scholarly journals Krill Oil Ameliorates Mitochondrial Dysfunctions in Rats Treated with High-Fat Diet

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Alessandra Ferramosca ◽  
Annalea Conte ◽  
Vincenzo Zara

In recent years, several studies focused their attention on the role of dietary fats in the pathogenesis of hepatic steatosis. It has been demonstrated that a high-fat diet is able to induce hyperglycemia, hyperinsulinemia, obesity, and nonalcoholic fatty liver disease. On the other hand, krill oil, a novel dietary supplement of n-3 PUFAs, has the ability to improve lipid and glucose metabolism, exerting possible protective effects against hepatic steatosis. In this study we have investigated the effects of krill oil on mitochondrial energetic metabolism in animals fed a high-fat diet. To this end, male Sprague-Dawley rats were divided into three groups and fed for 4 weeks with a standard diet (control group), a diet with 35% fat (HF group), or a high-fat diet supplemented with 2.5% krill oil (HF+KO group). The obtained results suggest that krill oil promotes the burning of fat excess introduced by the high-fat diet. This effect is obtained by stimulating mitochondrial metabolic pathways such as fatty acid oxidation, Krebs cycle, and respiratory chain complexes activity. Modulation of the expression of carrier proteins involved in mitochondrial uncoupling was also observed. Overall, krill oil counteracts the negative effects of a high-fat diet on mitochondrial energetic metabolism.

2014 ◽  
Vol 112 (6) ◽  
pp. 868-875 ◽  
Author(s):  
Masatoshi Kondoh ◽  
Takashi Shimada ◽  
Kazutake Fukada ◽  
Mayuko Morita ◽  
Kazuhiro Katada ◽  
...  

A high-fat diet (HFD) is one of the causes of hepatic steatosis. We previously demonstrated that Enterococcus faecalis FK-23 (FK-23), a type of lactic acid bacteria, exhibits an anti-obesity effect in mice fed a HFD. In the present study, we examined the effects of FK-23 on HFD-induced hepatic steatosis. Male C57BL/6 mice were divided into four groups and given one of four treatments: standard diet (SD); standard diet supplemented with FK-23 (SD+FK); HFD; or HFD supplemented with FK-23 (HFD+FK). For the administration of FK-23, the drinking water was supplemented with FK-23 at a concentration of 2 % (w/w). After 11 weeks, histological findings revealed hepatic steatosis in the liver of HFD-fed mice; however, this effect was attenuated by the administration of FK-23. The expression levels of genes involved in fatty acid oxidation in the liver tissue were significantly reduced in the HFD group compared with the SD group, but FK-23 supplementation tended to up-regulate the expression levels of these genes. Our findings show that the inhibitory effect of FK-23 against hepatic steatosis in HFD-fed mice can be explained by the prevention of fat accumulation in the liver through the modulation of the activities of genes involved in hepatic fatty acid oxidation.


Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2037 ◽  
Author(s):  
Petra Kroupova ◽  
Evert M. van Schothorst ◽  
Jaap Keijer ◽  
Annelies Bunschoten ◽  
Martin Vodicka ◽  
...  

Antisteatotic effects of omega-3 fatty acids (Omega-3) in obese rodents seem to vary depending on the lipid form of their administration. Whether these effects could reflect changes in intestinal metabolism is unknown. Here, we compare Omega-3-containing phospholipids (krill oil; ω3PL-H) and triacylglycerols (ω3TG) in terms of their effects on morphology, gene expression and fatty acid (FA) oxidation in the small intestine. Male C57BL/6N mice were fed for 8 weeks with a high-fat diet (HFD) alone or supplemented with 30 mg/g diet of ω3TG or ω3PL-H. Omega-3 index, reflecting the bioavailability of Omega-3, reached 12.5% and 7.5% in the ω3PL-H and ω3TG groups, respectively. Compared to HFD mice, ω3PL-H but not ω3TG animals had lower body weight gain (−40%), mesenteric adipose tissue (−43%), and hepatic lipid content (−64%). The highest number and expression level of regulated intestinal genes was observed in ω3PL-H mice. The expression of FA ω-oxidation genes was enhanced in both Omega-3-supplemented groups, but gene expression within the FA β-oxidation pathway and functional palmitate oxidation in the proximal ileum was significantly increased only in ω3PL-H mice. In conclusion, enhanced intestinal FA oxidation could contribute to the strong antisteatotic effects of Omega-3 when administered as phospholipids to dietary obese mice.


2017 ◽  
Vol 42 (2) ◽  
pp. 209-215 ◽  
Author(s):  
Natalia de las Heras ◽  
María Valero-Muñoz ◽  
Beatriz Martín-Fernández ◽  
Sandra Ballesteros ◽  
Antonio López-Farré ◽  
...  

Hypolipidemic and hypoglycemic properties of ginger in animal models have been reported. However, information related to the mechanisms and factors involved in the metabolic effects of ginger at a hepatic level are limited. The aim of the present study was to investigate molecular factors involved in the hypoglycemic and hypolipidemic effects of a hydroethanolic ginger extract (GE) in the liver of rats fed a high-fat diet (HFD). The study was conducted in male Wistar rats divided into the following 3 groups: (i) Rats fed a standard diet (3.5% fat), the control group; (ii) rats fed an HFD (33.5% fat); and (iii) rats fed an HFD treated with GE (250 mg·kg−1·day−1) for 5 weeks (HFD+GE). Plasma levels of glucose, insulin, lipid profile, leptin, and adiponectin were measured. Liver expression of glycerol phosphate acyltransferase (GPAT), cholesterol 7 alpha-hydroxylase, peroxisome proliferator-activated receptors (PPAR), PPARα and PPARγ, glucose transporter 2 (GLUT-2), liver X receptor, sterol regulatory element-binding protein (SREBP1c), connective tissue growth factor (CTGF), and collagen I was measured. Data were analyzed using a 1-way ANOVA, followed by a Newman−Keuls test if differences were noted. The study showed that GE improved lipid profile and attenuated the increase of plasma levels of glucose, insulin, and leptin in HFD rats. This effect was associated with a higher liver expression of PPARα, PPARγ, and GLUT-2 and an enhancement of plasma adiponectin levels. Furthermore, GE reduced liver expression of GPAT, SREBP1c, CTGF, and collagen I. The results suggest that GE might be considered as an alternative therapeutic strategy in the management of overweight and hepatic and metabolic−related alterations.


2021 ◽  
Vol 65 (s1) ◽  
Author(s):  
Proshanta Roy ◽  
Ilenia Martinelli ◽  
Michele Moruzzi ◽  
Federica Maggi ◽  
Consuelo Amantini ◽  
...  

Evidence suggests that transient receptor potential (TRP) ion channels dysfunction significantly contributes to the physiopathology of metabolic and neurological disorders. Dysregulation in functions and expression in genes encoding the TRP channels cause several inherited diseases in humans (the so-called ‘TRP channelopathies’), which affect the cardiovascular, renal, skeletal, and nervous systems. This study aimed to evaluate the expression of ion channels in the forebrain of rats with diet-induced obesity (DIO). DIO rats were studied after 17 weeks under a hypercaloric diet (high-fat diet, HFD) and were compared to the control rats with a standard diet (CHOW). To determine the systemic effects of HFD exposure, we examined food intake, fat mass content, fasting glycemia, insulin levels, cholesterol, and triglycerides. qRT-PCR, Western blot, and immunochemistry analysis were performed in the frontal cortex (FC) and hippocampus (HIP). After 17 weeks of HFD, DIO rats increased their body weight significantly compared to the CHOW rats. In DIO rats, TRPC1 and TRPC6 were upregulated in the HIP, while they were downregulated in the FC. In the case of TRPM2 expression, instead was increased both in the HIP and in the FC. These could be related to the increase of proteins and nucleic acid oxidation. TRPV1 and TRPV2 gene expression showed no differences both in the FC and HIP. In general, qRT-PCR analyses were confirmed by Western blot analysis. Immunohistochemical procedures highlighted the expression of the channels in the cell body of neurons and axons, particularly for the TRPC1 and TRPC6. The alterations of TRP channel expression could be related to the activation of glial cells or the neurodegenerative process presented in the brain of the DIO rat highlighted with post synaptic protein (PSD 95) alterations. The availability of suitable animal models may be useful for studying possible pharmacological treatments to counter obesity-induced brain injury. The identified changes in DIO rats may represent the first insight to characterize the neuronal alterations occurring in obesity. Further investigations are necessary to characterize the role of TRP channels in the regulation of synaptic plasticity and obesity-related cognitive decline.


2017 ◽  
Vol 61 (4) ◽  
pp. 517-525
Author(s):  
Barbara Stawiarska-Pięta ◽  
Jolanta Zalejska-Fiolka ◽  
Magdalena Wyszyńska ◽  
Anna Kleczka ◽  
Beata Janiga ◽  
...  

AbstractIntroduction:The aim of the study was to assess the influence of α-lipoic acid (ALA) on the morphology of the aorta and liver of rabbits fed high fat diet with addition of oxidised (ORO) and non-oxidised rapeseed oil (N-ORO).Material and Methods:The study was conducted on male chinchilla rabbits divided into six groups. The control group (C) was fed a breeding standard diet (BSD), group I received BSD with the addition of ALA in the dose of 10 mg/kg b.w., groups II and III received BSD enriched with 10% addition of N-ORO or ORO, whereas rabbits from groups IV and V received BSD with 10% addition of N-ORO or ORO and ALA.Results:Addition of ORO caused necrosis and steatosis of hepatocytes, as well as atherosclerotic plaques of various intensification in the aorta. In the liver of rabbits from group II (N-ORO) infiltrations of mononuclear cells was observed in the area of liver triads and between liver lobules. The beneficial influence of ALA was demonstrated in rabbits fed a diet containing N-ORO or ORO. In case of ORO, the activity of ALA was not fully effective.Conclusion:Diet supplementation with ALA counteracts the changes generated in the liver and aorta under increased exposure to higher fat content in diet, in particular thermally treated fats.


2020 ◽  
Vol 21 (5) ◽  
pp. 1870
Author(s):  
Do Yeon Kim ◽  
Sang Ryong Kim ◽  
Un Ju Jung

To test the hypothesis that myricitrin (MYR) improves type 2 diabetes, we examined the effect of MYR on hyperglycemia, glucose intolerance, hepatic steatosis, and inflammation in high-fat diet (HFD) and streptozotocin (STZ)-induced type 2 diabetic mice. Male C57BL/6J mice were randomly divided into three groups: non-diabetic, diabetic control, and MYR (0.005%, w/w)-supplemented diabetic groups. Diabetes was induced by HFD and STZ, and MYR was administered orally for 5 weeks. Myricitrin exerted no significant effects on food intake, body weight, fat weight, or plasma lipids levels. However, MYR significantly decreased fasting blood glucose levels, improved glucose intolerance, and increased pancreatic β-cell mass compared to the diabetic control group. Myricitrin administration also markedly increased glucokinase mRNA expression and activity as well as lowered glucose-6-phosphatase and phosphoenolpyruvate carboxykinase mRNA expression and activity in the liver. In addition, liver weight, hepatic triglyceride content, and lipid droplet accumulation were markedly decreased following MYR administration. These changes were seemingly attributable to the suppression of the hepatic lipogenic enzymes—fatty acid synthase and phosphatidate phosphohydrolase. Myricitrin also significantly lowered plasma MCP-1 and TNF-α levels and the mRNA expression of hepatic pro-inflammatory genes. These results suggest that MYR has anti-diabetic potential.


Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2176 ◽  
Author(s):  
Jungbin Song ◽  
Young-Sik Kim ◽  
Linae Kim ◽  
Hyo Jin Park ◽  
Donghun Lee ◽  
...  

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.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Valeria Cagnon ◽  
Ellen Lima ◽  
Celina Lamas ◽  
Andressa Baseggio ◽  
Larissa Kido ◽  
...  

Abstract Objectives Brazilian berries, such as Myrciaria jaboticaba (Vell.) Berg, present a high polyphenol concentration in the peel, showing an antioxidative property. The aim herein was to evaluate the antiangiogenic, antioxidant and proliferative effects of the Jaboticaba peel extract (patent BR 1020170054624) in early adenocarcinoma development in association with high-fat diet intake Methods Tramp mice were divided into 5 groups: Control group 8 (C8): 8 week-old mice; Control group 16 (C16): 16 week-old mice, standard diet; High-fat diet group (CH16): 16 week-old mice, high-fat diet; Jaboticaba standard diet group (JC): 16 week-old mice, standard diet and Jaboticaba intake; Jaboticaba high-fat diet group (HF): 16 week-old mice, high-fat diet and Jaboticaba intake. The 5.8 g Jaboticaba/Kg/body weight dose was administered five days per week for 2 months. The prostate was evaluated for proliferative, antiangiogenic and antioxidative markers, using morphology, immunohistochemistry and Western Blotting analyses. Results The prostate showed increased high grade prostatic intraepithelial neoplasia (HGPIN) and well-differentiated adenocarcinoma in the CH16 group. The Jaboticaba peel (JH group) led to decreased HGPIN. In both the JC and JH groups, a frequency increase of healthy prostatic epithelium was verified. A well-differentiated adenocarcinoma decrease was seen in the JC group. PCNA showed an increase in the CH16 group and a decrease in the JH group. VEGF had an increase in the CH16 group and a decrease after Jaboticaba peel extract intake. Catalase, SOD2, GR and 4HNE showed an increase in the CH16 group and all these molecules presented a decrease after Jaboticaba peel intake in the JH group. The TGFα protein level increased in the C16 and CH16 groups and decreased in the JC and JH groups. Conclusions To conclude, the high-fat diet intake intensified the severity of prostatic lesions. The Jaboticaba peel extract was effective in delaying prostatic adenocarcinoma progression, when administered at the early grades of cancer and considering the lesion severity. Jaboticaba peel intake showed antiangiogenic and antioxidant effects in the prostate, especially, after high-fat diet intake in Tramp mice, indicating a possible coadjuvant role of this natural compound in prostatic cancer therapy. Funding Sources Fapesp 18 045797.


2011 ◽  
Vol 106 (12) ◽  
pp. 1810-1813 ◽  
Author(s):  
Jason K. Higa ◽  
Wanyu Liu ◽  
Marla J. Berry ◽  
Jun Panee

Monocyte chemoattractant protein-1 (MCP-1) is an inflammatory chemokine up-regulated in obese subjects, contributing to the development of type 2 diabetes. The present study investigated the inhibitory effect of an ethanol–water extract from bamboo (BEX,Phyllostachys edulis) on the blood concentration of MCP-1. C57BL/6J mice were fed a standard diet or a high-fat diet with or without the BEX supplement (11 g dry mass/17 000 kJ) for 6 months. A total of ten mice were used in each group. Body weight and food consumption were measured weekly. After euthanisation, the weight of visceral fat and circulating MCP-1 concentration were measured. In comparison with the standard control group, the high-fat control group had increased body weight, abdominal fat storage and serum MCP-1 concentration by 60 % (P < 0·001), 266 % (P < 0·001) and 180 % (P < 0·01), respectively. In comparison with the high-fat control group, the high-fat BEX group showed a 3 % decrease in body weight (P < 0·01), 24 % decrease in mesenteric fat depot (P < 0·01) and 49 % decrease in serum MCP-1 concentration (P < 0·05). The present study suggests that the BEX supplement in the high-fat diet ameliorates elevated MCP-1 concentrations in the blood, and whether this is related to modulated endocrine properties of the visceral fat is to be studied.


2019 ◽  
Vol 9 (4) ◽  
pp. 276
Author(s):  
Yoshihiko Shibayama ◽  
Masanobu Nagano ◽  
Kazunori Hashiguchi ◽  
Akira Fujii ◽  
Ken Iseki

Background: Hepatic steatosis is among the most common causes of chronic liver diseases, although established effective treatments are not evident.  Previous studies reported that Kurozu improved hypercholesterolemia and carbohydrate metabolism. However, the effect of Kurozu on the incidence of hepatic steatosis is not clear.Objective: The effect of Kurozu on the onset of hepatic steatosis by administering a high-fat diet (HFD) for 110 weeks was evaluated in C57BL/6J mice. Methods: HFD treatment for 110 weeks accelerated the onset of hepatic steatosis more than a standard diet, whereas concentrated Kurozu (CK) supplementation ameliorated the effect of an HFD feeding. The effect of supplementation with resveratrol in an HFD on the onset of hepatic steatosis was also evaluated. To elucidate the mechanism of the effect of Kurozu on the expression of lipid metabolism genes, acute treatment for 10 days with Kurozu was also examined.Results: Supplementation with resveratrol in HFD-fed mice did not ameliorate hepatic steatosis. Body weights were significantly lower in the CK + HFD and Resveratrol + HFD groups than in the control HFD group in middle age. No significant differences in all-cause mortality were observed following supplementation with CK or resveratrol. CK and resveratrol supplements significantly inhibited decreases in dehydroepiandrosterone sulphate serum levels at postnatal week 120. CK and resveratrol supplements did not affect the survival of mice. The ingestion of Kurozu for 10 days significantly elevated the expression levels of Sirt1, Pgc-1α, Lpin1, and Igfbp1 in the liver. Conclusion: These results suggest that ingesting CK may delay the onset of hepatic steatosis HFD feeding causes.Keywords: Kurozu, steatosis, Sirt1, Igfbp1, Lpin1, Pgc-1α, resveratrol


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