|Effect of dietary resveratrol on the metabolic profile of nutrients in obese OLETF rats.|
|Jump to Full Text|
|PMID: 23374859 Owner: NLM Status: MEDLINE|
|BACKGROUND: Resveratrol (trans-3,4',5-trihydroxystilbene) is a naturally occurring phytoalexin produced by plants in response to various stresses. Several studies have shown that resveratrol is present in significant amounts in a variety of human diets, including wines, grapes, berries, and peanuts, and it possesses several beneficial health properties, such as atheroprotective, anti-obesity, anti-cancer, anti-inflammatory and antioxidant activities. In this study, we evaluated the effect of resveratrol on the pathogenesis of obesity and the metabolic profile of nutrients in non-high fat-fed obese OLETF rats.
RESULTS: Although lipid parameters in the serum and liver were not changed, the accumulation of abdominal white adipose tissues was markedly prevented in resveratrol diet-fed OLETF rats after 4 weeks of feeding. The results of the respiratory gas analysis indicated that dietary resveratrol induced the partial enhancement of fat metabolism and sparing actions for carbohydrate and protein at 1 week and 3 weeks of feeding in OLETF rats. Additionally, the adipose mRNA level of carnitine palmitoyltransferase in the resveratrol diet-fed OLETF rats was higher than the control rats after 4 weeks of feeding.
CONCLUSION: Our study demonstrated that dietary resveratrol can prevent obesity through a change in the metabolic profile of nutrients in obese OLETF rats.
|Koji Nagao; Tomoyuki Jinnouchi; Shunichi Kai; Teruyoshi Yanagita|
Related Documents :
|24630669 - Supplemental fat for dairy calves during mild cold stress.
23606129 - Beneficial effects of allium sativum l. stem extract on lipid metabolism and antioxidan...
24094539 - Genetic parameters of different measures of cheese yield and milk nutrient recovery fro...
24870269 - Growth performance, gastrointestinal function and meat quality in growing-finishing tur...
24563229 - Residual feed intake as a feed efficiency selection tool and its relationship with feed...
508699 - The effect of pectin on the structure and function of the rat small intestine.
19871239 - Effects of excess dietary cysteic acid, dl-methionine, and taurine on the rat liver.
23712399 - Performance and characteristics of carcass and non-carcass components of lambs fed peac...
6537869 - Hypocholesterolemic effect of dietary soy protein versus casein in rhesus monkeys (maca...
|Type: Journal Article Date: 2013-02-04|
|Title: Lipids in health and disease Volume: 12 ISSN: 1476-511X ISO Abbreviation: Lipids Health Dis Publication Date: 2013|
|Created Date: 2013-04-17 Completed Date: 2013-06-27 Revised Date: 2013-07-11|
Medline Journal Info:
|Nlm Unique ID: 101147696 Medline TA: Lipids Health Dis Country: England|
|Languages: eng Pagination: 8 Citation Subset: IM|
|Department of Applied Biochemistry and Food Science, Saga University, Saga 840-8502, Japan. email@example.com|
|APA/MLA Format Download EndNote Download BibTex|
Adipose Tissue, White
Body Weight / drug effects
Carnitine O-Palmitoyltransferase / genetics, metabolism
Cholesterol / metabolism
Gene Expression / drug effects
Glycogen / metabolism
Lipid Metabolism / drug effects*
Liver / drug effects*, metabolism
Obesity / metabolism*, prevention & control*
RNA, Messenger / genetics
Rats, Inbred OLETF
Stilbenes / administration & dosage*
Triglycerides / metabolism
|0/RNA, Messenger; 0/Stilbenes; 0/Triglycerides; 57-88-5/Cholesterol; 9005-79-2/Glycogen; EC 22.214.171.124/Carnitine O-Palmitoyltransferase; Q369O8926L/resveratrol|
Journal ID (nlm-ta): Lipids Health Dis
Journal ID (iso-abbrev): Lipids Health Dis
Publisher: BioMed Central
Copyright ©2013 Nagao et al.; licensee BioMed Central Ltd.
Received Day: 23 Month: 12 Year: 2012
Accepted Day: 31 Month: 1 Year: 2013
collection publication date: Year: 2013
Electronic publication date: Day: 4 Month: 2 Year: 2013
Volume: 12First Page: 8 Last Page: 8
PubMed Id: 23374859
Publisher Id: 1476-511X-12-8
|Effect of dietary resveratrol on the metabolic profile of nutrients in obese OLETF rats|
|Koji Nagao1||Email: firstname.lastname@example.org|
|Tomoyuki Jinnouchi1||Email: email@example.com|
|Shunichi Kai1||Email: firstname.lastname@example.org|
|Teruyoshi Yanagita12||Email: email@example.com|
1Department of Applied Biochemistry and Food Science, Saga University, Saga, 840-8502, Japan
2Department of Health and Nutrition Sciences, Nishikyushu University, Kanzaki, 842-8585, Japan
Lifestyle-related diseases, such as hyperlipidemia, arteriosclerosis, diabetes mellitus, and hypertension, are widespread and increasingly prevalent in industrialized countries and contribute to the increase in cardiovascular morbidity and mortality [1,2]. Accompanied by the rapid increase in the number of elderly people, they are important not only medically but also socioeconomically. Although the pathogenesis of lifestyle-related diseases is complicated and the precise mechanisms have not been elucidated, obesity has emerged as one of the major cardiovascular risk factors according to epidemiologic studies [3-5]. Obesity is defined as an increased mass of adipose tissue, and its prevalence and severity are markedly increasing in Westernized countries.
Diet has been recognized as a factor that contributes to the development and prevention of lifestyle-related diseases, and various natural molecules in plants and fruits have been used in folk medicines throughout the world for treating those diseases [6-10]. Resveratrol (trans-3,4′,5-trihydroxystilbene) is a naturally occurring phytoalexin produced by plants in response to various stresses. Several studies have shown that resveratrol is present in significant amounts in a variety of human diets, including wines, grapes, berries, and peanuts, and it possesses several beneficial health properties, such as atheroprotective, anti-cancer, anti-inflammatory and antioxidant activities [11-13]. Recent studies have also reported that resveratrol has anti-obesity effects in high-fat-fed mice and rats [14,15]. However, the effects of resveratrol on the metabolic profile of nutrients and body fat accumulation in non-high-fat diet-fed rodents have not been fully evaluated. Otsuka Long-Evans Tokushima fatty (OLETF) rats develop a syndrome with multiple metabolic and hormonal disorders that shares many features with human obesity [16-18]. OLETF rats have hyperphagia because they lack receptors for cholecystokinin, and they become obese even by consuming a normal diet (AIN-76, 7% fat diet) [19-21]. Therefore, we evaluated the effect of resveratrol on the pathogenesis of obesity and the metabolism of carbohydrate, fat, and protein in obese OLETF rats.
All aspects of the experiment were conducted according to the guidelines provided by the ethical committee for experimental animal care of Saga University. Six-week-old male OLETF rats were purchased from Hoshino Laboratory Animals, Inc. (Ibaraki, Japan). The rats were individually housed in metal cages in a temperature-controlled room (24°C) under a 12 h light/dark cycle. After a 1-week adaptation period on a powder chow diet (CE-2, Clea Japan, Tokyo), they were assigned to two groups (six rats each), each fed one of two diets: (i) a semi-synthetic diet containing (in weight %): casein, 20; corn oil, 7; cornstarch, 15; vitamin mixture (AIN-76™), 1; mineral mixture (AIN-76™), 3.5; DL-methionine, 0.3; choline bitartrate, 0.2; cellulose, 5; and sucrose, 45 (control group); or (ii) a semi-synthetic diet supplemented with 0.5% of resveratrol (Wako Pure Chemicals, Tokyo, Japan) at the expense of sucrose. The animals received the different diets for 4 weeks. The composition of the semi-synthetic diets is shown in Table 1. The rats were subjected to respiratory gas analysis after 1 week and 3 weeks of consuming the experimental diets. At the end of the feeding period and after a 9 h starvation period, all rats were killed by aortic exsanguination under diethyl ether anesthesia. The abdominal (perirenal, epididymal, and omental) white adipose tissue (WAT) and livers were excised immediately, and the serum was separated from the blood.
The liver lipids were extracted, and the concentrations of triglyceride and cholesterol were determined as described elsewhere . The glycogen levels were determined according to the method of Lo et al. .
The serum triglyceride, cholesterol, and glucose levels were measured using commercial enzyme assay kits (Wako Pure Chemicals, Tokyo, Japan).
The instruments and software used for the measurement of the oxygen consumption and respiratory quotient in the rats were obtained from Arco system (Chiba, Japan). The system consisted of six acrylic metabolic chambers, a mass spectrometer (model WSMR-1400), a gas sampler (model WGSS-1000), and a switching controller (model WMSC-2000). Each metabolic chamber had a 210 cm2 floor and was 11.5 cm in height. Room air was pumped through the chambers at a rate 1.8 L/min. Expired air was dried in a cotton-thin column and then directed to a mass spectrometer. Air from each chamber was sampled for 1 min. Therefore, air from each chamber was measured every 7 min, and data were recorded in a spreadsheet. The respiratory quotient (RQ) and energy production rate were calculated by the software using the following formulas: RQ = VCO2/VO2 and energy production rate = (2.96*RQ + 2.49)*VO2, where VO2 is the oxygen consumption, and VCO2 is the carbon dioxide exhaustion. Additionally, 24 h urine samples were collected, and oxygen production from protein metabolism (VO2-P) was calculated from the urinary nitrogen concentration (UN). The UN was determined using an assay kit (Urinary nitrogen test from Wako Pure Chemicals, Tokyo, Japan), and VO2-P was calculated using the following formula: VO2-P = UN*5.923. Thus, the energy metabolism was compared between the two groups using the values of non-protein oxygen consumption and non-protein energy expenditure. After 1 week or 3 weeks of consuming the semi-synthetic diets, each animal was placed into a metabolic chamber for 24 h respiratory gas analysis. During the analysis, the animals were pair-fed and had free access to water. The sampled gases were analyzed in a separate room to avoid stressing the rats.
Total RNA was extracted from 0.1 g of WAT using an RNeasy Lipid Tissue Mini Kit (Qiagen, Tokyo, Japan). A TaqMan Universal PCR Master Mix (Applied Biosystems, Tokyo, Japan) and Assay-on-Demand Gene Expression Products (Rn00569117_m1 for fatty acid synthase (FAS), Rn00580702_m1 for carnitine palmitoyltransferase (CPT), Rn00566193_m1 for peroxisome proliferator-activated receptor (PPAR)-α, Rn00565707_m1 for PPAR-δ, Rn00440945_m1 for PPAR-γ, and Hs99999901_s1 for 18S RNA, Applied Biosystems) were used for quantitative real-time RT-PCR analysis of FAS, CPT, PPARα, PPARδ, PPARγ, and 18S RNA expression in the liver. Amplification was performed with a real-time PCR system (ABI Prism 7000 Sequence Detection System; Applied Biosystems). The results were quantified with a comparative method and expressed as a relative value after normalization to 18S RNA expression.
All of the values are expressed as the mean ± standard error. The significance of the differences between the means of the two groups was determined by Student’s t-test. Differences were considered to be significant at p < 0.05.
The two groups of OLETF rats did not differ in their initial body weight, final body weight, or food intake during or after the 4-week feeding period (Table 2). Although lipid parameters in the serum and liver were not changed (Table 2), the accumulation of abdominal WAT was markedly prevented in the resveratrol-diet-fed OLETF rats after 4 weeks of feeding (Figure 1). These results indicate that resveratrol can prevent obesity in non-high-fat diet-fed obese OLETF rats.
Several studies have shown that functional food components produce anti-obesity effects by altering energy metabolism [24-27]. Their actions may have altered the energy expenditure or influenced the balance of nutrient metabolism, which affects body composition. To examine the effect of the resveratrol diet on the oxidation of nutrients, respiratory gas analysis was performed at 1 week and 3 weeks of feeding in OLETF rats. Because amount of food intake affects energy metabolism, rats were fed same amount of diets (12 g at 1 week and 14 g at 3 weeks) during the measurement. As the results, the total oxygen consumption and energy expenditure were not altered by dietary resveratrol at 1 week or 3 weeks of feeding (data not shown). However, carbohydrate oxidation (control, 4.87 ± 0.12; resveratrol, 4.43 ± 0.12 g/day/100 g body weight; P < 0.05) and protein oxidation (control, 0.402 ± 0.030; resveratrol, 0.286 ± 0.036 g/day/100 g body weight; P < 0.05) were significantly lowered in the resveratrol diet-fed OLETF rats at the 1 week of feeding period. Moreover, dietary resveratrol induced the partial enhancement of fat oxidation (Figure 2B) and suppressed carbohydrate (Figure 2A &2C) and protein (Figure 2E) oxidation after 3 weeks of feeding in OLETF rats. These results suggest that dietary resveratrol has an anti-obesity effect through the alteration of metabolic profiles of nutrients in obese OLETF rats.
Glycogen is the storage form of carbohydrates and is primarily found in the liver and muscles, and hepatic glycogen is converted into glucose for use throughout the body. Fat (or adipose tissue) is also storage fuel and is recruited for energy fuel when glycogen stores are depleted. In addition, the depletion of glycogen stores has been associated with fatigue and converting structural proteins into fuel sources. Although serum glucose levels were not different between groups, the hepatic glycogen content was 51.6% (not statistically significant) higher in the resveratrol diet-fed OLETF rats after 4 weeks of feeding (Figure 3).
A growing amount of evidence has demonstrated that some strategies can make the body recruit fat rather than glycogen to meet energy demands . A previous study demonstrated that AMPK activity and fuel selection in muscle in response to exercise can be manipulated by diet . Another study also reported that AMPK activation in the liver leads to the stimulation of fatty acid oxidation and inhibition of lipogenesis, glucose production and protein synthesis . Because dietary resveratrol has the potential to activate AMPK , it is possible that resveratrol induced sparing actions for carbohydrates and protein (which contribute to the anti-obesity effect) in OLETF rats.
To gain insight into the effect of dietary resveratrol on lipid metabolism in adipose tissue, we analyzed the mRNA expression of lipid metabolism-related genes by real-time RT-PCR. Previous studies have reported that body fat-lowering effect of resveratrol is mediated by down-regulation of adipogenesis in high-fat-fed mice and rats [14,15]. In contrast, the mRNA levels of FAS, a key enzyme in fatty acid synthesis, were not altered by dietary resveratrol in non-high-fat diet-fed OLETF rats (Figure 4). These results suggest that resveratrol is likely to modulate lipogenesis in a dietary fat-dependent manner. On the other hand, the mRNA levels of CPT, a key enzyme in fatty acid beta-oxidation, were significantly increased in the perirenal WAT of resveratrol-fed OLETF rats (Figure 4). Although the mRNA levels of PPARs, nuclear receptors related to the regulation of lipolysis and adipocyte differentiation, were not altered in this study (Figure 4), previous reports indicated that resveratrol regulates gene expression as a PPARα agonist in vitro[31,32]. Therefore, dietary resveratrol may enhance lipolytic gene expression through the activation of PPARα as a ligand in obese rats. Thus, we propose that the increase in CPT mRNA expression (possibly through the activation of PPARα) might contribute to the partial enhancement of fat oxidation by dietary resveratrol in non-high-fat diet-fed OLETF rats.
In conclusion, our study showed that resveratrol has the potential to suppress body fat accumulation in non-high-fat diet-fed obese OLETF rats. The effect was, at least in part, attributable to the enhancement of fat oxidation and sparing actions for carbohydrates and protein in resveratrol-fed OLETF rats. Further studies are necessary to evaluate the effect of dietary resveratrol on nutrient metabolism in several animal models and determine the lowest effective concentration.
CPT: Carnitine palmitoyltransferase; FAS: Fatty acid synthase; OLETF: Otsuka Long-Evans Tokushima fatty; PPAR: Peroxisome proliferator-activated receptor; RQ: Respiratory quotient; UN: Urinary nitrogen; WAT: White adipose tissue.
The authors declare that they have no competing interests.
KN made substantial contributions to the conception and design of the study, performing the experiment, assembling, analyzing and interpreting the data and drafting the manuscript. TJ and SK participated in the experimental work and in collecting, assembling, analyzing the data. TY contributed to planning the experiment and discussing the results. All authors read and approved the final manuscript.
This work was supported by a research grant from the Japanese Ministry of Education, Culture, Sports, Science and Technology.
|Kissebah AH,Krakower GR,Regional adiposity and morbidityPhysiol RevYear: 1994127618117938225|
|Must A,Spadano J,Coakley EH,Field AE,Colditz G,Detz WH,The disease burden associated with overweight and obesityJAMAYear: 1999121523152910.1001/jama.282.16.152310546691|
|Adler A,Obesity and target organ damage: diabetesInt J Obes Relat Metab DisordYear: 200212S11S1410.1038/sj.ijo.080221212457293|
|Fiegal KM,Carroll MD,Ogden CL,Johnson CL,Prevalence and trends in obesity among U.S. adults 1999–2000AMAYear: 2002121723172710.1001/jama.288.14.1723|
|Pi-Sunyer FX,The medical risks of obesityObes SurgYear: 200212S6S1110.1381/096089202762552601|
|Manach C,Mazur A,Scalbert A,Polyphenols and prevention of cardiovascular diseasesCurr Opin LipidolYear: 200512778410.1097/00041433-200502000-0001315650567|
|Nagao K,Inoue N,Inafuku M,Shirouchi B,Morooka T,Nomura S,Nagamori N,Yanagita T,Mukitake mushroom (Panellus serotinus) alleviates nonalcoholic fatty liver disease through the suppression of monocyte chemoattractant protein-1 production in db/db miceJ Nutr BiochemYear: 20101241842310.1016/j.jnutbio.2009.01.02119423319|
|Inafuku M,Nagao K,Nomura S,Shirouchi B,Inoue N,Nagamori N,Nakayama H,Toda T,Yanagita T,Protective effects of fractional extracts from Panellus serotinus on nonalcoholic fatty liver disease in obese, diabetic db/db miceBr J NutrYear: 20121263964610.1017/S000711451100348521787451|
|Nagao K,Yamano N,Shirouchi B,Inoue N,Murakami S,Sasaki T,Yanagita T,Effects of citrus auraptene (7-geranyloxycoumarin) on hepatic lipid metabolism in vitro and in vivoJ Agric Food ChemYear: 2010129028903210.1021/jf1020329|
|Tsuruta Y,Nagao K,Kai S,Yoshimura T,Tsuge K,Koganemaru K,Yanagita T,Polyphenolic extract of lotus root (edible rhizome of Nelumbo nucifera) alleviates hepatic steatosis in obese diabetic db/db miceLipids Health DisYear: 20111220210.1186/1476-511X-10-20222067945|
|Huang X,Zhu HL,Resveratrol and its analogues: promising antitumor agentsAnticancer Agents Med ChemYear: 20111247949010.2174/18715201179567742721524243|
|Do GM,Jung UJ,Park HJ,Kwon EY,Jeon SM,McGregor RA,Choi MS,Resveratrol ameliorates diabetes-related metabolic changes via activation of AMP-activated protein kinase and its downstream targets in db/db miceMol Nutr Food ResYear: 2012121282129110.1002/mnfr.20120006722715031|
|Gómez-Zorita S,Fernández-Quintela A,Macarulla MT,Aguirre L,Hijona E,Bujanda L,Milagro F,Martínez JA,Portillo MP,Resveratrol attenuates steatosis in obese Zucker rats by decreasing fatty acid availability and reducing oxidative stressCardiovasc Br J NutrYear: 20121220221010.1017/S0007114511002753|
|Kim S,Jin Y,Choi Y,Park T,Resveratrol exerts anti-obesity effects via mechanisms involving down-regulation of adipogenic and inflammatory processes in miceBiochem PharmacolYear: 2011121343135110.1016/j.bcp.2011.03.01221439945|
|Alberdin G,Rodríguez VM,Miranda J,Macarulla MT,Arias N,Andrés-Lacueva C,Portillo MP,Changes in white adipose tissue metabolism induced by resveratrol in ratsNutr MetabYear: 2011122910.1186/1743-7075-8-29|
|Nagao K,Inoue N,Wang YM,Hirata J,Shimada Y,Nagao T,Matsui T,Yanagita T,The 10trans,12cis isomer of conjugated linoleic acid suppresses the development of hypertension in Otsuka Long-Evans Tokushima fatty ratsBiochem Biophys Res CommunYear: 20031213413810.1016/S0006-291X(03)00929-X12788078|
|Arao K,Wang YM,Inoue N,Hirata J,Cha JY,Nagao K,Yanagita T,Dietary effect of pomegranate seed oil rich in 9cis,11trans,13cis conjugated linolenic acid on lipid metabolism in obese, hyperlipidemic OLETF RatsLipids Health DisYear: 2004122410.1186/1476-511X-3-2415533261|
|Wang YM,Nagao K,Inoue N,Ujino Y,Shimada Y,Nagao T,Iwata T,Kamegai T,Yamauchi-Sato Y,Yanagita T,Isomer-specific anti-obese and hypolipidemic properties of conjugated linoleic acid in obese OLETF ratsBiosci Biotechnol BiochemYear: 20061235536210.1271/bbb.70.35516495650|
|Shirouchi B,Nagao K,Inoue N,Ohkubo T,Hibino H,Yanagita T,Effect of dietary omega 3 phosphatidylcholine on obesity-related disorders in obese Otsuka Long-Evans Tokushima Fatty ratsJ Agric Food ChemYear: 2007127170717610.1021/jf071225x17661494|
|Inoue N,Nagao K,Sakata K,Yamano N,Gunawardena ERP,Han SY,Matsui T,Nakamori T,Furuta H,Takamatsu K,Yanagita T,Screening of soy protein-derived hypotriglyceridemic di-peptides in vitro and in vivoLipids Health DisYear: 2011128510.1186/1476-511X-10-8521600040|
|Inoue N,Nagao N,Nomura S,Shirouchi B,Inafuku M,Hirabaru H,Nakahara N,Nishizono S,Tanaka T,Yanagita T,Effect of Vaccinium ashei reade leaf extracts on lipid metabolism in obese OLETF ratsBiosci Biotechnol BiochemYear: 2011122304230810.1271/bbb.11045122146710|
|Shirouchi B,Nagao K,Inoue N,Furuya K,Koga S,Matsumoto H,Yanagita T,Dietary phosphatidylinositol prevents the development of nonalcoholic fatty liver disease in Zucker (fa/fa) ratsJ Agric Food ChemYear: 2008122375237910.1021/jf703578d18324772|
|Lo S,Russell JC,Taylor AW,Determination of glycogen in small tissue samplesJ Appl PhysiolYear: 1970122342365413312|
|Nagao K,Wang YM,Inoue N,Han SY,Buang Y,Noda T,Kouda N,Okamatsu H,Yanagita T,The 10trans,12cis isomer of conjugated linoleic acid promotes energy metabolism in OLETF ratsNutritionYear: 20031265265610.1016/S0899-9007(03)00060-112831953|
|Ikeda I,Konno R,Shimizu T,Ide T,Takahashi N,Kawada T,Nagao K,Inoue N,Yanagita T,Hamada T,Morinaga Y,Tomoyori H,Imaizumi K,Suzuki K,Campest-5-en-3-one, an oxidized derivative of campesterol, activates PPARα, promotes energy consumption and reduces visceral fat deposition in ratsBiochim Biophys ActaYear: 20061280080710.1016/j.bbagen.2006.02.01716616424|
|Nagao K,Yanagita T,Bioactive lipids in metabolic syndromeProg Lipid ResYear: 20081212714610.1016/j.plipres.2007.12.00218177744|
|Nagao K,Yanagita T,Medium-chain fatty acids: Functional lipids for the prevention and treatment of the metabolic syndromePharm ResYear: 20101220821210.1016/j.phrs.2009.11.007|
|Yeo WK,Carey AL,Burke L,Spriet LL,Hawley JA,Fat adaptation in well-trained athletes: effects on cell metabolismPhysiol Nutr MetabYear: 201112122210.1139/H10-089|
|Yeo WK,Lessard SJ,Chen ZP,Garnham AP,Burke LM,Rivas DA,Kemp BE,Hawley JA,Fat adaptation followed by carbohydrate restoration increases AMPK activity in skeletal muscle from trained humansJ Appl PhysiolYear: 2008121519152610.1152/japplphysiol.90540.200818801964|
|Viollet B,Foretz M,Guigas B,Horman S,Dentin R,Bertrand L,Hue L,Andreelli F,Activation of AMP-activated protein kinase in the liver: a new strategy for the management of metabolic hepatic disordersJ PhysiolYear: 200612415310.1113/jphysiol.2006.10850616644802|
|Cheng G,Zhang X,Gao D,Jiang X,Dong W,Resveratrol inhibits MMP-9 expression by up-regulating PPAR α expression in an oxygen glucose deprivation-exposed neuron modelNeurosci LettYear: 20091210510810.1016/j.neulet.2008.12.04519135132|
|Takahashi S,Nakashima Y,Repeated and long-term treatment with physiological concentrations of resveratrol promotes NO production in vascular endothelial cellsBr J NutrYear: 20121277478010.1017/S000711451100358821791144|
[Figure ID: F1]
The relative abdominal white adipose tissue weights in OLETF rats. The rats were fed a control diet or the resveratrol diet for 4 weeks. The values are expressed as the mean ± standard error for six mice. See Table 1 for the composition of the diets. * Significant (P < 0.05) difference between the control and resveratrol groups of OLETF rats.
[Figure ID: F2]
Carbohydrate oxidation (A, C), fat oxidation (B, D), and protein oxidation (E) in the rats fed the control diet or the resveratrol diet at 3 weeks of feeding. The values are expressed as the mean ± standard error for six mice. See Table 1 for the composition of the diets. * Significant (P < 0.05) difference between the control and resveratrol groups of OLETF rats.
[Figure ID: F3]
Serum glucose levels and liver glycogen contents in OLETF rats. The rats were fed a control diet or the resveratrol diet for 4 weeks. The values are expressed as the mean ± standard error for six mice. See Table 1 for the composition of the diets.
[Figure ID: F4]
The abundance of mRNAs related to lipid metabolism in white adipose tissue of OLETF rats. The rats were fed a control diet or the resveratrol diet for 4 weeks. The values are expressed as the mean ± standard error for six mice. See Table 1 for the composition of the diets. * Significant (P < 0.05) difference between the control and resveratrol groups of OLETF rats. CPT, carnitine palmitoyltransferase; FAS, fatty acid synthase; PPAR, peroxisome proliferator-activated receptor.
The composition of the experimental diets
|Mineral mixture (AIN-76)
|Vitamin mixture (AIN-76)
The effect of resveratrol on growth and lipid parameters in OLETF rats
|Initial body weight (g)
||132 ± 3
||132 ± 3
|Final body weight (g)
||294 ± 3
||299 ± 3
|Food intake (g)
||498 ± 3
||499 ± 3
|Serum cholesterol (mg/dL)
||135 ± 4
||122 ± 5
|Serum triglyceride (mg/dL)
||76.3 ± 5.0
||96.5 ± 10.6
|Hepatic cholesterol (mg/g liver)
||3.34 ± 0.11
||3.35 ± 0.13
|Hepatic triglyceride (mg/g liver)||14.8 ± 1.4||16.4 ± 1.4|
The values are expressed as the mean ± standard error for six mice.
Keywords: Resveratrol, Respiratory gas analysis, Metabolic profile, Obesity, OLETF rat.
Previous Document: Virological outcome and patterns of HIV-1 drug resistance in patients with 36 months' antiretroviral...
Next Document: Increased distractor vulnerability but preserved vigilance in patients with schizophrenia: Evidence ...