• IMMUNE NETWORK
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• v.11 no.2
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• pp.107-113
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• 2011

Background: Metabolic disorders, including type II diabetes and obesity, present major health risks in industrialized countries. AMP-activated protein kinase (AMPK) has become the focus of a great deal of attention as a novel therapeutic target for the treatment of metabolic syndromes. In this study, we evaluated whether dietary aloe could reduce obesity-induced inflammation and adipogenesis. Methods: Male C57BL/6 obese mice fed a high-fat diet for 54 days received a supplement of aloe formula (PAG, ALS, Aloe QDM, and Aloe QDM complex) or pioglitazone (PGZ) and were compared with unsupplemented controls (high-fat diet; HFD) or mice fed a regular diet (RD). RT-PCR and western blot analysis were used to quantify the expression of obesity-induced inflammation. Results: Aloe QDM complex downregulated fat size through suppressed expression of scavenger receptors on adipose tissue macrophages (ATMs) compared with HFD. Both white adipose tissue (WATs) and muscle exhibited increased AMPK activation through aloe supplementation, and in particular, the Aloe QDM complex. Obesity-induced inflammatory cytokines (IL-$1{\beta}$ and -6) and $HIF1{\alpha}$ mRNA and protein were decreased markedly, as was macrophage infiltration by the Aloe QDM complex. Further, the Aloe QDM complex decreased the translocation of NF-${\kappa}B$ p65 from the cytosol in the WAT. Conclusion: Dietary aloe formula reduced obesity-induced inflammatory responses by activation of AMPK in muscle and suppression of proinflammatory cytokines in the WAT. Additionally, the expression of scavenger receptors in the ATM and activation of AMPK in WAT led to reduction in the percent of body fat. Thus, we suggest that the effect of the Aloe QDM complex in the WAT and muscle are related to activation of AMPK and its use as a nutritional intervention against T2D and obesity-related inflammation.

• The Journal of Korean Academy of Prosthodontics
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• v.30 no.4
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• pp.541-564
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• 1992

The purpose of this experiment was to study the effect of implantation of the dense hydroxyapatite (HA) granules$(Apaceram^{(R)})$ in the fresh extraction sockets on the residual ridge resorption in normal and induced diabetic rabbits. Sixty-four white rabbits, weighing 3.0kg, were utilized in this study and they were divided into four group : group 1-sixteen normal rabbits without filling HA granules, group 2-sixteen normal rabbits with filling HA granules, group 3-sixteen diabetic rabbits without filling HA granules, group 4-sixteen diabetic rabbits with filling HA granules. HA granules were filled immediately after extraction in the extraction sockets of the mandibular left 1st, 2nd, and 3rd molar in group 2 and 4, and no HA granules were filled in group 1 and 3. The calculation of residual ridge resoption was done at 4th week, 8th week, 12th week, and 16th week after surgery, and histologic examination was performed to study healing process at 2nd week, 4th week, 8th week, and 16th week after surgery. The results were as follows : 1. The amount of residual ridge resorption was largest in group 3, and smallest in group 2 in every interval. There was no statistically significant difference between group 1 and 4. 2. In all groups, the amount of residual ridge resorption was high until 4th week after surgery, but the rate of residual ridge resolution slowly decreased after 4th week 3. There was more active healing process in group 1 and 2 than in group 2 and 4. 4. According to filling of HA granules, there was no difference in the amount of new bone formation, but direct contact could be observed between newly formed bone and HA granules in group 2 and 4. 5. Group 1 and 3 showed marked bone resorption and adipose marrow from 8th-16th week after surgery, but group 2 and 4 did not show maeked bone resolution, and showed fibrous tissue and a little adipose tissue among trabeculae from 8th week.

• Molecules and Cells
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• v.47 no.3
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• pp.100007.1-100007.11
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• 2024

Recent evidence establishes a pivotal role for obesity-induced inflammation in precipitating insulin resistance and type-2 diabetes. Central to this process is the proinflammatory M1 adipose-tissue macrophages (ATMs) in epididymal white adipose tissue (eWAT). Notably, natural killer (NK) cells are a crucial regulator of ATMs since their cytokines induce ATM recruitment and M1 polarization. The importance of NK cells is shown by the strong increase in NK-cell numbers in eWAT, and by studies showing that removing and expanding NK cells respectively improve and worsen obesity-induced insulin resistance. It has been suggested that NK cells are activated by unknown ligands on obesity-stressed adipocytes that bind to NKp46 (encoded by Ncr1), which is an activating NK-cell receptor. This was supported by a study showing that NKp46-knockout mice have improved obesity-induced inflammation/insulin resistance. We therefore planned to use the NKp46-knockout mice to further elucidate the molecular mechanism by which NKp46 mediates eWAT NK-cell activation in obesity. We confirmed that obesity increased eWAT NKp46⁺ NK-cell numbers and NKp46 expression in wild-type mice and that NKp46-knockout ablated these responses. Unexpectedly, however, NKp46-knockout mice demonstrated insulin resistance similar to wild-type mice, as shown by fasting blood glucose/insulin levels and glucose/insulin tolerance tests. Obesityinduced increases in eWAT ATM numbers and proinflammatory gene expression were also similar. Thus, contrary to previously published results, NKp46 does not regulate obesity-induced insulin resistance. It is therefore unclear whether NKp46 participates in the development of obesity-induced inflammation and insulin resistance. This should be considered when elucidating the obesity-mediated molecular mechanisms that activate NK cells.

• The Journal of Korean Medicine
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• v.33 no.3
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• pp.184-199
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• 2012

Objectives: There is a steady increase in the prevalence of obesity worldwide and obesity is often accompanied by inflammation. Although much emphasis has been placed on the adipose tissue inflammation in obesity, a study with herbal medicine is few. This study aimed to investigate the antidiabetic and anti-inflammatory effect of a complex herbal medicine (CHM) composed of Cornus officinalis, Dioscorea rhizoma, Aurantii fructus, and Mori Foliumon on obese type 2 diabetes mice. Methods: Type 2 diabetes mellitus and obesity were induced by Surwit's high fat, high sucrose diet for 8 weeks. Mice were divided into ND (normal diet, n=10), HFD (high fat and high sucrose diet, n=10), CHM (high fat and high sucrose diet with complex herbal medicine, n=10) and Met (high fat and high sucrose diet with metformin, n=10) groups. The body weight, fructosamine and OGTT (oral glucose tolerance test) were measured. After 8 weeks the blood samples of all mice were taken from the heart, and lipid profiles were measured. Epididymal fat pad, histological size of the adipocyte tissue and liver weights were measured. Inflammatory markers such as leptin and adipocyte tissue macrophage were measured to evaluate the effect of CHM on adipocyte tissue inflammation. Results: Compared with the HFD group, there was an improvement in OGTT and epididymal fat decreased in the CHM group. White adipocyte size and adipocyte tissue macrophage decreased in CHM group. Conclusions: These results suggest that CHM has antidiabetic and anti-inflammatory effects in high fat, high sucrose diet induced obese mice.

• Journal of Physiology & Pathology in Korean Medicine
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• v.32 no.6
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• pp.384-395
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• 2018

The aim of this study was to investigate whether a novel formulation of an herbal extracts has an inhibitory effect on obesity. To determine its anti-obesity effects, we performed anti-obesity-related experiments in vitro and in vivo. Thus, our present study was carried out to evaluate the anti-obesity effect of herbal extracts using a high fat diet (HFD)-induced obese mouse model and 3T3-L1 adipose cells. The effects of each herbal extracts on lipid accumulation in 3T3-L1 cells were examined using Oil Red O staining. Results showed that treatment with each herbal extracts at $10{\sim}100{\mu}g/ml$ had no effect on cell morphology and viability. Without evidence of toxicity, herbal extracts treatment decreased lipid accumulation compared with the untreated adipocytes controls as shown by the lower absorbance of Oil Red O stain. Futhermore, compared with control-differentiated mature adipocytes, each herbal extracts significantly inhibited lipid accumulation in mature 3T3-L1 adipocytes. In the HFD-fed obese mice, body weight, liver weight and white adipose tissue weights were significantly reduced by mixture of herbal extracts administration in mouse skin. Futhermore, we found that mixture of herbal extracts administration suppressed serum triglyceride (TG), and total cholesterol (TCHO) in HFD-induced obese mouse model. The mixture of herbal extracts of permeability was estimated by measuring the transepithelial electrical resistance (TEER) value in pig skin. The optimized formulations of herbal extracts (Test 3 formulation) showed skin permeation. However, test 1 formulation containing essential oil as enhancer showed maximum skin permeation. After confirming the enhanced skin permeability, in vivo studies were performed to assess whether skin irritation potential on the basis of a primary irritation index (PII) in rabbit skin. Reactions were scored for erythema/edema reactions at 24 h, 48 h and 72 h post-application. It was concluded that the test 1 formulation was not irritation (PII = 0). The present study suggests that the test 1 formulation might be of therapeutic interest with respect to the treatment of obesity.

• The Korea Journal of Herbology
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• v.33 no.2
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• pp.59-67
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• 2018

Objective : Plantago asiatica L. has been used for many years in Korea, China, and Japan for the treatment of many diseases such as anti-inflammatory, anti-asthma and diuretic. But the anti-obesity effect of Plantaginis asiaticae Folium has not been studied yet. Thus, this study aimed to demonstrate the anti-obesity efficacy of Plantaginis asiaticae Folium water extract (PAF) in high fat diet-induced obesity animal model. Method : Male, five-weeks old C57BL/6 mice were divided into 5 groups; ND (normal diet + 0.9% saline), HFD (high-fat diet + 0.9% saline), PC (high-fat diet + Garcinia cambogia 500 mg/kg), PAF 100, 300 (high-fat diet + PAF 100, 300 mg/kg. Treatments were performed daily for 6 weeks per os. We evaluated the changes of body weight, white adipose tissues weight, hepatic and fecal lipids level, pancreatic lipase activity and lipid profiles in plasma. Result : Body weights, adipose tissue weights and FER were significantly lower in mice fed the high-fat diet with PAF treatment than in mice fed the high-fat diet alone. In plasma, TG, TC, LDL-C, ATS and ALT levels significantly decreased in PAF groups compared with HFD group. Also, hepatic triglyceride (TG) levels decreased and fecal TG increased in PAF groups compared to HFD group. In addition, the activity of pancreatic lipase was decreased in the PAF groups compared to that of HFD group. Conclusion: These results suggest PAF extract is effective in preventing and improvement obesity, so it might be a potential and safe material for anti-obesity agent of weight control or functional supplements.

• Nutrition Research and Practice
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• v.8 no.5
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• pp.544-549
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• 2014

BACKGROUND/OBJECTIVES: Obesity-associated insulin resistance is a strong risk factor for type 2 diabetes mellitus. The aim of this study was to investigate the effect of myricetin on adiposity, insulin resistance, and inflammatory markers in mice with diet-induced insulin resistance. MATERIALS/METHODS: Five-week-old male C57BL/6J mice were fed a basal diet, a high-fat, high-sucrose (HFHS) diet, or the HFHS diet containing 0.06% myricetin or 0.12% myricetin for 12 weeks after a 1-week adaptation, and body weight and food intake were monitored. After sacrifice, serum lipid profiles, glucose, insulin, adipocyte-derived hormones, and proinflammatory cytokines were measured. The homeostasis model assessment for insulin resistance (HOMA-IR) was determined. RESULTS: Myricetin given at 0.12% of the total diet significantly reduced body weight, weight gain, and epidydimal white adipose tissue weight, and improved hypertriglyceridemia and hypercholesterolemia without a significant influence on food intake in mice fed the HFHS diet. Serum glucose and insulin levels, as well as HOMA-IR values, decreased significantly by 0.12% myricetin supplementation in mice fed the HFHS diet. Myricetin given at 0.12% of the total diet significantly reduced serum levels of leptin, tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interleukin-6 (IL-6) in mice fed the HFHS diet. CONCLUSIONS: These findings suggest that myricetin may have a protective effect against diet-induced obesity and insulin resistance in mice fed HFHS diet, and that alleviation of insulin resistance could partly occur by improving obesity and reducing serum proinflammatory cytokine levels.

• Journal of Microbiology and Biotechnology
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• v.15 no.4
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• pp.823-830
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• 2005

This study was undertaken to evaluate the effect of bacteria-derived $\beta$-glucan fiber on serum lipids, adiposity and uncoupling protein (UCP) expression in rats. In order to induce obesity, Sprague-Dawley weanling male rats were allowed free access to AIN-76A diet until 4 weeks of age, and fed high-fat diet (beef tallow, $40\%$ of calories as fat) for 6 weeks until 10 weeks of age. Rats were then fed with $0\%$ thigh- fat control group), $1\%$, or $5\%$ bacterial ~-glucan supplemented high-fat diets (w/w) for another 6 weeks. For comparison, normal control group was fed with AIN-76 diet $11.7\%$ fat). Supplementation with bacterial $\beta$-glucan resulted in a significant reduction of high-fat-induced white fat (i.e., visceral and peritoneal fat) development, adipocyte hypertrophy, and development of hyperinsulinemia and hyperleptinemia. Serum triglyceride, total cholesterol, and free fatty acid levels were greatly reduced, but, HDL-cholesterol concentrations were increased by bacterial $\beta$-glucan supplementation. Serum leptin level was lower in the $\beta$-glucan groups than in the high-fat group. The expression of UCPs (UCP1, UCP2, and UCP3) in brown adipose tissue (BAT) were significantly increased by $5\%$ bacterial $\beta$-glucan-containing diet. This study suggests that the anti-obesity effect of $5\%$ bacterial $\beta$-glucan is attributed to upregulation of UCPs and inefficient energy utilization.

• Nutrition Research and Practice
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• v.7 no.5
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• pp.352-358
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• 2013

Korean pine nut oil (PNO) has been reported to have favorable effects on lipid metabolism and appetite control. We investigated whether PNO consumption could influence weight gain, and whether the PNO-induced effect would result in an improvement of immune function in high-fat diet (HFD)-induced obese mice. C57BL/6 mice were fed control diets with 10% energy fat from either PNO or soybean oil (SBO), or HFDs with 45% energy fat from 10% PNO or SBO and 35% lard, 20% PNO or SBO and 25% lard, or 30% PNO or SBO and 15% lard for 12 weeks. The proliferative responses of splenocytes upon stimulation with concanavalin A (Con A) or lipopolysaccharide (LPS), Con A-stimulated production of interleukin (IL)-2 and interferon (IFN)-${\gamma}$, and LPS-stimulated production of IL-6, IL-$1{\beta}$, and prostaglandin $E_2$ ($PGE_2$) by splenocytes were determined. Consumption of HFDs containing PNO resulted in significantly less weight gain (17% less, P < 0.001), and lower weight gain was mainly due to less white adipose tissue (18% less, P = 0.001). The reduction in weight gain did not result in the overall enhancement in splenocyte proliferation. Overall, PNO consumption resulted in a higher production of IL-$1{\beta}$ (P = 0.04). Replacement of SBO with PNO had no effect on the production of IL-2, IFN-${\gamma}$, IL-6, or $PGE_2$ in mice fed with either the control diets or HFDs. In conclusion, consumption of PNO reduced weight gain in mice fed with HFD, but this effect did not result in the overall improvement in immune responses.

• IMMUNE NETWORK
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• v.12 no.3
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• pp.96-103
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• 2012

Obesity-induced disorders contribute to the development of metabolic diseases such as insulin resistance, fatty liver diseases, and type 2 diabetes (T2D). In this study, we evaluated whether the Aloe QDM complex could improve metabolic disorders related to blood glucose levels and insulin resistance. Male C57BL/6 obese mice fed a high-fat diet for 54 days received a supplement of Aloe QDM complex or pioglitazone (PGZ) or metformin (Met) and were compared with unsupplemented controls (high-fat diet; HFD) or mice fed a regular diet (RD). RT-PCR and western blot analysis were used to quantify the expression of obesity-induced inflammation. Dietary Aloe QDM complex lowered body weight, fasting blood glucose, plasma insulin, and leptin levels, and markedly reduced the impairment of glucose tolerance in obese mice. Also, Aloe QDM complex significantly enhanced plasma adiponectin levels and insulin sensitivity via AMPK activity in muscles. At the same time, Aloe QDM decreased the mRNA and protein of $PPAR{\gamma}/LXR{\alpha}$ and scavenger receptors in white adipose tissue (WAT). Dietary Aloe QDM complex reduces obesity-induced glucose tolerance not only by suppressing $PPAR{\gamma}/LXR{\alpha}$ but also by enhancing AMPK activity in the WAT and muscles, both of which are important peripheral tissues affecting insulin resistance. The Aloe QDM complex could be used as a nutritional intervention against T2D.