• Asian Pacific Journal of Cancer Prevention
• /
• v.17 no.1
• /
• pp.1-13
• /
• 2016

The evidence for the existence of a common pathway for health issues in men is presented in this review. Several epidemiological studies have shown that conditions like cardiovascular diseases (CVD), metabolic syndrome, diabetes, lower urinary tract symptom (LUTS), erectile dysfunction (ED), prostate cancer, hypogonadism, depression and suicide can be associated as risk factors for each other. Thus, the risk of CVD is significantly increased in men with metabolic syndrome, ED, hypogonadism, prostate cancer and/or LUTS. In addition, the above mentioned conditions are more prevalent in atherosclerotic patients. In addition, growing evidence indicates that low androgen levels can cause metabolic syndrome. In addition, obesity, dyslipidaemia and diabetes can further reduce androgen levels potentiating their adverse effect. Low testosterone levels are also associated with a higher incidence of aggressive prostate cancer on biopsy and on definitive pathology, and lower probability of abiraterone response in the metastatic setting. Several recent studies point towards diffuse endothelial dysfunction and dysregulated pro-inflammatory state as the biological link between all these disorders. Our current hypothesis is that oxidative stress caused by these dysfunctions explains the pathogenesis of each of these conditions.

• Molecules and Cells
• /
• v.41 no.6
• /
• pp.603-611
• /
• 2018

Triglyceride homeostasis is a key process of normal development and is essential for the maintenance of energy metabolism. Dysregulation of this process leads to metabolic disorders such as obesity and hyperlipidemia. Here, we report a novel function of the Drosophila flightless-I (fliI) gene in lipid metabolism. Drosophila fliI mutants were resistant to starvation and showed increased levels of triglycerides in the fat body and intestine, whereas fliI overexpression decreased triglyceride levels. These flies suffered from metabolic stress indicated by increased levels of trehalose in hemolymph and enhanced phosphorylation of eukaryotic initiation factor 2 alpha ($eIF2{\alpha}$). Moreover, upregulation of triglycerides via a knockdown of fliI was reversed by a knockdown of desat1 in the fat body of flies. These results indicate that fliI suppresses the expression of desat1, thereby inhibiting the development of obesity; fliI may, thus, serve as a novel therapeutic target in obesity and metabolic diseases.

• Journal of Ginseng Research
• /
• v.48 no.2
• /
• pp.129-139
• /
• 2024

Liver diseases are a significant global health burden and are among the most common diseases. Ginssennoside Rg3 (Rg3), which is one of the most abundant ginsenosides, has been found to have significant preventive and therapeutic effects against various types of diseases with minimal side effects. Numerous studies have demonstrated the significant preventive and therapeutic effects of Rg3 on various liver diseases such as viral hepatitis, acute liver injury, nonalcoholic liver diseases (NAFLD), liver fibrosis and hepatocellular carcinoma (HCC). The underlying molecular mechanism behind these effects is attributed to apoptosis, autophagy, antioxidant, anti-inflammatory activities, and the regulation of multiple signaling pathways. This review provides a comprehensive description of the potential molecular mechanisms of Rg3 in the development of liver diseases. The article focuses on the regulation of apoptosis, oxidative stress, autophagy, inflammation, and other related factors. Additionally, the review discusses combination therapy and liver targeting strategy, which can accelerate the translation of Rg3 from bench to bedside. Overall, this article serves as a valuable reference for researchers and clinicians alike.

• Journal of Preventive Medicine and Public Health
• /
• v.41 no.1
• /
• pp.39-44
• /
• 2008

Objectives : This study was conducted to investigate the associations of non alcoholic fatty liver with metabolic syndrome and the serum carotenoids. Methods : This study was conducted in a general hospital in South Korea from November, 2004 to August, 2005. The study subjects were 350 sampled persons who were aged from 40 years and older (males : 180, females : 170). They were grouped into the normal, mild and severe groups according to fat accumulation in their livers, as determined by ultrasonography. We analyzed the association between non alcoholic fatty liver and metabolic syndrome by multiple logistic regression analysis and we analyzed the association between non alcoholic fatty liver and the serum carotenoids by a general linear model(ANCOVA). Results : After adjustment for the effect of potential covariates, the prevalence of metabolic syndrome was associated with fat accumulation in the liver (p trend <0.001). If the odds ratio of normal group is 1.00, then that of the mild group is 2.80 (95% C.I=1.17-6.71) and that of the severe group is 7.29 (95% C.I=2.76-19.30). The prevalence of metabolic alterations fitting the criteria of metabolic syndrome, according to the class of fat accumulation in the liver, was significantly increased, except for criteria of high blood pressure, a large waist circumference and low HDL (high density lipoprotein) cholesterol level (p trend <0.001). The level of serum ${\beta}$-carotene was decreased according to the class of fat accumulation in the liver (p trend=0.036), but the levels of serum ${\alpha}$-carotene, lycopene, ${\beta}$-cryptoxanthin and lutein were not decreased. Conclusions : This study shows that non alcoholic fatty liver was associated with metabolic syndrome and with the serum ${\beta}$-carotene level.

• Korean Journal of Clinical Laboratory Science
• /
• v.53 no.4
• /
• pp.285-295
• /
• 2021

Sleep plays an important role in maintaining overall human health. There is increasing interest regarding the impact of sleep related disorders on metabolic diseases. Obstructive sleep apnea (OSA) is a common health problem, and in the last decade, the emergence of increasing obesity rates has further led to a remarkable increase in the prevalence of OSA, along with more prominent metabolic diseases. Obesity is the strongest risk factor for OSA. However, OSA is also known to cause obesity, suggesting an interaction between OSA and obesity. Although the underlying mechanisms leading to OSA-induced metabolic diseases are probably multi-factorial and are yet to be fully elucidated, the activation of inflammation and oxidative stress and the dysregulation of appetite-regulating hormones have emerged as important pathophysiological components of metabolic dysfunction and obesity observed in patients with OSA. Here, we will review the current state of research regarding the association of OSA with metabolic diseases and the possible pathophysiological mechanisms by which OSA could lead to such diseases. This will enhance our understanding of the potential interactions between OSA and obesity and between OSA and metabolic dysfunction.

• Journal of Oriental Neuropsychiatry
• /
• v.26 no.1
• /
• pp.63-78
• /
• 2015

Objectives: Pinelliae Rhizoma has traditionally been used as an anti-depressant in oriental medicine. This study is to investigate the effect of Pinelliae Rhizoma extract (PRe) on psychological stress in genome wild expression of mice. Methods: After giving physical stress to mice, PRe was orally administered with 100 mg/kg/day for five days. After extracting whole brain tissue from the mice, their genome changes were observed by micorarray analysis method. The genome changes were analyzed by IMAGENE 4.0, TREEVIEW, FatiGo algorithems, BOND database, cytoscape program, etc. Results: 1. PRe administered group were remained at normal level; 60% of increase was shown in expressed genes by physical stress, and 65% of decrease was shown in expressed genes by psychological stress. 2. Genes with increased expression in control group that remained at a normal state in PRe administered group were involved with the gene of a cellular metabolic process on biological process, protein binding on molecular function, and cell part on cell composition. The pathway was found to be cytokin-cytokin receptor interaction. 3. Genes with decreased expression in control group that remained at a normal state in PRe administered group were involved with the gene of a cellular metabolic process on biologiacl detail and coupled ATPaes activity on molecular function. This gene related path was Ubiquintin mediated proteolysis etc. 4. Core node genes analyzed by protein interaction network were Vinculin, Cell sdivision cycle 42 homolog (S. cerevisiae) etc. They played an important role in maintaining cytoskeleton and controlling cell cycle. Conclusions: Several genes were up-regulated and down-regulated in response to psychological stress. The expression of most of the genes that were altered in response to psychological stress was restored to normal levels in PRe treated mice. When the interaction network information was analyzed, the recovery of the core node genes in PRe treated mice indicates that this final set of genes may be the effective target of PRe.

• Nutrition Research and Practice
• /
• v.16 no.5
• /
• pp.549-564
• /
• 2022

BACKGROUND/OBJECTIVES: Oxidative stress is caused by an imbalance between harmful free radicals and antioxidants. Long-term oxidative stress can lead to an "exhausted" status of antioxidant defense system triggering development of metabolic syndrome and chronic inflammation. Green perilla (Perilla frutescens) is commonly used in Asian cuisines and traditional medicine in southeast Asia. Green perilla possesses numerous beneficial effects including anti-inflammatory and antioxidant functions. To investigate the potentials of green perilla leaf extract (PE) on oxidative stress, we induced oxidative stress by high-fat diet (HFD) in aging mice. MATERIALS/METHODS: C57BL/6J male mice were fed HFD continuously for 53 weeks. Then, mice were divided into three groups for 12 weeks: a normal diet fed reference group (NDcon), high-fat diet fed group (HDcon), and high-fat diet PE treated group (HDPE, 400 mg/kg of body weight). Biochemical analyses of serum and liver tissues were performed to assess metabolic and inflammatory damage and oxidative status. Hepatic gene expression of oxidative stress and inflammation related enzymes were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: PE improved hepatopathology. PE also improved the lipid profiles and antioxidant enzymes, including hepatic glutathione peroxidase (GPx) and superoxide dismutase (SOD) and catalase (CAT) in serum and liver. Hepatic gene expressions of antioxidant and anti-inflammatory related enzymes, such as SOD-1, CAT, interleukin 4 (IL-4) and nuclear factor erythroid 2-related factor (Nrf2) were significantly enhanced by PE. PE also reduced the levels of hydrogen peroxide (H₂O₂) and malondialdehyde (MDA) in the serum and liver; moreover, PE suppressed hepatic gene expression involved in pro-inflammatory response; Cyclooxygenase-2 (COX-2), nitric oxide synthase (NOS), interleukin 1 beta (IL-1β), and interleukin 6 (IL-6). CONCLUSIONS: This research opens opportunities for further investigations of PE as a functional food and possible anti-aging agent due to its attenuative effects against oxidative stress, resulting from HFD and aging in the future.

• The Plant Pathology Journal
• /
• v.17 no.2
• /
• pp.88-93
• /
• 2001

Oxidative stress is one of the major limiting factor in plant productivity. Reactive oxygens species (ROS) generated during metabolic processes damage cellular functions and consequently lead to disease, senescence and cell death. Plants have evolved an efficient defense system by which the ROS is scavenged by antioxidant enzymes such as superoxide dismutase (SOD) and ascorbate peroxidase (APX). Attempts to reduce oxidative damages under the stress conditions have included the manipulation of 갠 scavenging enzymes by gene transfer technology. Increased SOD activities of transgenic plants lead to increased resistance against oxidative stresses derived from methyl viologen (MV), and from photooxidative damage caused by high light and low temperature. Transgenic tobacco plants overexpressing APX showed reduced damage following either MV treatment of photooxidative treatment. Overexpression of glutathion reductase (GR) leads to increase in pool of ascorbate and GSH, known as small antioxidant molecules. These results indicate through overexpression of enzymes involved in ROS-scavenging could maintain or improve the plant productivities under environment stress condition. In this study, the rational approaches to develop stress-tolerant plants by gene manipulation of antioxidant enzymes will be introduced to provide solutions for the global food and environmental problems in the $21^\textrm{st}$ century.

• Asian-Australasian Journal of Animal Sciences
• /
• v.6 no.1
• /
• pp.87-89
• /
• 1993

Cortisol levels in plasma are known to be as an indication of reproductive and adrenal status of an animal. In this study it has been examined in relation to the oestrus induction by Progesterone oestrogen therapy in 3rd and 4th parity anoestrus animals. Cortisol was found higher in treated animals and levels raised within 6-12 hrs. after hormone therapy followed by elevation in glucose levels and depletion of total serum proteins. It shows the association of induction, occurrence and expression of oestrus with energy demanding metabolic stress in buffaloes.

• YAKHAK HOEJI
• /
• v.51 no.1
• /
• pp.75-82
• /
• 2007

Reactive oxygen species (ROS) are produced in the metabolic process of oxygen in cells. The superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in cells systemize the antioxidant enzymes to control the oxidative stress. Genistein is one of the isoflavonoids, and its role in controlling cellular oxidative stress is presently the active issue at question. In this study; we analyzed genistein-induced survival rates of the CHO-K1 cells, activities of antioxidant enzymes, ROS levels, and expression levels of antioxidant enzyme genes in order to investigate the effect of genistein on cellular ROS production and antioxidative systems in CHO-K1 cells. As results, the survival rate of cells was decreased as the dose of genistein increases (12.5${\sim}$200 ${\mu}$M). Genistein increased cellular ROS levels, while it reduced total SOD activities and the expression of CuZnSOD. In conclusion, we suggest that genistein may induce oxidative stress via down-regulation of SOD.