We hypothesized that the unsaturated fatty acid palmitoleic acid (POA) could promote the expression of adipogenic/lipogenic genes in bovine skeletal muscle satellite cells (BSCs). The BSCs were cultured in a growth medium containing 10% fetal bovine serum. When the cells reached 80%-90% confluence, we used the differentiation medium with 5% horse serum for differentiation for 96 h. The differentiation medium contained 50 µM, 100 µM and 200 µM POA. Control BSC were cultured only in differentiation media. Compared with the control BSC, the POA BSC significantly up-regulated the expression of paired box 3 (Pax3) and paired box 7 (Pax7) and down-regulated myogenin gene expression (p < 0.01), which indicates a depression in muscle fiber development. However, all POA treatments up-regulated the expression of the adipocyte transcription factors peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein alpha and beta (C/EBP α and C/EBP β), and other genes (p < 0.01) and increased the expression of PAT-family proteins and the concentration of adiponectin in the media. These results indicate that POA can convert part of BSCs into adipocytes.
BACKGROUND/OBJECTIVES: The $NAD^+$ precursor nicotinamide riboside (NR) is a type of vitamin $B_3$ found in cow's milk and yeast-containing food products such as beer. Recent studies suggested that NR prevents hearing loss, high-fat diet-induced obesity, Alzheimer's disease, and mitochondrial myopathy. The objective of this study was to investigate the effects of NR on inflammation and mitochondrial biogenesis in AML12 mouse hepatocytes. MATERIALS/METHODS: A subset of hepatocytes was treated with palmitic acid (PA; $250{\mu}M$) for 48 h to induce hepatocyte steatosis. The hepatocytes were treated with NR ($10{\mu}M$ and 10 mM) for 24 h with and without PA. The cell viability and the levels of sirtuins, inflammatory markers, and mitochondrial markers were analyzed. RESULTS: Cytotoxicity of NR was examined by PrestoBlue assay. Exposure to NR had no effect on cell viability or morphology. Gene expression of sirtuin 1 (Sirt1) and Sirt3 was significantly upregulated by NR in PA-treated hepatocytes. However, Sirt1 activities were increased in hepatocytes treated with low-dose NR. Hepatic pro-inflammatory markers including tumor necrosis factor-alpha and interleukin-6 were decreased in NR-treated cells. NR upregulated anti-inflammatory molecule adiponectin, and, tended to down-regulate hepatokine fetuin-A in PA-treated hepatocytes, suggesting its inverse regulation on these cytokines. NR increased levels of mitochondrial markers including peroxisome proliferator-activated receptor ${\gamma}$ coactivator-$1{\alpha}$, carnitine palmitoyltransferase 1, uncoupling protein 2, transcription factor A, mitochondrial and mitochondrial DNA in PA-treated hepatocytes. CONCLUSIONS: These data demonstrated that NR attenuated hepatic inflammation and increased levels of mitochondrial markers in hepatocytes.
Choi, Su-Young;Lee, Su Yeon;Jang, Da hye;Lee, Suk Jun;Cho, Jeong-Yong;Kim, Sung-Hak
Journal of Animal Science and Technology
/
v.62
no.6
/
pp.854-863
/
2020
This study was aimed to investigate the inhibitory effects of Porphyra dentata (P. dentata) extract on the adipogenesis of 3T3-L1 cells and evaluate its anti-obesity effect. The proliferation of 3T3-L1 cells and differentiation of adipocytes under treatment of P. dentata extract was examined by measuring the cell viability using alamarBlue assay and lipid droplets by Oil Red O staining. Results showed that P. dentata extract has no cytotoxicity effect and lipid droplets formation decreased in a concentration-dependent manner in 3T3-L1 cells. It has been confirmed that transcription factors affecting lipid accumulation and anti-adipogenic effects during cell differentiation are linked to P. dentata extract. We observed that P. dentata shows lowering the mRNA expression of peroxisome proliferator-activated receptor γ2 (PPARγ2), CCAAT/enhancer binding protein α (C/EBPα) that adipogenesis-associated key transcription factors and inhibiting adipogenesis in the early stages of differentiation. Treating the cells with P. dentata did not only suppressed PPARγ2 and C/EBPα but also significantly decreased the mRNA expression of adiponectin, Leptin, fatty acid synthase, adipocyte protein 2, and Acetyl-coA carboxylase 1. Overall, the P. dentata extract demonstrated inhibitory property in adipogenesis, which has a potential effect in anti-obesity in 3T3-L1 cells.
Seo, Seong-Wook;Kim, Min Ju;Kim, Kyoung;Chung, Dong-Min;Shin, Mi-Rae
The Korea Journal of Herbology
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v.37
no.4
/
pp.17-29
/
2022
Objective : The present study comparatively analyzed the anti-obesity effect of Arctium lappa L. roots with and without microwave processing. Methods : Four HFD groups except for the Normal group (n=8) were allocated: Control, microwave-processed dried Arctium lappa L. roots (MAL) extract 400 mg/kg/d (MAL400), MAL extract 800 mg/kg/d (MAL800), and the dried Arctium lappa L. roots (DAL) extract 800 mg/kg/d (DAL800). The efficacy of MAL and DAL was confirmed in terms of the serum biochemical index, protein expressions related to the synthesis of triglyceride (TG) and total cholesterol (TC) and 𝛽-oxidation, and histopathological staining. Results : Both MAL and DAL treatments significantly reduced final body weight and body weight gain. MAL800 treatment significantly reduced serum TG, TC, low-density lipoprotein cholesterol, and leptin levels, but the serum high-density lipoprotein cholesterol and adiponectin concentrations were dramatically increased. In particular, leptin in the MAL800 group was reduced by 14.1% compared with the DAL800 group. Moreover, the MAL800 treatment showed an effect superior to the DAL800 treatment in the reduction of serum TC, the sirtuin 1 (Sirt1) activation, and the inhibition of 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMGCR) gene expression. In particular, unlike the DAL800 treatment, MAL treatment significantly led to the activation of peroxisome proliferator-activated receptor alpha (PPAR𝛼). Subsequently, PPAR𝛼 meaningfully regulated downstream proteins associated with 𝛽-oxidation. Conclusion : These findings suggest that Arctium lappa L. roots with microwave processing effectively ameliorate obesity through the regulation of leptin and TC and the promotion of 𝛽-oxidation compared with Arctium lappa L. roots without microwave processing.
Youri Lee;Navid Iqbal;Mi-Hwa Lee;Doo-Sang Park;Yong-Sik Kim
Journal of Microbiology and Biotechnology
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v.34
no.5
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pp.1073-1081
/
2024
Obesity is spawned by an inequality between the portion of energy consumed and the quantity of energy expended. Disease entities such as cardiovascular disease, arteriosclerosis, hypertension, and cancer, which are correlated with obesity, influence society and the economy. Suppression of adipogenesis, the process of white adipocyte generation, remains a promising approach for treating obesity. Oil Red O staining was used to differentiate 3T3-L1 cells for screening 20 distinct Lactobacillus species. Among these, Lactobacillus acidophilus DS0079, referred to as YBS1, was selected for further study. YBS1 therapy decreased 3T3-L1 cell development. Triglyceride accumulation and mRNA expression of the primary adipogenic marker, peroxisome proliferator-activated receptor gamma (PPARγ), including its downstream target genes, adipocyte fatty acid binding protein 4 and adiponectin, were almost eliminated. YBS1 inhibited adipocyte differentiation at the early stage (days 0-2), but no significant difference was noted between the mid-stage (days 2-4) and late-stage (days 4-6) development. YBS1 stimulated the activation of p38 mitogen-activated protein kinase (p38 MAPK) during the early stages of adipogenesis; however, this effect was eliminated by the SB203580 inhibitor. The data showed that YBS1 administration inhibited the initial development of adipocytes via stimulation of the p38 MAPK signaling pathway, which in turn controlled PPARγ expression. In summary, YBS1 has potential efficacy as an anti-obesity supplement and requires further exploration.
Objective: This study investigated the effects of dietary n-6:n-3 polyunsaturated fatty acid (PUFA) ratio on growth performance, blood indexes, tissue fatty acid composition and the gene expression in finishing pigs. Methods: Seventy-two crossbred ([Duroc×Landrace]×Yorkshire) barrows (68.5±1.8 kg) were fed one of four isoenergetic and isonitrogenous diets with n-6:n-3 PUFA ratios of 2:1, 3:1, 5:1, and 8:1. Results: Average daily gain, average daily feed intake and gain-to-feed ratio had quadratic responses but the measurements were increased and then decreased (quadratic, p<0.05). The concentrations of serum triglyceride, total cholesterol and interleukin 6 were linearly increased (p<0.05) with increasing of dietary n-6:n-3 PUFA ratio, while that of high-density lipoprotein cholesterol tended to decrease (p = 0.062), and high-density lipoprotein cholesterol:low-density lipoprotein cholesterol ratio and leptin concentration were linearly decreased (p<0.05). The concentration of serum adiponectin had a quadratic response but the measurement was decreased and then increased (quadratic, p<0.05). The proportion of C18:3n-3 was linearly decreased (p<0.05) in the longissimus thoracis (LT) and subcutaneous adipose tissue (SCAT) as dietary n-6:n-3 PUFA ratio increasing, while the proportion of C18:2n-6 and n-6:n-3 PUFA ratio were linearly increased (p<0.05). In addition, the expression levels of peroxisome proliferator-activated receptor gamma (PPARγ) and lipoprotein lipase in the LT and SCAT, and adipocyte fatty acid binding protein and hormone-sensitive lipase (HSL) in the SCAT had quadratic responses but the measurements were increased and then decreased (quadratic, p<0.05). The expression of HSL in the LT was linearly decreased (p<0.05) with increasing of dietary n-6:n-3 PUFA ratio. Conclusion: Dietary n-6:n-3 PUFA ratio could regulate lipid and fatty acid metabolism in blood and tissue. Reducing dietary n-6:n-3 PUFA ratio (3:1) could appropriately suppress expression of related genes in PPARγ signaling, and result in improved growth performance and n-3 PUFA deposition in muscle and adipose tissue in finishing pigs.
SH21B is a natural composition composed of seven herbs: Scutellaria baicalensis Georgi, Prunus armeniaca Maxim, Ephedra sinica Stapf, Acorus gramineus Soland, Typha orientalis Presl, Polygala tenuifolia Willd and Nelumbo nucifera Gaertner (Ratio 3:3:3:3:3:2:2). In our previous study, we reported that SH21B inhibited adipogenesis and fat accumulation in 3T3-L1 cells through modulation of various regulators in the adipogenesis pathway. The aim of this study was to analyze the transcriptome profiles for the anti-adipogenic effects of SH21B in 3T3-L1 cells. Total RNAs from SH21B-treated 3T3-L1 cells were reverse-transcribed into cDNAs and hybridized to Affymetrix Mouse Gene 1.0 ST array. From microarray analyses, we identified 2,568 genes of which expressions were changed more than two-fold by SH21B, and the clustering analyses of these genes resulted in 9 clusters. Three clusters among the 9 showed down-regulation by SH21B (cluster 4, cluster 6 and cluster 9), and two clusters showed up-regulation by SH21B (cluster 7 and cluster 8) during the adipogenesis of 3T3-L1 cells. It was found that many genes related to cell proliferation and adipogenesis were included in these clusters. Clusters 4, 6 and 9 included genes which were related with adipogenesis induction and cell cycle arrest. Clusters 7 and 8 included genes related to cell proliferation as well as adipogenesis inhibition. These results suggest that the mechanisms of the anti-adipogenic effects of SH21B may be the modulation of genes involved in cell proliferation and adipogenesis.
Journal of the Korean Society of Food Science and Nutrition
/
v.42
no.10
/
pp.1576-1584
/
2013
This study is carried out to assess the relative effects of different doses of dietary glucose or fructose on non-alcoholic fatty liver disease (NAFLD) and hepatic metaflammation in a rodent model of type 2 diabetes. KK/HlJ male mice were fed experimental diets as follows: 1) control (CON), 2) moderate glucose (MG, 30% of total calories as glucose), 3) high glucose (HG, 60% of total calories as glucose), 4) moderate fructose (MF, 30% of total calories as fructose), and 5) high fructose (HF, 60% of total calories as fructose) for three weeks. Food intake was not affected by treatments. Compared with HF, HG not only increased serum fasting glucose and area under the curve during oral glucose tolerance test, but also decreased the levels of serum insulin and adiponectin. It indicated that glucose control was complicated via high glucose intake. High fructose treatment led to increased triglyceride in the serum and liver. In comparison to HG, high fructose diet activated NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome consisting of apoptosis-associated speck-like protein containing a CARD (ASC), NLRP3 and caspase 1, which increases interleukin (IL)-$1{\beta}$ maturation and secretion. The activation of NLRP3 inflammasome was accompanied by increased levels of tumor necrosis factor alpha (TNF-${\alpha}$) and IL-6. However, the expression of NLRP3 inflammasome components and pro-inflammatory cytokines did not differ between CON and HG. These data suggested that dietary fructose triggers hepatic metaflammation accompanied by NLRP3 inflammasome activation and has deleterious effects on NAFLD.
Go, Eun Ji;Ryu, Byung Ryeol;Yang, Su Jin;Baek, Jong Suep;Ryu, Su Ji;Kim, Hyun Bok;Lim, Jung Dae
Korean Journal of Medicinal Crop Science
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v.28
no.6
/
pp.395-411
/
2020
Background: This study investigated the anti-obesity effect of the flavonoid rich fraction (FRF) and its constituent, rutin obtained from the leaf of Morus alba L., on the lipid accumulation mechanism in 3T3-L1 adipocyte and C57BL/6 mouse models. Methods and Results: In Oil Red O staining, FRF (1,000 ㎍/㎖) treatments showed inhibition rate of 35.39% in lipid accumulation compared to that in the control. AdipoRedTM assay indicated that the triglyceride content in 3T3-L1 adipocytes treated with FRF (1,000 ㎍/㎖) was reduced to 23.22%, and free glycerol content was increased to 106.04% that of the control. FRF and its major constituent, rutin affected mRNA gene expression. Rutin contributed to the inhibition of Sterol regulatory element binding protein-1c (SREBP-1c) gene expression, and inhibited the transcription factors SREBP-1c, peroxisome proliferator-activated receptor gamma (PPAR-γ), CCAAT/enhancer binding protein α (C/EBPα), fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC). In addition, the effect of FRF administration on obesity development in C57BL/6 mice fed high-fat diet (HFD) was investigated. FRF suppressed weight gain, and reduced liver triglyceride and leptin secretion. FRF exerted potential anti-inflammatory effects by improving insulin resistance and adiponectin levels, and could thus be used to help counteract obesity. The mRNA expressions of PPAR-γ, FAS, ACC, and CPT-1 were determined in liver tissue. Quantitative real-time PCR analysis was also performed to evaluate the expression of IL-1β, IL-6, and TNF-α in epididymal adipose tissue. Compared to the control group, mice fed the HFD showed the up-regulation in PPAR-γ, FAS, IL-6, and TNF-α genes, and down-regulation in CPT1 gene expression. FRF treatement markedly reduced the expression of PPAR-γ, FAS, IL-6, and TNF-α compared to those in HFD control, whereas increased the expression level of CPT1. Conclusions: These results suggest that the FRF and its major active constituent, rutin, can be used as effective anti-obesity agents.
It was reported that the novel compounds (LP9M80-H) of $Liriope$$platyphylla$ regulate glucose transporter (Glut) biosynthesis by activating the insulin-signaling pathway in the liver and brain of ICR mice. To investigate the therapeutic effects of LP9M80-H on the pathology of diabetes and obesity, alterations of key factors related to symptoms were analyzed in the Otsuka Long Evans Tokushima Fatty (OLETF) rats treated with LP9M80-H for 2 weeks. The abdominal fat masses in the LP9M80-H-treated group were lower than the vehicle-treated group, although there was no difference in body weight between the two groups. Additionally, when compared to the vehicle-treated group, LP9M80-H treatment induced a significant decrease in glucose levels and an increase in the insulin concentration in the blood of OLETF rats. A high level of insulin protein was also detected in pancreatic ${\beta}$ cells of LP9M80-H-treated OLETF rats. A significant reduction in the concentration of lipids and adiponectin was detected only in LP9M80-H-treated OLETF rats. Furthermore, the expression of insulin receptor ${\beta}$ and the insulin receptor substrate (IRS) was dramatically decreased in LP9M80-H-treated OLETF rats compared to the vehicle-treated group. Of the glucose transporters located downstream of the insulin-signaling pathway, glucose transporters (Glut) -2 and -3 were significantly decreased in LP9M80-H-treated OLETF rats, while the level of Glut-4 was maintained under all conditions. Therefore, these results suggest that LP9M80-H may contribute to relieving symptoms of diabetes and obesity through glucose homeostasis and regulation of lipid concentration.
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