• Microbiology and Biotechnology Letters
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• v.50 no.1
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• pp.135-146
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• 2022

Obesity is closely associated with profound dyslipidemia, insulin resistance, and fatty liver disease. Recent reports have suggested that alterations in gut microbiota can be linked to diet-induced obesity. In this study, the anti-obesity effects of Weissella confusa WIKIM51 isolated from kimchi were investigated, as evidenced by: i) reduced lipid accumulation and downregulated adipogenesis-related genes in 3T3-L1 adipocytes; ii) suppressed gains in body weight and epididymal fat mass; iii) reduced serum lipid levels, for example, triglyceride and total cholesterol; iv) increased serum adiponectin levels and reduced serum leptin levels; v) downregulated lipogenesis and upregulated β-oxidation-related genes in the epididymal fat; and vi) altered microbial communities. The collective evidence indicate the potential value of W. confusa WIKIM51 as a functional food supplement for the prevention and amelioration of obesity.

• Nutrition Research and Practice
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• v.16 no.1
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• pp.60-73
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• 2022

BACKGROUND/OBJECTIVES: The extract from Dendropanax morbifera exhibited diverse therapeutic potentials. We aimed to evaluate the efficacy and safety of D. morbifera leaf extract for improving metabolic parameters in human. SUBJECTS/METHODS: A 12-week, double blind, placebo-controlled and randomized trial included a total of 74 adults, and they were assigned to the placebo group (n = 38) or 700 mg/day of D. morbifera group (n = 36). The efficacy endpoints were changes in glycemic, lipid, obesity, and blood pressure (BP) parameters, in addition to the prevalence of metabolic syndrome (MetS) and the numbers of MetS components. Safety was assessed by monitoring adverse events (AEs). RESULTS: After 12 weeks of treatment, the hemoglobin A1c (HbA1c) level significantly decreased in the D. morbifera group compared to that of the placebo group (difference: -0.13 ± 0.20% vs. 0.00 ± 0.28%, P = 0.031; % of change: -2.27 ± 3.63% vs. 0.10 ± 5.10%, P = 0.025). The homeostatic model assessment for insulin resistance level also decreased significantly from its baseline in the D. morbifera group. The systolic BP of D. morbifera group decreased significantly than that of placebo group (difference: -3.9 ± 9.8 mmHg vs. 3.3 ± 11.7 mmHg, P = 0.005; % of change: -2.8 ± 7.7% vs. 3.3 ± 10.2%, P = 0.005). However, the lipid parameters and body composition including body weight did not differ between the groups. The prevalence of MetS (36.8% vs. 13.9%, P = 0.022) and the incidence of MetS (10.5% vs. 13.9%, P = 0.027) at 12 weeks was significantly lower in the D. morbifera group than it was in the placebo group. No serious AEs occurred in either group. CONCLUSIONS: Supplementation with D. morbifera extracts over a 12-week period improved metabolic parameters such as HbA1c and BP and reduced the prevalence of MetS.

• Journal of Life Science
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• v.32 no.6
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• pp.476-481
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• 2022

Ubiquitin signaling regulates virtually all aspects of eukaryotic biology and dynamic processes in which protein substrates are modified by ubiquitin. To regulate these processes, deubiquitinating enzymes (DUBs) cleave ubiquitin or ubiquitin-like proteins from these substrates. DUBs have been implicated in the pathogenesis of cancer, leading to the development of increasing numbers of small-molecule DUB inhibitors. On the other hand, recent studies have focused on the function of DUBs in metabolic diseases such as obesity, diabetes, and fatty liver diseases. DUBs play a positive or negative role in the progression and development of metabolic diseases. Their involvement in cell pathology and regulation of major transcription factors in metabolic syndrome has been examined in vitro and in animal and human biopsies. UCH, USP7, and USP19 were linked to adipocyte differentiation, body weight gain, and insulin resistance in genetic or diet-induced obesity. CYLD, USP4, and USP18 were found to be closely associated with fatty liver diseases. In addition, these liver diseases were accompanied by body weight change in certain cases. Collectively, in this review, we discuss the current understanding of DUBs in metabolic diseases with a particular focus on obesity. We also provide basic knowledge and regulatory mechanisms of DUBs and suggest these enzymes as therapeutic targets for metabolic diseases.

• Journal of Life Science
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• v.33 no.3
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• pp.295-303
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• 2023

Immune and metabolic systems are important factors in maintaining homeostasis. Immune response and metabolic regulation are highly associated, so, when the normal metabolism is disturbed, the immune response changed followed the metabolic diseases occur. Likewise, obesity is highly related to immune response. Obesity, which is caused by an imbalance in energy metabolism, is associated with metabolic diseases, such as insulin resistance, type 2 diabetes, fatty liver diseases, atherosclerosis and hypertension. As known, obesity is characterized in chronic low-grade inflammation. In obesity, the microenvironment of immune cells became inflammatory by the unique activation phenotypes of immune cells such as macrophage, natural killer cell, T cell. Also, the immune cells interact each other in cellular or cytokine mechanisms, which intensify the obesity-induced inflammatory response. This phenomenon suggests the possibility of regulating the activation of immune cells as a pharmacological therapeutic strategy for obesity in addition to the common pharmacological treatment of obesity which is aimed at inhibiting enzymes such as pancreatic lipase and α-amylase or inhibiting differentiation of preadipocytes. In this review, we summarize the activation phenotypes of macrophage, natural killer cell and T cell, and their aspects in obesity. We also summarize the pharmacological substances that alleviates obesity by regulating the activation of immune cells.

• Journal of Ginseng Research
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• v.47 no.3
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• pp.376-384
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• 2023

Background: Hepatic lipid disorder impaired mitochondrial homeostasis and intracellular redox balance, triggering development of non-alcohol fatty liver disease (NAFLD), while effective therapeutic approach remains inadequate. Ginsenosides Rc has been reported to maintain glucose balance in adipose tissue, while its role in regulating lipid metabolism remain vacant. Thus, we investigated the function and mechanism of ginsenosides Rc in defending high fat diet (HFD)-induced NAFLD. Methods: Mice primary hepatocytes (MPHs) challenged with oleic acid & palmitic acid were used to test the effects of ginsenosides Rc on intracellular lipid metabolism. RNAseq and molecular docking study were performed to explore potential targets of ginsenosides Rc in defending lipid deposition. Wild type and liver specific sirtuin 6 (SIRT6, 50721) deficient mice on HFD for 12 weeks were subjected to different dose of ginsenosides Rc to determine the function and detailed mechanism in vivo. Results: We identified ginsenosides Rc as a novel SIRT6 activator via increasing its expression and deacetylase activity. Ginsenosides Rc defends OA&PA-induced lipid deposition in MPHs and protects mice against HFD-induced metabolic disorder in dosage dependent manner. Ginsenosides Rc (20mg/kg) injection improved glucose intolerance, insulin resistance, oxidative stress and inflammation response in HFD mice. Ginsenosides Rc treatment accelerates peroxisome proliferator activated receptor alpha (PPAR-α, 19013)-mediated fatty acid oxidation in vivo and in vitro. Hepatic specific SIRT6 deletion abolished ginsenoside Rc-derived protective effects against HFD-induced NAFLD. Conclusion: Ginsenosides Rc protects mice against HFD-induced hepatosteatosis by improving PPAR-α-mediated fatty acid oxidation and antioxidant capacity in a SIRT6 dependent manner, and providing a promising strategy for NAFLD.

• Nutrition Research and Practice
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• v.18 no.5
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• pp.633-646
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• 2024

BACKGROUND/OBJECTIVES: Cladophora glomerata extract (CGE), rich in polyphenols, was reported to exhibit antidiabetic and renoprotective effects by modulating the functions of protein kinases-mediated organic anion transporter 1 (Oat1) and 3 (Oat3) in rats with type 2 diabetes mellitus (T2DM). Nevertheless, the antioxidant effects of CGE on such renoprotection have not been investigated. This study examined the mechanisms involved in the antioxidant effects of CGE on renal organic anion transport function in an in vivo study. MATERIALS/METHODS: Diabetes was induced in the rats through a high-fat diet combined with a single dose of 40 mg/kg body weight (BW) streptozotocin. Subsequently, normal-diet rats were supplemented with a vehicle or 1,000 mg/kg BW of CGE, while T2DM rats were supplemented with a vehicle, CGE, or 200 mg/kg BW of vitamin C for 12 weeks. The study evaluated the general characteristics of T2DM and renal oxidative stress markers. The renal organic transport function was assessed by measuring the para-aminohippurate (PAH) uptake using renal cortical slices and renal inflammatory cytokine expression in the normal diet (ND) and ND + CGE treated groups. RESULTS: CGE supplementation significantly reduced hyperglycemia, hypertriglyceridemia, insulin resistance, and renal lipid peroxidation in T2DM rats. This was accompanied by the normalization of high expressions of renal glutathione peroxidase and nuclear factor kappa B by CGE and vitamin C. The renal anti-inflammation of CGE was evidenced by the reduction of tumor necrosis factor-1α and interleukin-1β. CGE directly blunted sodium nitroprusside-induced renal oxidative/nitrosative stresses and mediated the PAH uptake in the normally treated CGE in rats was particularly noteworthy. These data also correlated with reduced nitric oxide production, highlighting the potential of CGE as a therapeutic agent for managing T2DM-related renal complications. CONCLUSION: These findings suggest that CGE has antidiabetic effects and directly prevents diabetic nephropathy through oxidative/nitrosative stress pathways.

• Journal of Life Science
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• v.28 no.5
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• pp.621-626
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• 2018

We introduced the physiological responses of aging, active aging and also suggest the impact of physical exercise on body health status and elderly immunity. In this purpose, we searched the Pub Med data base for the articles (include our experimental papers) and review papers having the terms 'Aging', 'Active aging' and 'Physical activity and elderly' in the title, published from 1999 until 2018. The results were as follows: Exercise training has been extensively studied about the reduction of inflammation, oxidative stress, disease, and aging in syndrome X patients and elderly. Combined and aerobic or resistance exercise training could reduce obesity, insulin resistance, type 2 diabetes and hypertension. Exercise training has been extensively studied in cancer settings as part of prevention or treatment strategies. From this research, regular exercise has the potential to target tumor growth through regulation of inflammation and immune responses such as lactate clearance, NK cell activation (innate immunity), activation of cytotoxic immune cells, T cell activation (adaptive immunity), and immune surveillance. However, Endurance physical activity not only induces thermogenesis and diverse sports injuries but also elicits mobilization and functional enhancement of monocytes, neutrophils (which is caused by the cytokine changes such as TNF-alpha, IL-1) whereas it suppresses cell mediated immunity causing to increased susceptibility to inflammation and infections like cough and URTIs (upper respiratory track infections) in young and especially in elderly people. Therefore, Strategies to prevent physical fatigue, sports injuries include avoid overtraining, Adequate recovery and various type of rest during and after physical activity and assuring adequate nutrition supplementation such as glutamine, vitamin B, vitamin C, carbohydrate, ion or berry-contain sports beverages is helpful in physically active elderly.

• Clinical and Experimental Pediatrics
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• v.52 no.10
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• pp.1109-1118
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• 2009

Purpose : Metabolic syndrome (MS), characterized by obesity and insulin resistance, elicits risk factors such as hyperlipidemia, hypertension, and glucose intolerance with additive effects on atherosclerosis, leading to cardiovascular diseases. The purposes of this study were to evaluate the prevalence of MS among overweight and obese adolescents and to investigate the impact of obesity on the cardiovascular system. Methods : In all, 684 adolescents were included in the study. Blood pressure, body mass index (BMI), fasting blood glucose, total cholesterol, triglyceride, low-density-lipoprotein (LDL)-cholesterol, high-density-lipoprotein (HDL)-cholesterol, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and high-sensitive C-reactive protein (hs-CRP) were measured in the patients with a BMI of >85 percentile. Brachial-ankle pulse wave velocity (BaPWV) and ankle brachial index were measured using Vascular Profiler (VP)-1000. Results : MS was confirmed in 19.5% of the overweight and obese adolescents and 50.8% of the obese adolescents. The systolic and diastolic blood pressure, height, weight, fat mass, %fat, BMI, obesity index, and waist circumference were higher in the overweight and obese adolescents with MS. Moreover, the triglyceride, AST, ALT, and hs-CRP levels were higher, whereas HDL-cholesterol level was significantly lower in this group. The overweight and obese adolescents with MS showed shorter diastolic and systolic times, higher heart rate and BaPWV, and longer E-wave deceleration time by echocardiography. Conclusion : Overweight and obese adolescents showed characteristic MS features such as hypertension and hyperlipidemia. Thus, obese adolescents predisposed to MS should be provided early treatment for obesity.

• Journal of Veterinary Clinics
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• v.29 no.5
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• pp.361-367
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• 2012

Diabetes-related complications in human and veterinary medicine have been shown to be associated with hyperglycemia-induced inflammation. It has been recently suggested that the onset of insulin resistance may be caused by over-production of inflammatory cytokines such as tumor necrosis factor (TNF)-${\alpha}$ from immune cells. Conjugated linoleic acid (CLA) regulates inflammatory response through modulation of TNF-${\alpha}$ expression. The objective of this study was to examine the effect of CLA on nuclear factor kappaB (NF-${\kappa}B$) p65 binding activity, inhibitory kappaB ($I{\kappa}B$)-${\alpha}$ expression, and TNF-${\alpha}$ production from high glucose-treated RAW 264.7 cells. CLA was added to RAW cells that had been previously cultured with low or high concentration of glucose. The levels of TNF-${\alpha}$ protein in the culture supernatant of RAW cells exposed to high concentrations of glucose were higher than those of cells exposed to low concentrations of glucose. The treatment with the high concentration of glucose in RAW cells increased levels of NF-${\kappa}B$ p65 binding activity and the decreased $I{\kappa}B-{\alpha}$ expression when compared with those of low glucose. The treatments in combination with CLA and glucose (low and high) glucose in RAW cells increased TNF-${\alpha}$ production when compared with that glucose alone. These treatments with CLA increased TNF-${\alpha}$ production in high glucose-treated RAW cells than those with low glucose. These treatments of CLA also showed higher NF-${\kappa}B$ p65 binding activity and lower $I{\kappa}B-{\alpha}$ expression in high glucose than those in low glucose condition. This suggests that CLA can increase NF-${\kappa}B$ p65 binding activity and TNF-${\alpha}$ production from high glucose-treated RAW 264.7 cells and is likely to promote hyperglycemia-induced inflammation.

• Korean Journal of Plant Resources
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• v.29 no.1
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• pp.1-10
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• 2016

Obesity is a pro-inflammatory state that contributes to the development of metabolic disorders such as hyperlipidemia, insulin resistance, type 2 diabetes, non-alcoholic fatty liver, and cardiovascular disease. In this study, we evaluated the inhibition of adipogenesis in 3T3-L1 cells and in high-fat diet (HFD)-induced obese mice by Peucedanum japonicum Thunberg L. water extract (PJT). Lipid accumulation measurement indicates that PJT markedly inhibited adipogenesis in a dose-dependent manner. RT-PCR results demonstrated that the mRNA expression of adipogenic transcription factors such as peroxisome proliferator-activated receptor-γ (PPARγ) and CCAAT/enhancer binding protein-α (C/EBPα) in 3T3-L1 cells were significantly down-regulated by PJT treatment. Oral administration of PJT (100, 300, and 500 ㎎/㎏, b.w/daily for 4 weeks) was conducted in high-fat diet induced obese mice and C57BL/6 mice. The PJT-administered group of HFD-induced mice had a lower body weight gain, along with decreased serum levels of glucose, triglycerides, and total cholesterol compared with the control mice, however, the HDL-cholesterol/total cholesterol ratio was increased. Furthermore, the elevated mRNA expression levels of adipogenesis related genes in the white adipose tissue of obese mice were significantly suppressed by PJT. These results indicate that PJT exhibits anti-obesity effects in obese mice by decreasing in serum lipid levels and lipogenesis related gene.