatty acid-binding protein 4 (FABP4). DBM was observed to exert its inhibitory effect on lipid accumulation in the early adipogenic stage (days 0-2) by regulating early adipogenic factors including CCAAT-enhancer-binding protein-β (C/EBPβ) and Krueppel-like factor (KLF) 2. DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.

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Cholecalciferol inhibits lipid accumulation by regulating early adipogenesis in cultured adipocytes and zebrafish

Cited by 20 publications

References 25 publications

Caffeine-Stimulated Intestinal Epithelial Cells Suppress Lipid Accumulation in Adipocytes

Caffeine-Stimulated Intestinal Epithelial Cells Suppress Lipid Accumulation in Adipocytes

Caffeic acid and hydroxytyrosol have anti-obesogenic properties in zebrafish and rainbow trout models

Dibenzoylmethane Suppresses Lipid Accumulation and Reactive Oxygen Species Production through Regulation of Nuclear Factor (Erythroid-Derived 2)-Like 2 and Insulin Signaling in Adipocytes

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