scholarly journals Leucine imparts cardioprotective effects by enhancing mTOR activity and mitochondrial fusion in a myocardial ischemia/reperfusion injury murine model

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Atsushi Morio ◽  
Rie Tsutsumi ◽  
Shiho Satomi ◽  
Takashi Kondo ◽  
Hirotsugu Miyoshi ◽  
...  
Keyword(s):  
Infarct Size ◽  
High Fat Diet ◽  
Ischemia Reperfusion ◽  
Mitochondrial Fusion ◽  
Control Group ◽  
Obese Mice ◽  
High Fat ◽  
Rat Cardiomyocytes ◽  
Cardioprotective Effects ◽  
Mtor Activity

Abstract Background Coronary artery disease is a leading cause of morbidity and mortality among patients with diabetes. Previously, we demonstrated that branched-chain amino acids (BCAAs) showed cardioprotective effects against cardiac ischemia/reperfusion (I/R) injury. A recent study suggested that leucine (Leu), a BCAA, is a key amino acid involved in mammalian target of rapamycin (mTOR) activity and mitochondrial function. However, whether Leu has cardioprotective effects on diabetic hearts is unclear. In this study, we examined the preconditioning effect of Leu treatment on high-fat diet (HFD)-induced obese mouse which simulate prediabetic heart. Methods In vivo mice models of I/R injury were divided into the following groups: control, mTOR+/−, and high-fat diet (HFD)-induced obese groups. Mice were randomly administered with Leu, the mTOR inhibitor rapamycin (Rap), or Leu with Rap. Isolated rat cardiomyocytes were subjected to simulated I/R injury. Biochemical and mitochondrial functional assays were performed to evaluate the changes in mTOR activity and mitochondrial dynamics caused by Leu treatment. Results Leu-treated mice showed a significant reduction in infarct size when compared with the control group (34.8% ± 3.8% vs. 43.1% ± 2.4%, n = 7, p < 0.05), whereas Rap-treated mice did not show the protective effects of Leu. This preconditioning effect of Leu was attenuated in mTOR+/− mice. Additionally, Leu increased the percentage of fused mitochondria and the mitochondrial volume, and decreased the number of mitochondria per cell in isolated cardiomyocytes. In HFD-induced obese mice, Leu treatment significantly reduced infarct size (41.0% ± 1.1% vs. 51.0% ± 1.4%, n = 7, p < 0.05), which was not induced by ischemic preconditioning, and this effect was inhibited by Rap. Furthermore, we observed enhanced mTOR protein expression and mitochondrial fusion with decreased reactive oxygen species production with Leu treatment in HFD-induced obese mice, but not in mTOR+/− mice. Conclusions Leu treatment improved the damage caused by myocardial I/R injury by promoting mTOR activity and mitochondrial fusion on prediabetic hearts in mice.

scholarly journals Discordant signaling and autophagy response to fasting in hearts of obese mice: Implications for ischemia tolerance

2016 ◽  
Vol 311 (1) ◽  
pp. H219-H228 ◽  
Author(s):  
Allen M. Andres ◽  
Joel A. Kooren ◽  
Sarah J. Parker ◽  
Kyle C. Tucker ◽  
Nandini Ravindran ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Ischemia Reperfusion ◽  
Fasting Blood Glucose ◽  
Nutrient Sensing ◽  
Nutrient Deprivation ◽  
Autophagic Flux ◽  
Obese Mice ◽  
Energy Status ◽  
High Fat

Autophagy is regulated by nutrient and energy status and plays an adaptive role during nutrient deprivation and ischemic stress. Metabolic syndrome (MetS) is a hypernutritive state characterized by obesity, dyslipidemia, elevated fasting blood glucose levels, and insulin resistance. It has also been associated with impaired autophagic flux and larger-sized infarcts. We hypothesized that diet-induced obesity (DIO) affects nutrient sensing, explaining the observed cardiac impaired autophagy. We subjected male friend virus B NIH (FVBN) mice to a high-fat diet, which resulted in increased weight gain, fat deposition, hyperglycemia, insulin resistance, and larger infarcts after myocardial ischemia-reperfusion. Autophagic flux was impaired after 4 wk on a high-fat diet. To interrogate nutrient-sensing pathways, DIO mice were subjected to overnight fasting, and hearts were processed for biochemical and proteomic analysis. Obese mice failed to upregulate LC3-II or to clear p62/SQSTM1 after fasting, although mRNA for LC3B and p62/SQSTM1 were appropriately upregulated in both groups, demonstrating an intact transcriptional response to fasting. Energy- and nutrient-sensing signal transduction pathways [AMPK and mammalian target of rapamycin (mTOR)] also responded appropriately to fasting, although mTOR was more profoundly suppressed in obese mice. Proteomic quantitative analysis of the hearts under fed and fasted conditions revealed broad changes in protein networks involved in oxidative phosphorylation, autophagy, oxidative stress, protein homeostasis, and contractile machinery. In many instances, the fasting response was quite discordant between lean and DIO mice. Network analysis implicated the peroxisome proliferator-activated receptor and mTOR regulatory nodes. Hearts of obese mice exhibited impaired autophagy, altered proteome, and discordant response to nutrient deprivation.

scholarly journals Anti-Obesity Effects of the Flower of Prunus persica in High-Fat Diet-Induced Obese Mice

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2176 ◽  
Author(s):  
Jungbin Song ◽  
Young-Sik Kim ◽  
Linae Kim ◽  
Hyo Jin Park ◽  
Donghun Lee ◽  
...  
Keyword(s):  
Fatty Acid ◽  
High Fat Diet ◽  
Fatty Acid Synthase ◽  
Prunus Persica ◽  
Quantitative Polymerase Chain Reaction ◽  
Water Extract ◽  
Control Group ◽  
Acid Oxidation ◽  
Obese Mice ◽  
High Fat

Prunus persica (L.) Batsch is a deciduous fruit tree cultivated worldwide. The flower of P. persica (PPF), commonly called the peach blossom, is currently consumed as a tea for weight loss in East Asia; however, its anti-obesity effects have yet to be demonstrated in vitro or in vivo. Since PPF is rich in phytochemicals with anti-obesity properties, we aimed to investigate the effects of PPF on obesity and its underlying mechanism using a diet-induced obesity model. Male C57BL/6 mice were fed either normal diet, high-fat diet (HFD), or HFD containing 0.2% or 0.6% PPF water extract for 8 weeks. PPF significantly reduced body weight, abdominal fat mass, serum glucose, alanine transaminase and aspartate aminotransferase levels, and liver and spleen weights compared to the HFD control group. Real-time quantitative polymerase chain reaction analysis revealed that PPF suppressed lipogenic gene expression, including stearoyl-CoA desaturase-1 and -2 and fatty acid synthase, and up-regulated the fatty acid β-oxidation gene, carnitine palmitoyltransferase-1, in the liver. Our results suggest that PPF exerts anti-obesity effects in obese mice and these beneficial effects might be mediated through improved hepatic lipid metabolism by reducing lipogenesis and increasing fatty acid oxidation.

scholarly journals Effects of different intensities of physical exercise on insulin sensitivity and protein kinase B/Akt activity in skeletal muscle of obese mice

2014 ◽  
Vol 12 (1) ◽  
pp. 82-89 ◽  
Author(s):  
Rodolfo Marinho ◽  
Leandro Pereira de Moura ◽  
Bárbara de Almeida Rodrigues ◽  
Luciana Santos Souza Pauli ◽  
Adelino Sanchez Ramos da Silva ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Protein Kinase ◽  
High Fat Diet ◽  
Protein Kinase B ◽  
Whole Body ◽  
Control Group ◽  
Standard Diet ◽  
Obese Mice ◽  
High Fat

Objective : To investigate the effects of different intensities of acute exercise on insulin sensitivity and protein kinase B/Akt activity in skeletal muscle of obese mice. Methods : Swiss mice were randomly divided into four groups, and fed either a standard diet (control group) or high fat diet (obese sedentary group and obese exercise group 1 and 2) for 12 weeks. Two different exercise protocols were used: swimming for 1 hour with or without an overload of 5% body weight. The insulin tolerance test was performed to estimate whole-body sensitivity. Western blot technique was used to determine protein levels of protein kinase B/Akt and phosphorylation by protein Kinase B/Akt in mice skeletal muscle. Results : A single bout of exercise inhibited the high fat diet-induced insulin resistance. There was increase in phosphorylation by protein kinase B/Akt serine, improve in insulin signaling and reduce of fasting glucose in mice that swam for 1 hour without overload and mice that swan for 1 hour with overload of 5%. However, no significant differences were seen between exercised groups. Conclusion : Regardless of intensity, aerobic exercise was able to improve insulin sensitivity and phosphorylation by protein kinase B/Ak, and proved to be a good form of treatment and prevention of type 2 diabetes.

Gut carbohydrate metabolism instead of fat metabolism regulated by gut microbes mediates high-fat diet-induced obesity

2014 ◽  
Vol 5 (3) ◽  
pp. 335-344 ◽  
Author(s):  
M. Li ◽  
D. Gu ◽  
N. Xu ◽  
F. Lei ◽  
L. Du ◽  
...  
Keyword(s):  
Weight Gain ◽  
Carbohydrate Metabolism ◽  
Normal Control ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Control Group ◽  
Obese Mice ◽  
High Fat ◽  
Gut Microbes ◽  
Diet Induced Obesity

The aim of this study was to investigate the mechanisms underlying the involvement of gut microbes in body weight gain of high-fat diet-fed obesity-prone (obese) and obesity-resistant (lean) mice. C57BL/6 mice were grouped into an obese group, a lean group and a normal control group. Both obese and lean mice were fed a high-fat diet while normal control mice were fed a normal diet; they were observed for six weeks. The results showed that lean mice had lower serum lipid levels, body fat and weight gain than obese mice. The ATPase, succinate dehydrogenase and malate dehydrogenase activities in liver as well as oxygen expenditure and rectal temperature of lean mice were significantly lower than in obese mice. As compared with obese mice, the absorption of intestinal carbohydrates but not of fats or proteins was significantly attenuated in lean mice. Furthermore, 16S rRNA abundances of faecal Firmicutes and Bacteroidetes were significantly reduced in lean mice. In addition, faecal β-D-galactosidase activity and short chain fatty acid levels were significantly decreased in lean mice. Expressions of peroxisome proliferator-activated receptor gamma 2 and CCAAT/enhancer binding protein-β in visceral adipose tissues were significantly downregulated in lean mice as compared with obese mice. Resistance to dyslipidaemia and high-fat diet-induced obesity was mediated by ineffective absorption of intestinal carbohydrates but not of fats or proteins, probably through reducing gut Bacteroidetes and Firmicutes contents and lowering of gut carbohydrate metabolism. The regulation of intestinal carbohydrates instead of fat absorption by gut microbes might be a potential treatment strategy for high-fat diet-induced obesity.

scholarly journals Comparative evaluation of metformin and liraglutide cardioprotective effect in rats with impaired glucose tolerance

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Anna Simanenkova ◽  
Sarkis Minasian ◽  
Tatiana Karonova ◽  
Timur Vlasov ◽  
Natalya Timkina ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Reperfusion Injury ◽  
High Fat Diet ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Hemodynamic Parameters ◽  
High Fat ◽  
Once Daily

AbstractImpaired glucose tolerance (IGT) increases cardiovascular risk and can enlarge myocardial infarction (MI) incidence and severity. There is lack of information about cardioprotective potential of glucose-lowering drugs in IGT. We aimed to evaluate the sustainability of myocardium to ischemia–reperfusion injury in diabetic and IGT rats and to study cardioprotective action of metformin and liraglutide. Type 2 diabetes mellitus (DM) and IGT were modelled in Wistar rats by high-fat diet and streptozotocin + nicotinamide. 4 weeks after rats were divided into 4 groups: DM (without treatment) (n = 4), IGT (without treatment) (n = 4), IGT + MET (metformin 200 mg/kg per os once daily 8 weeks) (n = 4), IGT + LIRA (liraglutide 0.06 mg/kg s.c. once daily for 8 weeks) (n = 4). Control (n = 6) and high-fat diet (n = 8) groups were made for comparison. After 8 weeks ischemia–reperfusion injury in isolated hearts was performed. Hemodynamic parameters were evaluated and MI size was measured by staining of myocardium slices in triphenyltetrazolium chloride solution. Blood glucose level was measured during the study. Both IGT and DM led to similar worsening of hemodynamic parameters during ischemia–reperfusion period, in comparison with control group. MI size in IGT (56.76 (51.58; 69.07) %) and DM (57.26 (45.51; 70.08) %) groups was significantly larger than that in control group (42.98 (33.26; 61.84) %) and did not differ between each other. MI size in high-fat diet group (56.98 (47.11; 62.83) %) was as large as in IGT and DM groups (p > 0.05). MI size in IGT + MET (42.11 (38.08; 71.96) %) and IGT + LIRA (42.50 (31.37; 60.40) %) was smaller than in both DM and IGT groups (p < 0.05 for multiple comparison). Myocardium damage size did not differ in IGT + MET and IGT + LIRA groups (p >  0.05). Only LIRA, but not MET administration to IGT rats led to ischemic contracture reduction. Glycemic control was similarly satisfactory in IGT, IGT + MET, IGT + LIRA groups. Thus, IGT and DM have similarly pronounced negative influence on hemodynamics and MI size in rat transient global ischemia ex vivo. Obesity development also has negative impact on the MI size. Both MET and LIRA have infarct-limiting effect independent on their influence on glucose level. LIRA, but not MET, diminishes ischemic contracture in IGT rats.

scholarly journals Exercise ameliorates the FGF21–adiponectin axis impairment in diet-induced obese mice

2019 ◽  
Vol 8 (5) ◽  
pp. 596-604 ◽  
Author(s):  
Wenqi Yang ◽  
Ling Liu ◽  
Yuan Wei ◽  
Chunlu Fang ◽  
Fu Zhou ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Metabolism ◽  
High Fat Diet ◽  
Fasting Blood Glucose ◽  
Control Group ◽  
Adipose Tissue Inflammation ◽  
Obese Mice ◽  
High Fat ◽  
High Molecular Weight Adiponectin ◽  
Tissue Inflammation

Objective The protective effects of exercise against glucose dysmetabolism have been generally reported. However, the mechanism by which exercise improves glucose homeostasis remains poorly understood. The FGF21–adiponectin axis participates in the regulation of glucose metabolism. Elevated levels of FGF21 and decreased levels of adiponectin in obesity indicate FGF21–adiponectin axis dysfunction. Hence, we investigated whether exercise could improve the FGF21–adiponectin axis impairment and ameliorate disturbed glucose metabolism in diet-induced obese mice. Methods Eight-week-old C57BL/6J mice were randomly assigned to three groups: low-fat diet control group, high-fat diet group and high-fat diet plus exercise group. Glucose metabolic parameters, the ability of FGF21 to induce adiponectin, FGF21 receptors and co-receptor levels and adipose tissue inflammation were evaluated after 12 weeks of intervention. Results Exercise training led to reduced levels of fasting blood glucose and insulin, improved glucose tolerance and better insulin sensitivity in high-fat diet-induced obese mice. Although serum FGF21 levels were not significantly changed, both total and high-molecular-weight adiponectin concentrations were markedly enhanced by exercise. Importantly, exercise protected against high-fat diet-induced impaired ability of FGF21 to stimulate adiponectin secretion. FGF21 co-receptor, β-klotho, as well as receptors, FGFR1 and FGFR2, were upregulated by exercise. We also found that exercise inhibited adipose tissue inflammation, which may contribute to the improvement in the FGF21–adiponectin axis impairment. Conclusions Our data indicate exercise protects against high-fat diet-induced FGF21–adiponectin axis impairment, and may thereby exert beneficial effects on glucose metabolism.

Systematic Investigation of the Effects of Long-Term Administration of a High-Fat Diet on Drug Transporters in the Mouse Liver, Kidney and Intestine

2019 ◽  
Vol 20 (9) ◽  
pp. 742-755 ◽  
Author(s):  
Xianyuan Lu ◽  
Yaqian Dong ◽  
Zhichao Jian ◽  
Qingyun Li ◽  
Linna Gong ◽  
...  
Keyword(s):  
Western Blot ◽  
Mrna Expression ◽  
High Fat Diet ◽  
Drug Transporters ◽  
Control Group ◽  
Obese Mice ◽  
High Fat ◽  
Protein Levels ◽  
Term Administration

Background: Long-term intake of a high-fat diet is a crucial factor contributing to obesity, which has become a global public health problem. Progressive obesity subsequently leads to hepatic injury, renal damage and intestinal atrophy. Transporters expressed in the liver, kidney and intestine play important roles in the deposition of nutrients and drugs, but researchers have not clearly determined whether/how the expression of transporters changes after long-term administration of a High-Fat Diet (HFD). This study aims to explore the effects of the long-term administration of a HFD on the expression of drug transporters in the liver, kidney and intestine in mice and to provide useful information for medical applications in the clinic. Methods: Male C57BL/6J mice were fed either a basal diet or HFD for 24 weeks, and oral glucose tolerance tests were performed after 3, 11 and 23 weeks. Serum was obtained to measure lipid metabolism, inflammatory mediators, renal function and hepatic function. Adipose tissues, kidney, pancreas and liver were collected for hematoxylin and eosin (H&E) staining after 4, 12 and 24 weeks. The mRNA and proteins expression of drug transporters in the liver, kidney and intestine were detected using real-time PCR and western blot, respectively. Results: Compared with the control group, long-term HFD administration significantly increased the adipose index. The serum lipid levels, including Total Cholesterol (TC), Triglyceride (TG), and Low-Density Lipoprotein Cholesterol (LDL-C), as well as the levels of the inflammatory cytokines Interleukin-10 (IL-10) and tumor necrosis factor-α (TNF-α) were significantly elevated in HFD-induced obese mice. H&E staining revealed pathological changes in the adipose cells, liver, kidney and pancreas from the obese group following the long-term administration of the HFD. The liver of the obese group presented increased mRNA expression of the efflux transporter Mrp2 and uptake transporter Oat2 at 24 weeks. The relative expression of Oat2 increased 4.08-fold and the protein expression of Oat2 was upregulated at 24 weeks in HFD-fed mice, while the mRNA expression of the uptake transporters Oct1, Oatp1b2 and Oatp1a4 decreased by 79%, 61% and 19%, respectively. The protein expression of Oct1 was significantly downregulated in obese mice at 12 weeks. The mRNA expression of the efflux transporter Mdr1a was significantly reduced in HFD-fed mice compared with the control group at 24 weeks. Western blot showed that the trend of protein level of Mdr1 was consistent with the mRNA expression. In the kidney, the level of the Oct2 mRNA increased 1.92- and 2.46-fold at 4 and 12 weeks in HFD-fed mice, respectively. The expression of the Oat1 and Oat3 mRNAs was markedly downregulated in the kidneys of mice with HFD-induced obesity at 4 weeks. The decrease of 72% and 21% in Mdr1a mRNA expression was observed in the obese model at 4 weeks and 12 weeks, respectively. Western blot showed that the protein levels of Mdr1 and Oat1 were consistent with the mRNA expression. The qPCR experiments showed a 2.87-fold increase in Bcrp mRNA expression at 24 weeks, and the expression of the Pept1 mRNA increased 2.84-fold in intestines of obese mice subjected to long-term administration of the HFD compared with control mice at 12 weeks. Western blot showed that the trend of protein levels of Mdr1 and Mrp2 were consistent with the mRNA expression. Conclusion: The expression of uptake and efflux transporters mRNAs and protein levels were altered in obese mice compared with control mice, providing scientific evidence for future medical applications in the clinic.

Impaired Myocardial MIF/AMPK Activation Aggravates Myocardial Ischemia Reperfusion Injury in High-Fat Diet-Induced Obesity

2019 ◽  
Vol 19 (7) ◽  
pp. 1046-1054
Author(s):  
Fanqing Meng ◽  
Dongliang Li ◽  
Bingfeng Song ◽  
Liang Li
Keyword(s):  
Myocardial Ischemia ◽  
High Fat Diet ◽  
Ischemia Reperfusion ◽  
Ampk Activation ◽  
Obese Mice ◽  
High Fat ◽  
Glut4 Expression ◽  
Diet Induced Obesity ◽  
Myocardial Ischemia Reperfusion ◽  
Lean Group

Background: Obese patients are more sensitive to myocardial ischemia, which has been linked with high mortality rates. The following study investigates the effects of impaired macrophage Migration Inhibitory Factor (MIF)/AMP-Activated Protein Kinase (AMPK) activation on increased susceptibility to myocardial ischemia/reperfusion (I/R) in high-fat diet-induced obesity. Methods: Male C57BL/6J mice were fed with a normal diet (10% kcal as fat, lean group) or a high-fat diet (60kcal as fat, obese group) for 12 consecutive weeks. To detect the MIF expression and AMPK activation in response to I/R in isolated hearts from lean and obese mice, myocardial samples were collected from left ventricular areas at different time points. To determine whether MIF supplementation is protective against I/R injury, recombined MIF (10 ng/mL) was applied before ischemia. Myocardial infarct size was estimated by triphenyltetrazolium staining. Western blot was used to detect myocardial MIF expression, AMPK activation and membrane glucose transporter 4 (Glut4) expression. Results: The expression of MIF was remarkably higher in obese group compared to lean group. Ischemia increased myocardial MIF expression and phosphorylation of AMPK in lean mice, whereas it had no significant effect on obese mice. Furthermore, administration of recombinant MIF increased ischemic AMPK activation and membrane Glut4 expression in both lean and obese mice, while it reduced the infarct size in lean mice only. Conclusion: An impaired MIF/AMPK activation response and consequent reduced membrane Glut4 expression may play an important role in increasing myocardial susceptibility to I/R in obesity.

scholarly journals Comparative Evaluation of Metformin and Liraglutide Cardioprotective Effect in Rats With Impaired Glucose Tolerance

2020 ◽  
Author(s):  
Anna Simanenkova ◽  
Sarkis Minasian ◽  
Tatiana Karonova ◽  
Timur Vlasov ◽  
Natalya Timkina ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Reperfusion Injury ◽  
High Fat Diet ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Hemodynamic Parameters ◽  
High Fat ◽  
Once Daily

Abstract Background: Impaired glucose tolerance (IGT) increases cardiovascular risk and can enlarge myocardial infarction (MI) incidence and severity. There is lack of information about cardioprotective potential of glucose-lowering drugs in IGT. We aimed to evaluate the sustainability of myocardium to ischemia-reperfusion injury in diabetic and IGT rats and to study cardioprotective action of metformin and liraglutide. Methods: Type 2 diabetes mellitus (DM) and IGT were modelled in Wistar rats by high-fat diet and streptozotocin+nicotinamide. 4 weeks after rats were divided into 4 groups: DM (without treatment), IGT (without treatment), IGT+MET (metformin 200 mg/kg per os once daily 8 weeks), IGT+LIRA (liraglutide 0.06 mg/kg s.c. once daily for 8 weeks). Control and high-fat diet groups were made for comparison. After 8 weeks ischemia-reperfusion injury of isolated hearts was performed. Hemodynamic parameters were evaluated and MI size was measured by staining of myocardium slices in triphenyltetrazolium chloride solution. Blood glucose level was measured during the study.Results: Both IGT and DM led to similar worsening of hemodynamic parameters during ischemia-reperfusion period, in comparison with control group. MI size in IGT (56.76 (51.58; 69.07) %) and DM (57.26 (45.51; 70.08) %) groups was significantly large than in control group (42.98 (33.26; 61.84) %) and did not differ between each other. MI size in high-diet group (56.98 (47.11; 62.83) %) was similarly large as in IGT and DM groups (p>0.05). MI size in IGT+MET (42.11 (38.08; 71.96) %) and IGT+LIRA (42.50 (31.37; 60.40) %) was smaller than in both DM and IGT groups (p<0.05 for multiple comparison). Myocardium damage size did not differ in IGT+MET and IGT+LIRA groups (p>0.05). Only LIRA, but not MET administration to IGT rats led to ischemic contracture reduction. Glycemic control was similar satisfactory in IGT, IGT+MET, IGT+LIRA groups. Conclusions: IGT and DM have similarly pronounced negative influence on hemodynamics and MI size in transient global rat ischemia ex vivo. Obesity development also has negative impact on the myocardial infarct size. Both MET and LIRA have infarct-limiting effect independent on their influence on glucose level. LIRA, but not MET, diminishes ischemic contracture in IGT rats.

scholarly journals Role of resveratrol and chrysin on inflammation and liver function in obese mice

2021 ◽  
Author(s):  
Pipit Pitriani ◽  
◽  
Wang-Lok Lee ◽  
Hee-Geun Park ◽  
◽  
...  
Keyword(s):  
Body Weight ◽  
Liver Function ◽  
High Fat Diet ◽  
Diet Group ◽  
Normal Diet ◽  
Calorie Intake ◽  
Control Group ◽  
Obese Mice ◽  
High Fat ◽  
Impaired Liver Function

The incidence of obesity has been spreading throughout the world. Many of the complications caused by obesity, such as inflammation and impaired liver function. This study aimed to determine the effect of supplementation resveratrol and chrysin on inflammation and liver function of obese mice fed a high-fat diet. 40 mice (C57BL/6) were randomly divided into four groups: 10 in the normal diet (NC), 10 control group on a high-fat diet (HC), 10 in the high-fat diet with resveratrol (HRE), and 10 in the high-fat diet group with chrysin (HCH). Resveratrol 25 mg and 50mg of chrysin supplement per kg body weight were orally given with 0.1ml solution of Dimethyl Sulfoxide (DMSO) dissolved in for 15 weeks (4 times/week). The calorie intake of the group supplemented by resveratrol and chrysin significantly decreased. Group with high-fat diet, resveratrol, and chrysin increased body weight significantly compared to the normal diet group. The liver weight decreased in the resveratrol but not in the chrysin group. TNFα did not decrease in the resveratrol and chrysin group while IL1β significantly decreased. TLR 4 significantly decreased only in the chrysin group, while IL10 only increased in the resveratrol group. The collagen was decreased by resveratrol and chrysin supplementation while fibronectin was not affected by resveratrol or chrysin. The inflammatory process in the liver of obese mice fed a high-fat diet can be reduced by supplementing resveratrol and chrysin.

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