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 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 Fat Encapsulation Reduces Diarrhea in Piglets Partially by Repairing the Intestinal Barrier and Improving Fatty Acid Transport

Animals ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 28
Author(s):  
Min Tian ◽  
Jiaming Chen ◽  
Zhihui Wu ◽  
Hanqing Song ◽  
Fei Yang ◽  
...  
Keyword(s):  
Small Intestine ◽  
Fatty Acid ◽  
Soybean Oil ◽  
Mrna Expression ◽  
Transport System ◽  
Palm Oil ◽  
Control Group ◽  
Fatty Acid Transport ◽  
Acid Transport ◽  
Fatty Acid Binding

(1) Background: Nutritional strategies to enhance gut function and reduce the piglet diarrhea rate are critical to increase the growth performance of piglets. The purpose of this study was to investigate whether dietary fat types and/or fat microencapsulation techniques are involved in regulating the fatty acid transport system and the mechanical and immunological barriers of the small intestine. (2) Methods: Three hundred twenty-four weaning piglets were randomly divided into three groups fed a soybean oil diet (SBO, control group, 6.0% soybean oil), palm oil diet (PO, 6.0% palm oil), or encapsulated palm oil diet (EPO, 7.5% encapsulated palm oil). (3) Results: A significantly lower mRNA expression of the claudin was observed in the duodenum and jejunum of the PO group than in the SBO group (p < 0.05). However, the mRNA expression and protein abundance of claudin and ZO-1 in the jejunum of the EPO group were higher (p < 0.05) than in the PO group. Porcine β-defensin (pBD) secretion was not significantly different between the SBO and PO groups (p > 0.05), while the pBD-2 levels were significantly different (p < 0.05). Compared with the PO group, the EPO group exhibited a significantly increased secretion of pBD-2 and pBD-129 in the small intestine (p < 0.05) and pBD-1 in the jejunum and ileum (p < 0.05). The protein abundances of apolipoprotein AIV (Apo AIV) and intestinal fatty acid binding protein (I-FABP) were significantly lower in the PO group than in the SBO group (p < 0.05). Simultaneously, the protein abundances of fatty acid transport protein 4 (FATP4), fatty acid translocase (CD36), and I-FABP were higher in the EPO group than in the PO group. Furthermore, the low digestibility of palm oil (PO group) might negatively regulate intestinal tight junctions, fatty acid transporters, lipoproteins, and β-defensin through the activation of the AMPK/mTORC1 and AMPK/Sirt1/NF-κB pathways. (4) Conclusions: In summary, microencapsulation techniques might alleviate the negative effects of palm oil and help to improve the intestinal fatty acid transport system and barrier function.

scholarly journals Increased placental fatty acid transporter 6 and binding protein 3 expression and fetal liver lipid accumulation in a mouse model of obesity in pregnancy

2015 ◽  
Vol 309 (12) ◽  
pp. R1569-R1577 ◽  
Author(s):  
Paula Díaz ◽  
Jessica Harris ◽  
Fredrick J. Rosario ◽  
Theresa L. Powell ◽  
Thomas Jansson
Keyword(s):  
Fatty Acid ◽  
Mrna Expression ◽  
Lipid Accumulation ◽  
Plasma Membranes ◽  
Fetal Liver ◽  
Fatty Acid Transport ◽  
Acid Transport ◽  
Fatty Acid Binding ◽  
Obesity In Pregnancy ◽  
In Pregnancy

Obesity in pregnancy is associated with increased fetal growth and adiposity, which, in part, is determined by transplacental nutrient supply. Trophoblast uptake and intracellular trafficking of lipids are dependent on placental fatty acid transport proteins (FATP), translocase (FAT/CD36), and fatty acid binding proteins (FABP). We hypothesized that maternal obesity in mice leads to increased placental expression of FAT/CD36, FATPs, and FABPs, and lipid accumulation in the fetal liver. C57/BL6J female mice were fed either a control (C; n = 10) or an obesogenic (OB; n = 10) high-fat, high-sugar diet before mating and throughout pregnancy. At E18.5, placentas and fetal livers were collected. Trophoblast plasma membranes (TPM) were isolated from placental homogenates. Expression of FAT/CD36 and FATP (TPM) and FABP (homogenates) was determined by immunoblotting. Gene expression was assessed by RT-quantitative PCR. Sections of fetal livers were stained for Oil Red O, and lipid droplets were quantified. TPM protein expression of FAT/CD36, FATP 2, and FATP 4 was comparable between C and OB groups. Conversely, TPM FATP 6 expression was increased by 35% in OB compared with C placentas without changes in mRNA expression. FABPs 1, 3–5 and PPARγ were expressed in homogenates, and FABP 3 expression increased 27% in OB compared with C placentas; however, no changes were observed in mRNA expression. Lipid droplet accumulation was 10-fold higher in the livers of fetuses from OB compared with C group. We propose that increased lipid transport capacity in obese mice promotes transplacental fatty acid transport and contributes to excess lipid accumulation in the fetal liver.

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 Gene Expression in Livers of BALB/C and C57BL/6J Mice Fed a High-Fat Diet

2011 ◽  
Vol 40 (1) ◽  
pp. 71-82 ◽  
Author(s):  
Satomi Nishikawa ◽  
Jiro Sugimoto ◽  
Miyoko Okada ◽  
Tetsuya Sakairi ◽  
Shiro Takagi
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Mrna Expression ◽  
High Fat Diet ◽  
Fatty Acid Uptake ◽  
Blood Chemistry ◽  
Acid Uptake ◽  
High Fat ◽  
Hepatic Lipid Accumulation ◽  
The One

We previously demonstrated that high-fat diet (HFD)–induced hepatic lipid accumulation is more severe in BALB/c mice than in C57BL/6J (B6) mice. To understand the changes in liver metabolism, we studied blood chemistry, gene expression, and histopathological changes of the liver in nine-week HFD-fed BALB/c and B6 mice and one- or four-week HFD-fed BALB/c mice. Serum total cholesterol and triglyceride levels were significantly increased in all HFD-fed groups, and one- and four-week HFD-fed BALB/c groups, respectively. Histopathology revealed that vacuolation of hepatocytes was severe in nine-week HFD-fed BALB/c mice, although it was less severe in the other groups. Microarray analysis of mRNA expression of nine-week HFD-fed BALB/c mice showed up-regulation of genes involved in fatty acid uptake and biosynthesis, such as Cd36, Acaca, Acly, and Fasn. Some changes were observed in the one- and four-week HFD-fed BALB/c groups and the nine-week HFD-fed B6 group, however these changes in mRNA expression were not so marked. In conclusion, the fatty accumulation observed in BALB/c mice may be caused, at least in part, by up-regulation of fatty acid uptake and biosynthesis. Cd36, Acaca, Acly and Fasn may be involved in these metabolic processes.

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