scholarly journals Differential regulation of placental amino acid transport by saturated and unsaturated fatty acids

2014 ◽  
Vol 307 (8) ◽  
pp. C738-C744 ◽  
Author(s):  
Susanne Lager ◽  
Thomas Jansson ◽  
Theresa L. Powell

Fatty acids are critical for normal fetal development but may also influence placental function. We have previously reported that oleic acid (OA) stimulates amino acid transport in primary human trophoblasts (PHTs). In other tissues, saturated and unsaturated fatty acids have distinct effects on cellular signaling, for instance, palmitic acid (PA) but not OA reduces IκBα expression. We hypothesized that saturated and unsaturated fatty acids differentially affect trophoblast amino acid transport and cellular signaling. To test this hypothesis, PHTs were cultured in docosahexaenoic acid (DHA; 50 μM), OA (100 μM), or PA (100 μM). DHA and OA were also combined to test whether DHA could counteract the OA stimulatory effect on amino acid transport. The effects of fatty acids were compared against a vehicle control. Amino acid transport was measured by isotope-labeled tracers. Activation of inflammatory-related signaling pathways and the mechanistic target of rapamycin (mTOR) pathway were determined by Western blot analysis. Exposure of PHTs to DHA for 24 h reduced amino acid transport and phosphorylation of p38 MAPK, STAT3, mTOR, eukaryotic initiation factor 4E-binding protein 1, and ribosomal protein (rp)S6. In contrast, OA increased amino acid transport and phosphorylation of ERK, mTOR, S6 kinase 1, and rpS6. The combination of DHA with OA increased amino acid transport and rpS6 phosphorylation. PA did not affect amino acid transport but reduced IκBα expression. In conclusion, these fatty acids differentially regulated placental amino acid transport and cellular signaling. Taken together, these findings suggest that dietary fatty acids could alter the intrauterine environment by modifying placental function, thereby having long-lasting effects on the developing fetus.

1963 ◽  
Vol 41 (1) ◽  
pp. 397-407 ◽  
Author(s):  
E. Stachiewicz ◽  
J. H. Quastel

Nystatin, an antifungal antibiotic, inhibits the accumulation, by yeast cells, of glycine, leucine, arginine, and alanine at concentrations that have no effect on the respiration of the cells. The uptake of glycine by yeast cells that have been preincubated with nystatin and then suspended in a nystatin-free medium is much lower than that of normal cells. The longer the preincubation with nystatin, the greater is the inhibition of glycine uptake. Nystatin produces two distinct effects. At concentrations below 0.8 μg/ml, nystatin inhibits glycine or arginine uptake. At concentrations from 0.8 to 2.0 μg/ml, it causes an efflux of previously accumulated glycine or arginine. Fatty acids, such as oleic, linoleic, stearic, or palmitic acid, can protect the yeast cell from the action of nystatin. The presence of citrate or versene abolishes the protective action of these fatty acids. Calcium ions also protect the cell from the action of nystatin. The concentration of calcium ions giving complete protection depends upon the nystatin concentration. The implications of these facts on amino acid transport in yeast are discussed.


1963 ◽  
Vol 41 (2) ◽  
pp. 397-407 ◽  
Author(s):  
E. Stachiewicz ◽  
J. H. Quastel

Nystatin, an antifungal antibiotic, inhibits the accumulation, by yeast cells, of glycine, leucine, arginine, and alanine at concentrations that have no effect on the respiration of the cells. The uptake of glycine by yeast cells that have been preincubated with nystatin and then suspended in a nystatin-free medium is much lower than that of normal cells. The longer the preincubation with nystatin, the greater is the inhibition of glycine uptake. Nystatin produces two distinct effects. At concentrations below 0.8 μg/ml, nystatin inhibits glycine or arginine uptake. At concentrations from 0.8 to 2.0 μg/ml, it causes an efflux of previously accumulated glycine or arginine. Fatty acids, such as oleic, linoleic, stearic, or palmitic acid, can protect the yeast cell from the action of nystatin. The presence of citrate or versene abolishes the protective action of these fatty acids. Calcium ions also protect the cell from the action of nystatin. The concentration of calcium ions giving complete protection depends upon the nystatin concentration. The implications of these facts on amino acid transport in yeast are discussed.


1992 ◽  
Vol 286 (2) ◽  
pp. 405-411 ◽  
Author(s):  
P S Sohal ◽  
V E Baracos ◽  
M T Clandinin

The present study was designed to determine if dietary-fat-induced alterations in the fatty acid composition of skeletal-muscle lipid alters insulin-dependent and basal muscle metabolism, including glucose and amino acid transport, prostaglandin (PG) synthesis and protein turnover. Rats were fed on high-fat semi-purified diets providing 19% or 1% omega 3 fatty acids in the form of fish oil, for 6 weeks. After 3 weeks, half of the rats were made diabetic by a single injection of streptozotocin (50 mg/kg body wt.). After a further 3 weeks, contralateral epitrochlearis and extensor digitorum longus (EDL) muscles from each rat were incubated in vitro. High levels of dietary omega 3 fatty acids decreased PGE2 and PGF2 alpha synthesis in EDL and epitrochlearis muscle (P less than 0.0001). Diabetes and insulin had no effect on PG synthesis. Diet did not alter basal glucose or amino acid transport in EDL muscle from healthy or diabetic rats. Insulin increased glucose and amino acid transport (P less than 0.0001); the increase in glucose transport by insulin was significantly greater in muscles of rats fed on high levels of omega 3 fatty acids (P less than 0.05). Epitrochlearis from rats fed on high levels of omega 3 fatty acids showed decreased net protein degradation in the presence and absence of insulin, owing to decreased rates of protein degradation and synthesis. The data suggest that high levels of dietary omega 3 fatty acids that alter muscle membrane composition also result in alterations in glucose transport and the metabolism of muscle protein.


2019 ◽  
Vol 316 (5) ◽  
pp. E810-E816 ◽  
Author(s):  
O.R. Vaughan ◽  
T.L. Powell ◽  
T. Jansson

Apelin is an insulin-sensitizing hormone increased in abundance with obesity. Apelin and its receptor, APJ, are expressed in the human placenta, but whether apelin regulates placental function in normal body mass index (BMI) and obese pregnant women remains unknown. We hypothesized that apelin stimulates amino acid transport in cultured primary human trophoblast (PHT) cells and that maternal circulating apelin levels are elevated in obese pregnant women delivering large babies. Treating PHT cells with physiological concentrations of the pyroglutamated form [Pyr1]apelin-13 (0.1–10.0 ng/ml) for 24 h dose-dependently increased System A amino acid transport ( P < 0.05) but did not affect System L transport activity. Mechanistic target of rapamycin (mTOR), extracellular signal-regulated kinase-1/2 (ERK1/2), and AMP-activated protein kinase-α (AMPKα) signaling were unaffected by apelin ( P > 0.05). Plasma apelin was not different in obese women (BMI 35.8 ± 0.7, n = 21) with large babies compared with normal-BMI women (23.1 ± 0.5, n = 16) delivering normal birth weight infants. Apelin was highly expressed in placental villous tissue (20-fold higher vs. adipose), and APJ was present in syncytiotrophoblast microvillous membrane, but neither differed in abundance between normal-BMI and obese women. Phosphorylation (Thr172) of placental AMPKα strongly correlated with microvillous membrane APJ expression ( P < 0.01, R = 0.63) but negatively correlated with placental apelin abundance ( P < 0.01, R = −0.62). Neither placental APJ nor apelin abundance correlated with maternal BMI, plasma insulin, birth weight, or mTOR or ERK1/2 signaling ( P > 0.05). Hence, apelin stimulates trophoblast amino acid uptake, establishing a novel mechanism regulating placental function. We found no evidence that apelin constitutes an endocrine link between maternal obesity and fetal overgrowth.


2008 ◽  
Vol 68 (S 01) ◽  
Author(s):  
FM von Versen-Höynck ◽  
A Rajakumar ◽  
JM Roberts ◽  
W Rath ◽  
RW Powers

2020 ◽  
Vol 16 (2) ◽  
pp. 142-154 ◽  
Author(s):  
Hadi Emamat ◽  
Zahra Yari ◽  
Hossein Farhadnejad ◽  
Parvin Mirmiran

Recent evidence has highlighted that fat accumulation, particularly abdominal fat distribution, is strongly associated with metabolic disturbance. It is also well-recognized that the metabolic responses to variations in macronutrients intake can affect body composition. Previous studies suggest that the quality of dietary fats can be considered as the main determinant of body-fat deposition, fat distribution, and body composition without altering the total body weight; however, the effects of dietary fats on body composition have controversial results. There is substantial evidence to suggest that saturated fatty acids are more obesogen than unsaturated fatty acids, and with the exception of some isomers like conjugate linoleic acid, most dietary trans fatty acids are adiposity enhancers, but there is no consensus on it yet. On the other hand, there is little evidence to indicate that higher intake of the n-3 and the n-6 polyunsaturated fatty acids can be beneficial in attenuating adiposity, and the effect of monounsaturated fatty acids on body composition is contradictory. Accordingly, the content of this review summarizes the current body of knowledge on the potential effects of the different types of dietary fatty acids on body composition and adiposity. It also refers to the putative mechanisms underlying this association and reflects on the controversy of this topic.


2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Dunfang Wang ◽  
Xuran Ma ◽  
Shanshan Guo ◽  
Yanli Wang ◽  
Tao Li ◽  
...  

As a classic prescription, Huangqin Tang (HQT) has been widely applied to treat ulcerative colitis (UC), although its pharmacological mechanisms are not clear. In this study, urine metabolomics was first analysed to explore the therapeutic mechanisms of HQT in UC rats induced by TNBS. We identified 28 potential biomarkers affected by HQT that might cause changes in urine metabolism in UC rats, mapped the network of metabolic pathways, and revealed how HQT affects metabolism of UC rats. The results showed that UC affects amino acid metabolism and biosynthesis of unsaturated fatty acids and impairs the tricarboxylic acid cycle (TCA cycle). UC induced inflammatory and gastrointestinal reactions by inhibiting the transport of fatty acids and disrupting amino acid metabolism. HQT plays key roles via regulating the level of biomarkers in the metabolism of amino acids, lipids, and so on, normalizing metabolic disorders. In addition, histopathology and other bioinformatics analysis further confirm that HQT altered UC rat physiology and pathology, ultimately affecting metabolic function of UC rats.


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