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Luc Tappy - One of the best experts on this subject based on the ideXlab platform.
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fructose and metabolic diseases new findings new questions
Nutrition, 2010Co-Authors: Luc Tappy, Kim A Le, Christel Tran, Nicolas PaquotAbstract:There has been much concern regarding the role of Dietary fructose in the development of metabolic diseases. This concern arises from the continuous increase in fructose (and total added caloric sweeteners consumption) in recent decades, and from the increased use of High-Fructose corn syrup (HFCS) as a sweetener. A large body of evidence shows that a High-Fructose Diet leads to the development of obesity, diabetes, and dyslipidemia in rodents. In humans, fructose has long been known to increase plasma triglyceride concentrations. In addition, when ingested in large amounts as part of a hypercaloric Diet, it can cause hepatic insulin resistance, increased total and visceral fat mass, and accumulation of ectopic fat in the liver and skeletal muscle. These early effects may be instrumental in causing, in the long run, the development of the metabolic syndrome. There is however only limited evidence that fructose per se, when consumed in moderate amounts, has deleterious effects. Several effects of a High-Fructose Diet in humans can be observed with high-fat or high-glucose Diets as well, suggesting that an excess caloric intake may be the main factor involved in the development of the metabolic syndrome. The major source of fructose in our Diet is with sweetened beverages (and with other products in which caloric sweeteners have been added). The progressive replacement of sucrose by HFCS is however unlikely to be directly involved in the epidemy of metabolic disease, because HFCS appears to have basically the same metabolic effects as sucrose. Consumption of sweetened beverages is however clearly associated with excess calorie intake, and an increased risk of diabetes and cardiovascular diseases through an increase in body weight. This has led to the recommendation to limit the daily intake of sugar calories.
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a high fructose Diet impairs basal and stress mediated lipid metabolism in healthy male subjects
British Journal of Nutrition, 2008Co-Authors: Andrew Abdelsayed, Christophe Binnert, Murielle Bortolotti, Philippe Schneiter, Luc TappyAbstract:The effects of a 7 d High-Fructose Diet (HFrD) or control Diet on lipid metabolism were studied in a group of six healthy lean males. Plasma NEFA and beta-hydroxybutyrate concentrations, net lipid oxidation (indirect calorimetry) and exogenous lipid oxidation (13CO2 production) were monitored in basal conditions, after lipid loading (olive oil labelled with [13C]triolein) and during a standardised mental stress. Lactate clearance and the metabolic effects of an exogenous lactate infusion were also monitored. The HFrD lowered plasma concentrations of NEFA and beta-hydroxybutyrate as well as lipid oxidation in both basal and after lipid-loading conditions. In addition, the HFrD blunted the increase in plasma NEFA and exogenous lipid oxidation during mental stress. The HFrD also increased basal lactate concentrations by 31.8 %, and lactate production by 53.8 %, while lactate clearance remained unchanged. Lactate infusion lowered plasma NEFA with the control Diet, and net lipid oxidation with both the HFrD and control Diet. These results indicate that a 7 d HFrD markedly inhibits lipolysis and lipid oxidation. The HFrD also increases lactate production, and the ensuing increased lactate utilisation may contribute to suppress lipid oxidation.
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a 4 wk high fructose Diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans
The American Journal of Clinical Nutrition, 2006Co-Authors: David Faeh, Eric Ravussin, Chris Boesch, Roland Kreis, Michael Ith, Peter Vermathen, Rodrigue Stettler, Luc TappyAbstract:BACKGROUND: High fructose consumption is suspected to be causally linked to the epidemics of obesity and metabolic disorders. In rodents, fructose leads to insulin resistance and ectopic lipid deposition. In humans, the effects of fructose on insulin sensitivity remain debated, whereas its effect on ectopic lipids has never been investigated. OBJECTIVE: We assessed the effect of moderate fructose supplementation on insulin sensitivity (IS) and ectopic lipids in healthy male volunteers (n = 7). DESIGN: IS, intrahepatocellular lipids (IHCL), and intramyocellular lipids (IMCL) were measured before and after 1 and 4 wk of a High-Fructose Diet containing 1.5 g fructose . kg body wt(-1) . d(-1). Adipose tissue IS was evaluated from nonesterified fatty acid suppression, hepatic IS from suppression of hepatic glucose output (6,6-2H2-glucose), and muscle IS from the whole-body glucose disposal rate during a 2-step hyperinsulinemic euglycemic clamp. IHCL and IMCL were measured by 1H magnetic resonance spectroscopy. RESULTS: Fructose caused significant (P < 0.05) increases in fasting plasma concentrations of triacylglycerol (36%), VLDL-triacylglycerol (72%), lactate (49%), glucose (5.5%), and leptin (48%) without any significant changes in body weight, IHCL, IMCL, or IS. IHCL were negatively correlated with triacylglycerol after 4 wk of the High-Fructose Diet (r = -0.78, P < 0.05). CONCLUSION: Moderate fructose supplementation over 4 wk increases plasma triacylglycerol and glucose concentrations without causing ectopic lipid deposition or insulin resistance in healthy humans.
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effect of fructose overfeeding and fish oil administration on hepatic de novo lipogenesis and insulin sensitivity in healthy men
Diabetes, 2005Co-Authors: David Faeh, Kaori Minehira, Jeanmarc Schwarz, Raj Periasamy, Seongsoo Park, Luc TappyAbstract:High-Fructose Diet stimulates hepatic de novo lipogenesis (DNL) and causes hypertriglyceridemia and insulin resistance in rodents. Fructose-induced insulin resistance may be secondary to alterations of lipid metabolism. In contrast, fish oil supplementation decreases triglycerides and may improve insulin resistance. Therefore, we studied the effect of High-Fructose Diet and fish oil on DNL and VLDL triglycerides and their impact on insulin resistance. Seven normal men were studied on four occasions: after fish oil (7.2 g/day) for 28 days; a 6-day High-Fructose Diet (corresponding to an extra 25% of total calories); fish oil plus High-Fructose Diet; and control conditions. Following each condition, fasting fractional DNL and endogenous glucose production (EGP) were evaluated using [1-13C]sodium acetate and 6,6-2H2 glucose and a two-step hyperinsulinemic-euglycemic clamp was performed to assess insulin sensitivity. High-Fructose Diet significantly increased fasting glycemia (7 +/- 2%), triglycerides (79 +/- 22%), fractional DNL (sixfold), and EGP (14 +/- 3%, all P < 0.05). It also impaired insulin-induced suppression of adipose tissue lipolysis and EGP (P < 0.05) but had no effect on whole- body insulin-mediated glucose disposal. Fish oil significantly decreased triglycerides (37%, P < 0.05) after High-Fructose Diet compared with High-Fructose Diet without fish oil and tended to reduce DNL but had no other significant effect. In conclusion, High-Fructose Diet induced dyslipidemia and hepatic and adipose tissue insulin resistance. Fish oil reversed dyslipidemia but not insulin resistance.
C V Anuradha - One of the best experts on this subject based on the ideXlab platform.
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troxerutin reverses fibrotic changes in the myocardium of high fat high fructose Diet fed mice
Molecular and Cellular Biochemistry, 2015Co-Authors: Rajagopalan Geetha, Mutulur Krishnamoorthy Radika, Emayavaramban Priyadarshini, Krishnamurthy Bhavani, C V AnuradhaAbstract:A previous study from our laboratory showed that troxerutin (TX) provides cardioprotection by mitigating lipid abnormalities in a high-fat High-Fructose Diet (HFFD)-fed mice model of metabolic syndrome (MS). The present study aims to investigate the reversal effect of TX on the fibrogenic changes in the myocardium of HFFD-fed mice. Adult male Mus musculus mice were grouped into four and fed either control Diet or HFFD for 60 days. Each group was divided into two, and the mice were either treated or untreated with TX (150 mg/kg bw, p.o) from the 16th day. HFFD-fed mice showed marked changes in the electrocardiographic data. Increased levels of myocardial superoxide, p22phox subunit of NADPH oxidase, transforming growth factor (TGF), smooth muscle actin (α-SMA), and matrix metalloproteinases (MMPs)-9 and -2, and decreased levels of tissue inhibitors of MMPs-1 and -2 were observed. Furthermore, degradation products of troponin I and myosin light chain-1 were observed in the myocardium by immunoblotting. Rise in collagen was observed by hydroxyproline assay, while fibrotic changes were noticed by histology and Western blotting. Hypertrophy of cardiomyocytes and myocardial calcium accumulation were also observed in HFFD-fed mice. TX treatment exerted cardioprotective and anti-fibrotic effects in HFFD-fed mice by improving cardiac contractile function, reducing superoxide production and by favorably modifying the fibrosis markers. These findings suggest that TX could be cardioprotective through its antioxidant and antifibrogenic actions. This new finding could pave way for translation studies to human MS.
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troxerutin suppresses lipid abnormalities in the heart of high fat high fructose Diet fed mice
Molecular and Cellular Biochemistry, 2014Co-Authors: Rajagopalan Geetha, Baskaran Yogalakshmi, S Sreeja, Krishnamoorthy Bhavani, C V AnuradhaAbstract:The reversal effect of troxerutin (TX) on obesity, insulin resistance, lipid accumulation, oxidative damage, and hypertension induced in the high-fat–High-Fructose Diet (HFFD)-fed mice model of metabolic syndrome was investigated. Adult male Mus musculus mice of body weight 25–30 g were fed either control Diet or HFFD. Each group was divided into two and treated or untreated with TX (150 mg/kg bw, p.o.) from the 16th day. Assays were done in plasma and heart after 30 and 60 days of the experimental period. Significant increase in the levels of glucose and insulin, blood pressure (BP), and oxidative stress were observed after 30 days of HFFD feeding as compared to control. Animals fed HFFD for 60 days developed more severe changes in the above parameters compared to those fed for 30 days. Hearts of HFFD-fed mice registered downregulation of peroxisome proliferator-activated receptor-α and peroxisome proliferator-activated receptor gamma coactivator-1α, carnitine palmitoyl transferse-1b and AMP-activated protein kinase; and upregulation of cluster of differentiation 36, fatty acid-binding protein-1, and sterol regulatory element-binding protein-1c after 60 days. TX administration restricted obesity (as seen by Lee’s index); improved whole body insulin sensitivity; reduced BP, lipid accumulation, and oxidative damage; upregulated fatty acid (FA) oxidation; and downregulated FA transport and lipogenesis. Histology of heart revealed that TX diminishes inflammatory cell infiltration and fatty degeneration in HFFD-fed mice. The antioxidant property of TX and its ability to influence lipid regulatory genes could be the underlying mechanisms for its beneficial effects.
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dose dependent effect of galangin on fructose mediated insulin resistance and oxidative events in rat kidney
Redox Report, 2010Co-Authors: Allur Subramaniyan Sivakumar, P Viswanathan, C V AnuradhaAbstract:Abstract Galangin is an antioxidant flavonol present in high concentrations in the rhizome of Alpinia galanga. We investigated the effect of galangin on whole-body insulin resistance and kidney oxidative stress in a fructose-induced rat model of metabolic syndrome. Male albino Wistar rats were divided into 6 groups containing six animals each. Groups I and VI received a starch-based control Diet, while groups II, III, IV and V were fed a high fructose Diet (60 g/100 g). Groups III, IV and V additionally received galangin (50, 100 and 200 μg/kg body weight, respectively) while group VI received 200 μg galangin/kg body weight. At the end of 60 days, fructose-fed rats exhibited insulin resistance, increased levels of peroxidation end products and diminished antioxidant status. galangin, dose-dependently normalized blood glucose and insulin levels. The minimum effective dose was 100 μg galangin/kg body weight. At this dose, galangin also prevented the development of insulin resistance and the exaggerated the ...
Matić Gordana - One of the best experts on this subject based on the ideXlab platform.
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Impact of insulin and glucocorticoid signalling on hepatic glucose homeostasis in the rat exposed to High-Fructose Diet and chronic stress.
2020Co-Authors: Teofilović Ana, Matić Gordana, Đorđević Ana, Vojnović-milutinović Danijela, Tappy Luc, Brkljačić Jelena, Veličković NatašaAbstract:Overconsumption of fructose-enriched beverages and everyday stress are involved in the pathogenesis of metabolic disorders through modulation of hepatic glucose metabolism. The aim of the study was to investigate whether interaction of High-Fructose Diet and chronic stress alter insulin and glucocorticoid signalling thus affecting hepatic glucose homeostasis. High-Fructose Diet led to hyperinsulinemia, increased glucose transporter 2 level, elevated protein kinase B (Akt) phosphorylation, increased glucokinase mRNA and phospho-to-total glycogen synthase kinase 3 ratio and decreased expression of gluconeogenic genes. Fructose Diet also led to stimulated glucocorticoid prereceptor metabolism, but downstream signalling remained unchanged due to increased glucocorticoid clearance. Stress did not affect hepatic insulin and glucocorticoid signalling nor glucose metabolism, while the interaction of the factors was observed only for glucokinase expression. The results suggest that, under conditions of fructose-induced hyperinsulinemia, suppression of gluconeogenesis and glycogen synthase activation contribute to the maintenance of glucose homeostasis. The increased glucocorticoid inactivation may represent an adaptive mechanism to prevent hyperglycaemia
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Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with High-Fructose Diet
'Elsevier BV', 2018Co-Authors: Bursac Biljana, Gligorovska Ljupka, Veličković Nataša, Matić Gordana, Đorđević Ana, Vojnović-milutinović Danijela, Petrović, Snježana B., Teofilović Ana, Preitner Frederic, Tappy LucAbstract:Both fructose overconsumption and increased glucocorticoids secondary to chronic stress may contribute to overall dyslipidemia. In this study we specifically assessed the effects and interactions of Dietary fructose and chronic stress on lipid metabolism in the visceral adipose tissue (VAT) of male Wistar rats. We analyzed the effects of 9-week 20% high fructose Diet and 4-week chronic unpredictable stress, separately and in combination, on VAT histology, glucocorticoid prereceptor metabolism, glucocorticoid receptor subcellular redistribution and expression of major metabolic genes. Blood triglycerides and fatty acid composition were also measured to assess hepatic Delta 9 desaturase activity. The results showed that fructose Diet increased blood triglycerides and Delta 9 desaturase activity. On the other hand, stress led to corticosterone elevation, glucocorticoid receptor activation and decrease in adipocyte size, while phosphoenolpyruvate carboxykinase, adipose tissue triglyceride lipase, FAT/CD36 and sterol regulatory element binding protein-1c (SREBP-1c) were increased, pointing to VAT lipolysis and glyceroneogenesis. The combination of stress and fructose Diet was associated with marked stimulation of fatty acid synthase and acetylCoA carboxylase mRNA level and with increased 11 beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase protein levels, suggesting a coordinated increase in hexose monophosphate shunt and de novo lipogenesis. It however did not influence the level of peroxisome proliferator-activated receptor-gamma, SREBP-1c and carbohydrate responsive element-binding protein. In conclusion, our results showed that only combination of Dietary fructose and stress increase glucocorticoid prereceptor metabolism and stimulates lipogenic enzyme expression suggesting that interaction between stress and fructose may be instrumental in promoting VAT expansion and dysfunction
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Involvement of glucocorticoid prereceptor metabolism and signaling in rat visceral adipose tissue lipid metabolism after chronic stress combined with High-Fructose Diet.
2018Co-Authors: Bursać Biljana, Gligorovska Ljupka, Veličković Nataša, Đorđević Ana, Vojnović-milutinović Danijela, Teofilović Ana, Preitner Frederic, Tappy Luc, Petrović Snježana, Matić GordanaAbstract:Both fructose overconsumption and increased glucocorticoids secondary to chronic stress may contribute to overall dyslipidemia. In this study we specifically assessed the effects and interactions of Dietary fructose and chronic stress on lipid metabolism in the visceral adipose tissue (VAT) of male Wistar rats. We analyzed the effects of 9-week 20% high fructose Diet and 4-week chronic unpredictable stress, separately and in combination, on VAT histology, glucocorticoid prereceptor metabolism, glucocorticoid receptor subcellular redistribution and expression of major metabolic genes. Blood triglycerides and fatty acid composition were also measured to assess hepatic Δ9 desaturase activity. The results showed that fructose Diet increased blood triglycerides and Δ9 desaturase activity. On the other hand, stress led to corticosterone elevation, glucocorticoid receptor activation and decrease in adipocyte size, while phosphoenolpyruvate carboxykinase, adipose tissue triglyceride lipase, FAT/CD36 and sterol regulatory element binding protein-1c (SREBP-1c) were increased, pointing to VAT lipolysis and glyceroneogenesis. The combination of stress and fructose Diet was associated with marked stimulation of fatty acid synthase and acetyl-CoA carboxylase mRNA level and with increased 11β-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase protein levels, suggesting a coordinated increase in hexose monophosphate shunt and de novo lipogenesis. It however did not influence the level of peroxisome proliferator-activated receptor-gamma, SREBP-1c and carbohydrate responsive element-binding protein. In conclusion, our results showed that only combination of Dietary fructose and stress increase glucocorticoid prereceptor metabolism and stimulates lipogenic enzyme expression suggesting that interaction between stress and fructose may be instrumental in promoting VAT expansion and dysfunction
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High-Fructose Diet leads to visceral adiposity and hypothalamic leptin resistance in male rats - do glucocorticoids play a role?
2014Co-Authors: Bursac, Biljana N., Matić Gordana, Vojnović-milutinović Danijela, Vasiljevic, Ana D., Nestorović Nataša, Velickovic, Natasa A., Đorđević, Ana D.Abstract:Fructose overconsumption has been involved in the genesis and progression of the metabolic syndrome. Hypothalamus and adipose tissue, major organs for control of food intake and energy metabolism, play crucial roles in metabolic homeostasis. We hypothesized that glucocorticoid signaling mediates the effects of a fructose-enriched Diet on visceral adiposity by acting on neuropeptide Y (NPY) in the hypothalamus and altering adipogenic transcription factors in the visceral adipose tissue. We analyzed the effects of 9-week consumption of 60\% fructose solution on dyslipidemia, insulin and leptin sensitivity, and adipose tissue histology in male Wistar rats. Glucocorticoid signaling was assessed in both hypothalamus and visceral adipose tissue, while the levels of peroxisome-proliferator-activated receptor gamma (PPAR-gamma), sterol regulatory element-binding protein-1 (SREBP-1) and lipin-1, together with the levels of their target genes expression, were analyzed in the visceral adipose tissue. The results showed that long-term consumption of highly concentrated liquid fructose led to the development of visceral adiposity, elevated triglycerides and hypothalamic leptin resistance accompanied by stimulated glucocorticoid signaling and NPY mRNA elevation. Results from adipose tissue implied that fructose consumption shifted the balance between glucocorticoid receptor and adipogenic transcriptional factors (PPAR gamma, SREBP-1 and lipin-1) in favor of adipogenesis judged by distinctly separated populations of small adipocytes observed in this tissue. In summary, we propose that High-Fructose-Diet-induced alterations of glucocorticoid signaling in both hypothalamus and adipose tissue result in enhanced adipogenesis, possibly serving as an adaptation to energy excess in order to limit deposition of fat in nonadipose tissues. (C) 2014 Elsevier Inc. All rights reserved.Ministry of Education, Science and Technological Development of the Republic of Serbia {[}III41009
Takako Yokozawa - One of the best experts on this subject based on the ideXlab platform.
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the protective role of amla emblica officinalis gaertn against fructose induced metabolic syndrome in a rat model
British Journal of Nutrition, 2010Co-Authors: Hyun Young Kim, Tsutomu Okubo, Lekh Raj Juneja, Takako YokozawaAbstract:We investigated the effects of amla (Emblica officinalis Gaertn.) on fructose-induced metabolic syndrome using a rat model. Male Wistar rats were fed a High-Fructose (65 %) Diet or standard chow for 1 week, and treated with an ethyl acetate (EtOAc) extract of amla, a polyphenol-rich fraction, at 10 or 20 mg/kg body weight per d, or vehicle, for 2 weeks. Serum glucose, TAG, total cholesterol and blood pressure levels of the High-Fructose Diet-fed rats were increased compared with those of the normal rats (P < 0.001). However, the EtOAc extract of amla ameliorated the high fructose-induced metabolic syndrome, including hypertriacylglycerolaemia and hypercholesterolaemia. Also, the elevated levels of hepatic TAG and total cholesterol in rats given the High-Fructose Diet were significantly reduced by 33.8 and 24.6 %, respectively (P < 0.001), on the administration of the EtOAc extract of amla at the dose of 20 mg/kg with the regulation of sterol regulatory element-binding protein (SREBP)-1 expression. The protein levels of PPARalpha and SREBP-2 were not affected by the feeding of the High-Fructose Diet or EtOAc extract of amla. In addition, oral administration of the amla extract at the dose of 20 mg/kg significantly inhibited the increased serum and hepatic mitochondrial thiobarbituric acid-reactive substance levels (21.1 and 43.1 %, respectively; P < 0.001). Furthermore, the amla extract inhibited the increase of cyclo-oxygenase-2 with the regulation of NF-kappaB and bcl-2 proteins in the liver, while the elevated expression level of bax was significantly decreased by 8.5 and 10.2 % at the doses of 10 and 20 mg/kg body weight per d, respectively. These findings suggest that fructose-induced metabolic syndrome is attenuated by the polyphenol-rich fraction of amla.
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gravinol ameliorates high fructose induced metabolic syndrome through regulation of lipid metabolism and proinflammatory state in rats
Journal of Agricultural and Food Chemistry, 2008Co-Authors: Takako Yokozawa, Hyun Ju Kim, Eun Ju ChoAbstract:Using a rat model with fructose-induced metabolic syndrome, the effect of gravinol was investigated. Male Wistar rats were fed a 65% fructose Diet and administered 10 or 20 mg of gravinol/kg of body weight/day for 2 weeks. High-level fructose feeding led to hyperglycemia, hyperlipidemia, hypertri-glyceridemia, and hypertension. On the other hand, the administration of gravinol significantly lowered serum glucose and total cholesterol levels. The tail arterial blood pressure was significantly elevated with the High-Fructose Diet. However, rats given gravinol showed a lower blood pressure as compared with fructose-fed control rats. In addition, the triglyceride (TG) levels in serum and lipoprotein fraction were dose-dependently reduced in rats fed gravinol. The decreases of hepatic TG and total cholesterol by gravinol were responsible for the down-regulation of hepatic sterol regulatory element binding protein (SREBP)-1. However, gravinol did not affect the protein levels of hepatic peroxisome proliferator-activated receptor-alpha and SREBP-2. Moreover, gravinol administration in the fructose-fed rats markedly reduced the glycosylated protein and thiobarbituric acid-reactive substance levels in the serum and hepatic mitochondria, and it inhibited the increase of the cyclooxygenase-2 protein level as a result of the down-regulation of nuclear factor kappa B (NF-kappaB). Furthermore, the decrease of anti-apoptotic bcl-2 protein levels and the increase of pro-apoptotic bax protein levels by the High-Fructose Diet were reversed by gravinol. These findings suggest that fructose-induced metabolic syndrome is attenuated by gravinol administration, which is associated with the reduction of serum lipids and protection against the proinflammatory state induced by oxidative stress.
Rajagopalan Geetha - One of the best experts on this subject based on the ideXlab platform.
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troxerutin reverses fibrotic changes in the myocardium of high fat high fructose Diet fed mice
Molecular and Cellular Biochemistry, 2015Co-Authors: Rajagopalan Geetha, Mutulur Krishnamoorthy Radika, Emayavaramban Priyadarshini, Krishnamurthy Bhavani, C V AnuradhaAbstract:A previous study from our laboratory showed that troxerutin (TX) provides cardioprotection by mitigating lipid abnormalities in a high-fat High-Fructose Diet (HFFD)-fed mice model of metabolic syndrome (MS). The present study aims to investigate the reversal effect of TX on the fibrogenic changes in the myocardium of HFFD-fed mice. Adult male Mus musculus mice were grouped into four and fed either control Diet or HFFD for 60 days. Each group was divided into two, and the mice were either treated or untreated with TX (150 mg/kg bw, p.o) from the 16th day. HFFD-fed mice showed marked changes in the electrocardiographic data. Increased levels of myocardial superoxide, p22phox subunit of NADPH oxidase, transforming growth factor (TGF), smooth muscle actin (α-SMA), and matrix metalloproteinases (MMPs)-9 and -2, and decreased levels of tissue inhibitors of MMPs-1 and -2 were observed. Furthermore, degradation products of troponin I and myosin light chain-1 were observed in the myocardium by immunoblotting. Rise in collagen was observed by hydroxyproline assay, while fibrotic changes were noticed by histology and Western blotting. Hypertrophy of cardiomyocytes and myocardial calcium accumulation were also observed in HFFD-fed mice. TX treatment exerted cardioprotective and anti-fibrotic effects in HFFD-fed mice by improving cardiac contractile function, reducing superoxide production and by favorably modifying the fibrosis markers. These findings suggest that TX could be cardioprotective through its antioxidant and antifibrogenic actions. This new finding could pave way for translation studies to human MS.
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troxerutin suppresses lipid abnormalities in the heart of high fat high fructose Diet fed mice
Molecular and Cellular Biochemistry, 2014Co-Authors: Rajagopalan Geetha, Baskaran Yogalakshmi, S Sreeja, Krishnamoorthy Bhavani, C V AnuradhaAbstract:The reversal effect of troxerutin (TX) on obesity, insulin resistance, lipid accumulation, oxidative damage, and hypertension induced in the high-fat–High-Fructose Diet (HFFD)-fed mice model of metabolic syndrome was investigated. Adult male Mus musculus mice of body weight 25–30 g were fed either control Diet or HFFD. Each group was divided into two and treated or untreated with TX (150 mg/kg bw, p.o.) from the 16th day. Assays were done in plasma and heart after 30 and 60 days of the experimental period. Significant increase in the levels of glucose and insulin, blood pressure (BP), and oxidative stress were observed after 30 days of HFFD feeding as compared to control. Animals fed HFFD for 60 days developed more severe changes in the above parameters compared to those fed for 30 days. Hearts of HFFD-fed mice registered downregulation of peroxisome proliferator-activated receptor-α and peroxisome proliferator-activated receptor gamma coactivator-1α, carnitine palmitoyl transferse-1b and AMP-activated protein kinase; and upregulation of cluster of differentiation 36, fatty acid-binding protein-1, and sterol regulatory element-binding protein-1c after 60 days. TX administration restricted obesity (as seen by Lee’s index); improved whole body insulin sensitivity; reduced BP, lipid accumulation, and oxidative damage; upregulated fatty acid (FA) oxidation; and downregulated FA transport and lipogenesis. Histology of heart revealed that TX diminishes inflammatory cell infiltration and fatty degeneration in HFFD-fed mice. The antioxidant property of TX and its ability to influence lipid regulatory genes could be the underlying mechanisms for its beneficial effects.