scholarly journals Hepatic Gene Expression Profile of Lipid Metabolism of Obese Mice after treatment with Anti-obesity Drug

2020 ◽  
Author(s):  
Maha Al-Qeraiwi ◽  
Manar Al-Rashid ◽  
Nasser Rizk ◽  
Abdelrahman El Gamal ◽  
Amena Fadl
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
High Fat Diet ◽  
Fat Metabolism ◽  
Control Group ◽  
Fatty Acid Transport ◽  
Hepatic Gene Expression ◽  
High Fat ◽  
Beta Oxidation ◽  
Hepatic Fat

Obesity is a global disorder with multifactorial causes. The liver plays a vital role in fat metabolism. Disorder of hepatic fat metabolism is associated with obesity and causes fatty liver. High fat diet intake (HFD) to mice causes the development of dietinduced obesity (DIO). The study aimed to detect the effects of anti-obesity drugs (sulforaphane; SFN and leptin) on hepatic gene expression of fat metabolism in mice that were fed HFD during an early time of DIO. Twenty wild types (WT) CD1 male mice aged ten weeks were fed a high fat diet. The mice were treated with vehicle; Veh (control group), and SFN, then each group is treated with leptin or saline. Four groups of treatment were: control group (vehicle + saline), Group 2 (vehicle + leptin), group 3 (SFN + saline), and group 4 (SFN + leptin). Body weight and food intake were monitored during the treatment period. Following the treatments of leptin 24 hour, fasting blood samples and liver tissue was collected, and Total RNA was extracted then used to assess the gene expression of 84 genes involved in hepatic fat metabolism using RT-PCR profiler array technique. Leptin treatment upregulated fatty acid betaoxidation (Acsbg2, Acsm4) and fatty acyl-CoA biosynthesis (Acot6, Acsl6), and downregulated is fatty acid transport (Slc27a2). SFN upregulated acylCoA hydrolase (Acot3) and long chain fatty acid activation for lipids synthesis and beta oxidation (Acsl1). Leptin + SFN upregulated fatty acid beta oxidation (Acad11, Acam) and acyl-CoA hydrolase (Acot3, Acot7), and downregulated fatty acid elongation (Acot2). As a result, treatment of both SFN and leptin has more profound effects on ameliorating pathways involved in hepatic lipogenesis and TG accumulation and lipid profile of TG and TC than other types of intervention. We conclude that early intervention of obesity pa could ameliorate the metabolic changes of fat metabolism in liver as observed in WT mice on HFD in response to anti-obesity treatment.

scholarly journals Effect of a high fat diet on lipid absorption and fatty acid transport in a rat model of short bowel syndrome

2003 ◽  
Vol 19 (5) ◽  
pp. 385-390 ◽  
Author(s):  
Igor Sukhotnik ◽  
A. Semih Gork ◽  
Min Chen ◽  
Robert A. Drongowski ◽  
Arnold G. Coran ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Short Bowel Syndrome ◽  
Rat Model ◽  
High Fat Diet ◽  
Lipid Absorption ◽  
Fatty Acid Transport ◽  
Acid Transport ◽  
High Fat ◽  
Short Bowel

scholarly journals Benjankul supplementation improves hepatic fat metabolism in high-fat diet-induced obese rats

2020 ◽  
Vol 19 (4) ◽  
pp. 797-803
Author(s):  
Achiraya Kamchansuppasin ◽  
Kevalin Vongthoung ◽  
Pomthep Temrangsee ◽  
Narongsuk Munkong ◽  
Nusiri Lerdvuthisopon
Keyword(s):  
High Fat Diet ◽  
Fat Metabolism ◽  
High Fat ◽  
Obese Rats ◽  
Hepatic Fat

No Abstract.

scholarly journals Omega-3 Phospholipids from Krill Oil Enhance Intestinal Fatty Acid Oxidation More Effectively than Omega-3 Triacylglycerols in High-Fat Diet-Fed Obese Mice

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2037 ◽  
Author(s):  
Petra Kroupova ◽  
Evert M. van Schothorst ◽  
Jaap Keijer ◽  
Annelies Bunschoten ◽  
Martin Vodicka ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Acid Oxidation ◽  
Obese Mice ◽  
Krill Oil ◽  
Omega 3 ◽  
High Fat ◽  
Lower Body Weight

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.

Maternal high-fat diet during gestation and lactation alters hepatic gene expression in male rat offspring

Appetite ◽  
2011 ◽  
Vol 57 ◽  
pp. S15
Author(s):  
E.R. Ewald ◽  
B. Sun ◽  
R.H. Purcell ◽  
R.S. Lee ◽  
J.B. Potash ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Male Rat ◽  
Hepatic Gene Expression ◽  
High Fat ◽  
Rat Offspring

scholarly journals Maternal High-Fat Diet Increases Fetal Muscle Fat Metabolism and Fatty Acid Transporter Expression in an Ovine Model

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 799-799
Author(s):  
Asma Omar ◽  
Gerrit Bouma ◽  
Quinton Winger ◽  
Adam Chicco
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Mrna Expression ◽  
High Fat Diet ◽  
Fatty Acid Transport ◽  
Acid Transport ◽  
Ovine Model ◽  
High Fat ◽  
Oxidation Capacity ◽  
Fetal Muscle

Abstract Objectives Excessive maternal dietary fat consumption during pregnancy may be linked to adverse effects on offspring health, including greater risk of developing metabolic syndrome later in life. Metabolic syndrome is generally considered to be a preventable condition, but the extent to which it is “programmed” during fetal development remains unclear. The aim of this study was to determine the effect of a maternal high-fat diet (MHFD) during pregnancy on fetal muscle oxidative metabolism and related protein and mRNA expressions in an ovine model. Methods White-faced ewes were fed either a control diet (Show-rite NewCo Lamb Feed-17% protein, 5% Fat) or a high-fat diet (Show-rite NewCo Lamb Feed + 6% Rumen-protected Fat) from 2–3 weeks before pregnancy until mid-gestation (75 days), when a C-section was performed to collect the placenta and fetal tissues for analysis. Results MHFD tended to increase fetal body and organ weights, but only significantly increased fetal body length and liver mass (P < 0.05). MHFD increased mRNA expression of placental (cotyledon) fatty acid transport protein-1 (FATP-1) and peroxisome proliferator activated receptor gamma, suggesting an upregulation of placental fatty acid metabolism and transport. Fetal muscle fatty acid oxidation capacity was greater in animals from MHFD pregnancies, with no effect on pyruvate oxidation. This was associated with greater fetal muscle mRNA and protein expression of FATP4, while mRNA expression glucose transporters (GLUT1 and GLUT3) decreased. Muscle expression of insulin signaling enzymes reflected a mild decreases in insulin sensitivity, but these did not reach statistical significance. Conclusions These studies indicate that MHFD induces an increase in placental and fetal muscle fatty acid transport and oxidation capacity, and favors lower blood glucose uptake compared to controls. Whether these shifts in fetal metabolism predispose offspring from MHFD pregnancies to elevated blood sugar and Type 2 diabetes later in life merits further investigation. Funding Sources Colorado Agricultural Experiment Station.

scholarly journals Container-aided Integrative QTL and RNA-seq Analysis of Collaborative Cross Mice Supports Distinct Sex-Oriented Molecular Modes of Response in Obesity

2019 ◽  
Author(s):  
Ilona Binenbaum ◽  
Hanifa Abu-Toamih Atamni ◽  
Georgios Fotakis ◽  
Georgia Kontogianni ◽  
Theodoros Koutsandreas ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Complex Traits ◽  
Hepatic Gene Expression ◽  
High Fat ◽  
Mouse Population ◽  
Male And Female ◽  
Female Mice ◽  
Diet Induced Obesity ◽  
Genetic Mechanisms

Abstract Background: The CC mouse population is a valuable resource to study the genetic basis of complex traits, such as obesity. Although the development of obesity is influenced by environmental factors, the underlying genetic mechanisms play a crucial role in the response to these factors. The interplay between the genetic background and the gene expression pattern can provide further insight into this response, but we lack robust and easily reproducible workflows to integrate genomic and transcriptomic information in the CC mouse population. Results: We established an automated and reproducible integrative workflow to analyse complex traits in the CC mouse genetic reference panel at the genomic and transcriptomic levels. We implemented the analytical workflow to assess the underlying genetic mechanisms of host susceptibility to diet induced obesity and integrate these results with diet induced changes in the hepatic gene expression of susceptible and resistant mice. Hepatic gene expression differs significantly between obese and non-obese mice, with a significant sex effect, where male and female mice exhibit different responses and coping mechanisms. Conclusion: Integration of the data showed that different genes but similar pathways are involved in the genetic susceptibility and disturbed in diet induced obesity. Genetic mechanisms underlying susceptibility to high-fat diet induced obesity differ in female and male mice. The clear distinction we observe in the systemic response to the high-fat diet challenge and to obesity between male and female mice points to the need for further research into distinct sex-related mechanisms in metabolic disease.

scholarly journals High Fat Diet Stimulates Beta-Oxidation, Alters Electrical Properties and Induces Adipogenicity of Atria in Obese Mice

2020 ◽  
Author(s):  
Nadine Suffee ◽  
Elodie Baptista ◽  
Jérôme Piquereau ◽  
Maharajah Ponnaiah ◽  
Nicolas Doisne ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
High Fat Diet ◽  
Potassium Current ◽  
Obese Mice ◽  
High Fat ◽  
Beta Oxidation ◽  
Long Chain

SUMMARYMetabolic disorders such as obesity are risk factors of atrial fibrillation, not only by sharing comorbidities but likely through their direct impact on atria, notably its adipogenicity. Here, we submitted mice that lack cardiac adipose tissue to a high fat diet and first studied the atrial metabolomic and lipidomic phenotypes using liquid chromatography-mass spectrometry. We found an increased consumption of free fatty acid by the beta-oxidation and an accumulation of long-chain lipids in atria of obese mice. Free fatty acid was the main substrate of mitochondrial respiration studied in the saponin-permeabilized atrial muscle. Conducted action potential recorded in atrial trabeculae was short, and ATP-sensitive potassium current was increased in perforated patch-clamp atrial myocytes of obese mice. There was histological and phenotypical evidence for an accumulation of adipose tissue in obese mice atria. Thus, an obesogenic diet transforms the energy metabolism, causes fat accumulation and induces electrical remodeling of atria myocardium.HIGHLIGHTS- Untargeted metabolomic and lipidomic analysis revealed that a high fat diet induces profound transformation of atrial energy metabolism with beta-oxidation activation and long-chain lipid accumulation.- Mitochondria respiration studied in atrial myocardial trabecula preferentially used Palmitoyl-CoA as energy substrate in obese mice.- Atria of obese mice become vulnerable to atrial fibrillation and show short action potential due to the activation of K-ATP dependent potassium current.- Adipocytes and fat molecular markers were detected in atria of obese mice together with an inflammatory profile consistence with a myocardial accumulation of fat.

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