The application of polyphenols has attracted great interest in the field of functional foods and nutraceuticals due to their potential health benefits in humans. However, the effectiveness of polyphenols depends on their bioactivity and bioavailability. In the present study, the bioactive component from green tea extract (GTE) was administrated orally (50 mg/kg body weight/day) as free or in a microencapsulated form with maltodextrin in rats fed a high fructose diet. High fructose diet induced features of metabolic syndrome including hypertriglyceridemia, hyperuricemia, increased serum total cholesterol, and retroperitoneal obesity. In addition, myocardial fibrosis was increased. In rats receiving high fructose diet, the lowering of blood triglycerides, total cholesterol, non esterified fatty acid (NEFA) and uric acid, as well as the reduction in final body weight and retroperitoneal fat weight associated with the administration of GTE, led to a reversal of the features of metabolic syndrome (P < 0.05). In particular, the administration of microencapsulated GTE decreased myocardial fibrosis and increased liver catalase activity consistent with a further alleviation of serum NEFA, and hyperuricemia compared to administration of GTE. Taken together, our results suggest that microencapsulation of the bioactive components of GTE might have a protective effect on cardiovasucular system by attenuating the adverse features of myocardial fibrosis, decreasing uric acid levels and increasing hepatic catalase activity effectively by protecting their bioactivities.
Journal of The Korean Society of Inherited Metabolic disease
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v.15
no.2
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pp.55-58
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2015
Tetrahydrobiopterin ($BH_4$) can normalize blood phenylalanine (Phe) levels in $BH_4$ deficiency, but typically not in phenylketonuria (PKU). In 1999, Kure et al. reported that some PKU patients showed decreased blood Phe levels after $BH_4$ loading, and thereafter, those PKU patients were identified by neonatal PKU screening. A natural cofactor for phenylalanine hydroxylase (PAH) is a 6R-isomer of $BH_4$, which is first synthesized in Japan as Sapropterin dihydrochloride (Biopten$^{(R)}$) in 1982. In Japan, Biopten$^{(R)}$ is first approved for the treatment of $BH_4$ deficiency in 1992, and then for $BH_4$-responsive PAH deficiency (BPKU) in 2008. The discovery of BPKU has vast clinical implications. After Biopten$^{(R)}$ (Kuvan$^{(R)}$) is available for the treatment of BPKU, the QOL of both patients and their families were improved very much, since the serum phenylalanine levels were controlled within 4 mg/dL by $BH_4$ mono-therapy with a normal diet or $BH_4$ combined use of mild phenylalanine-restricted diet. Biopten$^{(R)}$ therapy in patients with BPKU is highly efficacious (70%) at maintaining serum Phe levels within recommended control range and provides excellent safety at least average use period of 10 years (range, 1-17 years) with no unwarranted side effects in Japan. In addition it has been confirmed that sapropterin therapy initiated before 4 years of age was very effective to maintain plasma Phe levels within the favorable range and was safe in Japanese patients with BPKU.
Background: Insulin resistance is an integral feature of metabolic syndromes, including obesity, hyperglycemia, and hyperlipidemia. In this study, we evaluated whether the aloe component could reduce obesity-induced inflammation and the occurrence of metabolic disorders such as blood glucose and insulin resistance. 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 lowered fasting blood glucose and plasma insulin compared with HFD. Obesity-induced inflammatory cytokine (IL-$1{\beta}$, -6, -12, TNF-${\alpha}$) and chemokine (CX3CL1, CCL5) mRNA and protein were decreased markedly, as was macrophage infiltration and hepatic triglycerides by Aloe QDM. At the same time, Aloe QDM decreased the mRNA and protein of $PPAR{\gamma}/LXR{\alpha}$ and $11{\beta}$-HSD1 both in the liver and WAT. Conclusion: Dietary aloe formula reduces obesity-induced glucose tolerance not only by suppressing inflammatory responses but also by inducing anti-inflammatory cytokines in the WAT and liver, both of which are important peripheral tissues affecting insulin resistance. The effect of Aloe QDM complex in the WAT and liver are related to its dual action on $PPAR{\gamma}$ and $11{\beta}$-HSD1 ression and its use as a nutritional intervention against T2D and obesity-related inflammation is suggested.
Background: Dietary fat has been suggested to be the cause of various health issues. Obesity, hypertension, cardiovascular disease, diabetes, dyslipidemia, and kidney disease are known to be associated with a high-fat diet (HFD). Obesity and associated conditions, such as type 2 diabetes mellitus and nonalcoholic fatty liver disease (NAFLD), are currently a worldwide health problem. Few prospective pharmaceutical therapies that directly target NAFLD are available at present. A Traditional Chinese Medicine, ginseng-plus-Bai-Hu-Tang (GBHT), is widely used by diabetic patients to control glucose level or thirst. However, whether it has therapeutic effects on fat-induced hepatic steatosis and metabolic syndrome remains unclear. Methods: This study was conducted to examine the therapeutic effect of GBHT on fat-induced obesity, hepatic steatosis, and insulin resistance in mice. Results: GBHT protected mice against HFD-induced body weight gain, hyperlipidemia, and hyperglycemia compared with mice that were not treated. GBHT inhibited the expansion of adipose tissue and adipocyte hypertrophy. No ectopic fat deposition was found in the livers of HFD mice treated with GBHT. In addition, glucose intolerance and insulin sensitivity in HFD mice was also improved by GBHT. Conclusion: GBHT prevents changes in lipid and carbohydrate metabolism in a HFD mouse model. Our findings provide evidence for the traditional use of GBHT as therapy for the management of metabolic syndrome.
BACKGROUND/OBJECTIVES: Non-alcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver disease and is closely associated with metabolic syndrome. In the present study, we observed the effect of ethanol extract of Allium fistulosum (EAF) on NAFLD and have suggested the possibility of using EAF as a natural product for application in the development of a treatment for NAFLD. MATERIALS/METHODS: The preventive effect on hepatic lipid accumulation was estimated by using an oleic acid (OA)-induced NAFLD model in vitro and a Western diet (high-fat high-sucrose; WD)-induced obese mouse model. Animals were divided into three groups (n = 7): normal diet group (ND), WD group, and WD plus 1% EAF group. RESULTS: EAF reduced OA-stimulated lipid accumulation in HepG2 cells in the absence of cellular cytotoxicity and significantly blocked transcriptional activation of sterol regulatory element-binding protein 1 and fatty acid synthase genes. Subsequently, we investigated these effects in vivo in mice fed either ND or WD in the presence or absence of EAF supplementation. In comparison to the ND controls, the WD-fed mice exhibited increases in body weight, liver weight, epididymal fat weight, and accumulation of fat in hepatocytes, and these effects were significantly attenuated by EAF supplementation. CONCLUSIONS: Allium fistulosum attenuates the development of NAFLD, and EAF elicits anti-lipogenic activity in liver. Therefore, EAF represents a promising candidate for use in the development of novel therapeutic drugs or drug combinations for the prevention and treatment of NAFLD.
Yoon, Nal Ae;Park, Juyeong;Jeong, Joo Yeon;Rashidova, Nilufar;Ryu, Jinhyun;Roh, Gu Seob;Kim, Hyun Joon;Cho, Gyeong Jae;Choi, Wan Sung;Lee, Dong Hoon;Kang, Sang Soo
Development and Reproduction
/
v.23
no.2
/
pp.129-138
/
2019
In many cases, obesity is associated with metabolic disorders. Recently, natural compounds that may be beneficial for improving obesity have received increasing attention. Bitter melon has received attention as a diabetes treatment. $NAD^+$-dependent deacetylase (Sirtuin 1, SIRT1) has emerged as a novel therapeutic target for metabolic diseases. In this study, ethanol extract of bitter melon (BME) suppressed adipocyte differentiation and significantly increased the expression of SIRT1 in fully differentiated 3T3-L1 cells. Moreover, it enhanced the activation of AMP-activated protein kinase (AMPK). In high-fat diet (HFD)-fed induced-obesity mice, BME suppressed HFD-induced increases in body weight and white adipose tissue (WAT) weight. BME also increased the expression of SIRT1 and suppressed peroxisome proliferator-activated receptor and sterol regulatory element binding protein 1 expressions of WAT from HFD-fed mice. These findings suggest that BME prevents obesity by activating the SIRT1 and AMPK pathway and that it may be a useful dietary supplement for preventing obesity.
This study was done to evaluate the effect of Ca source using fish (Tilapia mossambica) scales on the bone metabolism. Male Sprague-Dawley rats, 4 weeks of age, were fed low-calcium diet (0.15% Ca) for 2 weeks. The rats on the low-calcium diet were further assigned to one of following three groups for an additional 4 weeks: 1) Ca-depletion group (LoCa) given 0.15% Ca diet ($CaCO_3$), 2) Ca-repletion group (AdCa) given 0.5% Ca diet ($CaCO_3$), 3) Ca-repletion diet (AdFa) received 0.5% Ca diet (Ca source from Tilapia mossambica scales). Serum parathyroid (PTH) and calcitonin showed no differences among experimental groups. Whereas LoCa group elevated the turnover markers, serum ALP and osteocalcin, and urinary deoxypyridinoline (DPD), AdCa and AdFa groups reduced their values. Elevation in the femoral weight, ash and Ca contents was observed in AdCa and AdFa groups. Bone mineral density was increased in AdCa and AdFa groups by 25-26% compared with LoCa group. These data demonstrate that Ca repletion with either Ca source from Tilapia mossambica scales or $CaCO_3$ is similarly effective in the improvement of bone turnover markers and BMD, suggesting the usefulness of Tilapia mossambica scales in the prevention of bone loss compared with $CaCO_3$.
The purpose of this study was to investigate the effects of either chrysin or exercise on the inflammasome and thermogenic markers in the livers of high-fat fed mice. C57BL/6 mice were randomly assigned to four groups: normal diet control (NC; n=5), high-fat diet control (HC; n=5), high-fat diet with chrysin (Hch; n=5), and high-fat diet with moderate exercise (HME; n=5). The mice were fed a high-fat diet (60% of calories from fat) or normal diet (18% of calories from fat). Chrysin was supplemented orally as 50mg/kg/day dissolved in a 0.1ml solution of dimethyl sulfoxide. The exercised mice ran on a treadmill at 12-20 m/min for 30-60 min/day, 5 times/week, for 16 weeks. After the intervention, the epididymal fat and liver weights were significantly decreased in the HME group compared with HC and Hch groups. The adipocyte size was effectively decreased in the Hch and HME groups compared with the HC group. The inflammasome markers NLRP3, $IL-1{\beta}$, and caspase1 were significantly decreased in the Hch and HME groups compared with the HC group. The thermogenic markers $PGC-1{\alpha}$ and BMP7 were significantly lower in the HC than in the NC group. However, the HME group showed an increase in the thermogenic markers. In conclusion, chrysin and moderate exercise have positive effects on obese metabolic complications induced by high-fat diets by reducing inflammasome genes. However, chrysin supplementation had no effect on thermogenic gene expression. Moderate exercise would therefore seem to be more effective in controlling obesity-induced metabolic deregulation.
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.
Lee Chang Hyun;Han Woong;Kim Young Soo;Lee Kwang Gyu
Journal of Physiology & Pathology in Korean Medicine
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v.18
no.1
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pp.187-193
/
2004
Constipation is a common clinical problem that comprises of symptoms that include excessive straining, hard feces, feeling of incomplete evacuation and infrequent defecation. Although many conditions, such as metabolic problems, fiber deficiency, anorectal problem, an drug, can cause constipation. This study was examined the effects of Chilsun-Whan on intestinal mucosa and gastrointestinal transit time and plasma lipids in rats. Adult male rats were fed for weeks on diets containing no addition(basal diet group), 5% cellulose(cellulose group) and 2.5% . Chilsun-Whan group(Chilsun-Whan group). The results were as follows; 1. The fecal weght was significantly increased 2 times in Chilsun-Whan administrated group compare to basal diet group. 2. The gastrointestinal transit times was significantly decreased in Chilsun-Whan administrated group compare to basal diet. 3. Carmine red mixed with Chilsun-Whan, as a marker, was administered through a gastric tube for stomach or intracecally by a chronically implanted catheter for colon transit. Small intestinal transit and large intestinal transit time were significantly decreased in Chilsun-Whan administrated group compare to basal diet. 4. The height of jejunal villi was developed in Chilsun-Whan administrated group compare to basal diet The thickness of mucosa and muscle layer of colonic mucosa were significantly developed in Chilsun-Whan administrated group compare to basal diet group. 5. The change of goblet cell in colonic mucosa was increased acid mucin stained alcian blue in Chilsun-Whan administrated group compare to basal diet and cellulose group. 6. HDL-cholesterol of plasma lipid was increased in Chilsun-Whan administrated group compare to basal diet and cellulose groups. Theses results suggests that Chilsun-Whan may be used in prevention and treatment of constipation resulting in increase of fecal weight, decrease of gastrointestinal transit time. development of intestinal villi, intensify of stainability of acid mucin in colon.
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