• Preventive Nutrition and Food Science
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• v.20 no.4
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• pp.253-259
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• 2015

Chronic low-grade inflammation is associated with obesity. This study investigated effect of high hydrostatic pressure extract of red ginseng (HRG) on inflammation in rats with high-fat (HF) diet induced obesity. Male, Sprague-Dawley rats (80~110 g) were randomly divided into two groups, and fed a 45% HF diet (HF) and a 45% HF diet containing 1.5% HRG (HF+HRG) for 14 weeks. At the end of the experiment, the serum leptin level was reduced by the HRG supplementation. The mRNA expression of genes related to adipogenesis including peroxisome proliferator-activated receptor-gamma and adipocyte protein 2 was down-regulated in the white adipose tissue (WAT). The mRNA levels of major inflammatory cytokines such as tumor necrosis factor-${\alpha}$, monocyte chemoattractant protein 1, and interleukin-6 were remarkably down-regulated by the HRG in WAT. These results suggest that HRG might be beneficial in ameliorating the inflammation-associated health complications by suppressing adipogenic and pro-inflammatory gene expression.

• IMMUNE NETWORK
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• v.13 no.4
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• pp.123-132
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• 2013

Obesity is consistently increasing in prevalence and can trigger insulin resistance and type 2 diabetes. Many lines of evidence have shown that macrophages play a major role in inflammation associated with obesity. This study was conducted to determine metformin, a widely prescribed drug for type 2 diabetes, would regulate inflammation through down-regulation of scavenger receptors in macrophages from obesity-induced type 2 diabetes. RAW 264.7 cells and peritoneal macrophages were stimulated with LPS to induce inflammation, and C57BL/6N mice were fed a high-fat diet to generate obesity-induced type 2 diabetes mice. Metformin reduced the production of NO, $PGE_2$ and pro-inflammatory cytokines ($IL-1{\beta}$, IL-6 and $TNF-{\alpha}$) through down-regulation of $NF-{\kappa}B$ translocation in macrophages in a dose-dependent manner. On the other hand, the protein expressions of anti-inflammatory cytokines, IL-4 and IL-10, were enhanced or maintained by metformin. Also, metformin suppressed secretion of $TNF-{\alpha}$ and reduced the protein and mRNA expression of $TNF-{\alpha}$ in obese mice as well as in macrophages. The expression of scavenger receptors, CD36 and SR-A, were attenuated by metformin in macrophages and obese mice. These results suggest that metformin may attenuate inflammatory responses by suppressing the production of $TNF-{\alpha}$ and the expressions of scavenger receptors.

• The Journal of Internal Korean Medicine
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• v.35 no.4
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• pp.428-438
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• 2014

Objectives: Obesity is an important cause of insulin resistance that leads to obese type 2 diabetes. Recently it has been found that obesity is associated with adipose tissue accumulation which causes systemic inflammation. In this study, we investigated effects of Inula helenium on the inflammation in high fat diet-induced insulin resistance mouse. Methods: Insulin resistance was induced in C57BL/6 male mice (19~21 g) on a 60% fat diet. Mice were divided into 3 groups (n=6) of normal, control and Inula helenium. After 12 weeks, body weight, FBS, oral glucose tolerance test (OGTT), serum level of insulin, epididymal fat pad, liver weight and the gene expression of tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-6, interleukin (IL)-10 and cluster of differentiation (CD) 68 were measured. Also, adipose tissue macrophage was analyzed by fluorescence activated cell sorting. Results: Inula helenium significantly reduces oral glucose tolerance levels, insulin serum level and adipose tissue macrophage. Also Inula helenium increased IL-10 gene expression and decreased CD68 gene expression. Conclusions: These results show that Inula helenium has anti-insulin resistance and anti-inflammatory effects on a high fat diet-induced insulin resistance mouse model.

• Molecules and Cells
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• v.47 no.2
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• pp.100031.1-100031.13
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• 2024

It is now well-accepted that obesity-induced inflammation plays an important role in the development of insulin resistance and type 2 diabetes. A key source of the inflammation is the murine epididymal and human visceral adipose tissue. The current paradigm is that obesity activates multiple proinflammatory immune cell types in adipose tissue, including adipose-tissue macrophages (ATMs), T Helper 1 (Th1) T cells, and natural killer (NK) cells, while concomitantly suppressing anti-inflammatory immune cells such as T Helper 2 (Th2) T cells and regulatory T cells (Tregs). A key feature of the current paradigm is that obesity induces the anti-inflammatory M2 ATMs in lean adipose tissue to polarize into proinflammatory M1 ATMs. However, recent single-cell transcriptomics studies suggest that the story is much more complex. Here we describe the single-cell genomics technologies that have been developed recently and the emerging results from studies using these technologies. While further studies are needed, it is clear that ATMs are highly heterogeneous. Moreover, while a variety of ATM clusters with quite distinct features have been found to be expanded by obesity, none truly resemble classical M1 ATMs. It is likely that single-cell transcriptomics technology will further revolutionize the field, thereby promoting our understanding of ATMs, adipose-tissue inflammation, and insulin resistance and accelerating the development of therapies for type 2 diabetes.

• Nutrition Research and Practice
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• v.15 no.6
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• pp.798-806
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• 2021

BACKGROUND/OBJECTIVES: Obesity is associated with chronic inflammation. The spleen is the largest organ of the lymphatic system and has an important role in immunity. Obesity-induced inflammatory responses are triggered by Toll-like receptor (TLR)-myeloid differentiation primary response 88 (MyD88) pathway signaling. Phenethyl isothiocyanate (PEITC) and 3,3'-diindolylmethane (DIM), major dietary glucosinolates present in cruciferous vegetables, have been reported to produce anti-inflammatory effects on various diseases. However, the effects of PEITC and DIM on the obesity-induced inflammatory response in the spleen are unclear. The purpose of this study was to examine the anti-inflammatory effects of PEITC and DIM on the spleen and their mechanism in high fat/cholesterol diet (HFCD)-fed C57BL/6 mice. MATERIALS/METHODS: We established an animal model of HFCD-induced obesity using C57BL/6 mice. The mice were divided into six groups: normal diet with AIN-93G diet (CON), high fat diet (60% calories from fat) with 1% cholesterol (HFCD), HFCD with PEITC 30 mg/kg/day or 75 mg/kg/day (HFCD+P30, HFCD+P75), and HFCD with DIM 1.5 mg/kg/day or 7.5 mg/kg/day (HFCD+D1.5, HFCD+D7.5). Enzyme-linked immunosorbent assay was used to evaluate pro-inflammatory cytokine secretion. Western blot and quantitative polymerase chain reaction were used to analyze protein and mRNA levels of nuclear factor kappa B (NF-κB) p65, interleukin 6 (IL-6), cyclooxygenase 2 (COX-2), TLR2, TLR4, and MyD88 in spleen tissue. RESULTS: Serum IL-6 levels were significantly higher in the HFCD group than in groups fed a HFCD with PEITC or DIM. Levels of NF-κB p65 protein and TLR2/4, MyD88, NF-κB p65, IL-6, and COX-2 mRNA were significantly higher in the HFCD group than in the CON group and were reduced by the PEITC and DIM supplements. CONCLUSIONS: PEITC- and DIM-supplemented diets improved splenic inflammation by modulating the TLR2/4-MyD88 pathway in HFCD-fed mice. We suggest that dietary glucosinolates may at least partially improve obesity-induced inflammation of the spleen.

• Journal of Microbiology and Biotechnology
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• v.31 no.11
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• pp.1568-1575
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• 2021

Obesity and related metabolic diseases are major problems worldwide. Some probiotics are currently considered potential therapeutic strategies for obesity. We aimed to investigate the anti-obesity efficacy of Latilactobacillus sakei WIKIM31 in obese mice induced by a high fat diet. The administration of a high-fat diet with L. sakei WIKIM31 reduced body weight gain, epididymal fat mass, triglyceride and total cholesterol levels in the blood, and remarkably decreased the expression of lipogenesis-related genes in the epididymal adipose tissue and liver. Interestingly, intake of L. sakei WIKIM31 improved gut barrier function by increasing the gene expression of tight junction proteins and suppressing the inflammatory responses. Additionally, L. sakei WIKIM31 enhanced the production of short-chain fatty acids, such as butyrate and propionate, in the intestinal tract. These results showed that L. sakei WIKIM31 can be used as a potential therapeutic probiotic for obesity.

• Bulletin of Food Technology
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• v.23 no.1
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• pp.28-39
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• 2010

• Biomedical Science Letters
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• v.23 no.2
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• pp.144-153
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• 2017

It was demonstrated that Gangjihwan (DF), which is the herbal composition composed of Ephedra intermedia, Lithospermum erythrorhizon, and Rheum palmatum, inhibits obesity and hepatic steatosis in high fat diet (HFD)-fed obese mice. The aim of this study was to determine the effects of DF on visceral obesity, hepatic inflammation and fibrosis and the mechanism of actions involved in this process using in vivo and in vitro approaches. DF was extracted with water (DF-FW), 30% grain alcohol (DF-GA30), and 70% grain alcohol (DF-GA70). Administration of DF to HFD-fed control mice decreased visceral tissue mass and visceral adipocyte size without adverse effects. Visceral fat mass was decreased by DF-GA30 and DF-GA70, and visceral adipocyte size by all three DF extracts compared with obese control mice. Histological analysis revealed that three kinds of DF extracts reduced toluidine blue-stained mast cells and collagen accumulation in the liver, the extents of which were most eminent in DF-GA70-treated mice. DF-GA70 decreased the mRNA levels of the inflammation ($TNF{\alpha}$ and VCAM-1), fibrosis (${\alpha}-SMA$), and apoptosis (caspase 3) genes, but increasing the anti-apoptosis gene (Bcl-2) mRNA levels in the liver of obese control mice. Consistent with the in vivo data, GA-70 also altered the expression of inflammation genes ($TNF{\alpha}$ and MCP-1) in HepG2 cells. These results indicate that DF not only inhibits visceral obesity, but also ameliorates visceral obesity-induced hepatic inflammation and fibrosis and that this process may be mediated by regulating the hepatic expression of inflammatory and fibrogenic genes.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2018.04a
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• pp.9-9
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• 2018

Arctii Fructus (AF), which contains arctigenin (ARC) as a major constituent, is traditionally used as an anti-inflammatory medicine to treat inflammatory sore throat. Although several studies have proven its anti-inflammatory effects, there have been no reports on its use in inflammation related disorders such as obesity, cancer metastasis, and allergic responses. This study investigated the anti-obesity effect and anti-metastasis effect of AF and ARC. AF and ARC inhibited weight gain by reducing the mass of white adipose tissue in high fat diet (HFD)-induced obese mice. Serum cholesterol levels were also improved by AF and ARC. In in vitro experiments, AF and ARC decreased differentiation of white adipocytes. Furthermore, AF induced differentiation of brown adipocytes, which are able to consume surplus energy through non-shivering thermogenesis. Also, AF and ARC inhibited colon cancer and lung metastasis of colon cancer. They suppressed not only colorectal cancer cell progression by inhibiting cell growth, but also prohibited lung metastasis by regulating epithelial-mesenchymal transition (EMT), migration, and the invasion. These effects were confirmed in an experimental metastasis mouse model. In addition, AF and ARC inhibited mast cell mediated allergic responses. Collectively, our study suggests that AF and ARC might show inhibitory effects on inflammation related diseases, including obesity, cancer, cancer metastasis, and allergic responses.

• Journal of Microbiology and Biotechnology
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• v.27 no.9
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• pp.1617-1627
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• 2017

Dietary approaches using structured lipids, including medium-chain fatty acids and diacylglycerols, have been adopted for the prevention of obesity-induced chronic inflammation. In an extension to previous studies, medium-chain fatty acid-diacylglycerol enriched dietary oil (MCDG) was prepared by interesterification of canola oil and medium-chain fatty acid-triacylglycerols. The consequent MCDG product was applied to RAW264.7 macrophages followed by the assessment of multiple inflammatory responses. Compared with conventionally used canola and olive oil controls, MCDG suppressed macrophage phagocytosis, as assessed by the uptake of microsphere beads. Furthermore, the production of IL-6 and $TNF-{\alpha}$, transcription of COX-2 and iNOS, and expression of CD80 on cell surfaces were downregulated by MCDG in LPS-stimulated macrophages. Subsequently, differentiated 3T3-L1 adipocytes were evaluated for proinflammatory cytokine production and lipid accumulation. IL-6 production was marginally affected and lipid accumulation was inhibited by MCDG. Taken together, these results suggest that MCDG has potential as an alternative oil for cooking in order to prevent obesity-induced inflammation.