Effects Of Saturated Fatty Acids Research Articles

The association between circulating fatty acids and stroke in hypertensive patients

BackgroundStroke is prevalent in hypertensive population. It has been suggested that unsaturated fatty acids (USFA) have protective effect on stroke. The effect of saturated fatty acids (SFAs) on stroke is still unclear. Therefore, we studied the relationship between circulating fatty acids and acute ischemic stroke (AIS) in hypertensive patients. MethodsEighty-nine pairs including 100 men and 78 women matched by sex and age were recruited. Each pair included a hypertensive patient within 48h of AIS onset and a hypertensive patient without stroke. Six circulating fatty acids were methylated before concentration determination which was repeated twice with percent recovery estimated. ResultsThere were differences in educational level (P = 0.002) and occupation (P < 0.001) between stroke and non-stroke participants. All the 6 fatty acid levels were higher in non-stroke participants (P = 0.017 for palmitoleic acid, 0.001 for palmitic acid, <0.001 for linoleic acid, <0.001 for behenic acid, <0.001 for nervonic acid and 0.002 for lignoceric acid). In logistic regression analysis, AIS was inversely associated with fatty acid levels except for lignoceric acid. After adjustment for education and occupation, the palmitoleic acid and palmitic acid levels were no longer inversely associated with AIS. After further adjustment for systolic blood pressure, smoking, drinking, total cholesterol and triglyceride, the inverse associations of linoleic acid (OR = 0.965, 95%CI = 0.942-0.990, P = 0.005), behenic acid (OR = 0.778, 95%CI = 0.664-0.939, P = 0.009), nervonic acid (OR = 0.323, 95%CI = 0.121-0.860, P = 0.024) with AIS remained significant. ConclusionsCirculating fatty acids except lignoceric acid were inversely associated with AIS. Both USFAs and SFAs may have beneficial effect on stroke prevention in hypertensive population.

Effects of saturated fatty acids with lysophospholipids on production and nutrient digestibility in lactating cows

The objective of the experiment was to determine the effects of supplemental saturated fatty acid (SFA) sources, lysophospholipids (LPL), and their interaction on production and nutrient digestibility in lactating dairy cows. The experiment was conducted with 48 cows in a randomized complete block design. Cows were blocked (total 12 blocks) by parity and days in milk and randomly assigned to 4 dietary treatments in each block (2 × 2 factorial arrangement), i.e., 2 sources of fat supplements, C16:0 (palmitic acid, PA)- or C18:0 (stearic acid, SA)-enriched fat, with or without LPL. The experiment was conducted for 6 wk to measure daily dry matter intake and milk yield and weekly milk composition. During the last week of the experiment, spot fecal and urine samples were collected to determine total-tract nutrient digestibility. Milk samples in the last week were also collected to analyze for milk fatty acid (FA) profile. All data were analyzed using the mixed procedure of SAS where block was used as a random effect and FA, LPL, and the interaction of FA by LPL were used as fixed effects. Week and interactions of week by FA or LPL were included for production measures. Different sources of SFA did not affect dry matter intake and milk yield. However, PA increased (39.7 vs. 36.8 kg) energy-corrected milk compared with SA due to increased milk fat yield. No effect of LPL on production measures was observed. Total-tract digestibilities of dry matter, organic matter, crude protein, and total FA were not different between PA and SA, but PA increased (41.4 vs. 38.8%) neutral detergent fiber digestibility compared with SA. Supplementation of LPL increased (64.7 vs. 60.5%) total FA digestibility, especially 18-carbon FA (74.1 vs. 68.2%). An interaction of SFA by LPL was found for 16-carbon FA digestibility. The PA diet increased the concentration of 16-carbon FA in milk fat and SA increased the concentration of preformed FA (≥18 carbons). Supplementation of LPL decreased the concentration of trans-10 C18:1. No difference in N utilization and excretion among treatments was observed. In conclusion, PA was more effective in improving milk fat yield of lactating cows compared with SA. Supplementation of LPL increased digestibility of total FA, especially 18-carbon FA but did not affect production.

Effect of saturated fatty acids and Omega-3 on the survival, growth, and progression of neoplastic cells

Effect of saturated fatty acids and Omega-3 on the survival, growth, and progression of neoplastic cells

Effect of saturated and unsaturated fat on the physical properties of plant-based cheese

In many plant-based meat and dairy alternatives, coconut oil is frequently used to replicate the textural and structural properties of animal fats due to its high saturated fat content. Concerns about the health implications of saturated fat and the sustainability of coconut oil call for an exploration into alternative fat combinations in plant-based foods. The effects of saturated fatty acid (SFA) content on plant-based cheese physical characteristics were evaluated through five different ratios of coconut oil (CO) to sunflower oil (SO): 100%, 90%, 75%, 60%, 50%, 40%, 25%, 10%, and 0%. As determined through texture profile analysis, the hardness of the cheeses after setting at 5°C for 24h increased with increasing amounts of coconut oil due to the increasing solid fat content providing additional firmness. The samples with 100% coconut oil displayed satisfactory melt and stretch; however, the melt and stretch values were matched by adding as little as 25% sunflower oil. The melt and stretch values did not continue to increase with increasing saturated fat content but instead remained constant with increasing coconut oil addition. Rheological analysis of the cheeses during a temperature ramp from 20 to 95°C was assessed where the tanδ value at 95°C was used as a measure of cheese melt, where values ≥ 1 indicated a better melt. The 0% coconut oil cheese had the lowest tanδ (G″/G′) value of 0.3, whereas the addition of 25% coconut oil into the cheese resulted in the tanδ increasing to values greater than 0.5. The 25% CO cheese sample also achieved a more similar complex viscosity (η*) to that of dairy cheese than all samples but the 75% CO cheese. Therefore, there is an opportunity to decrease the amount of coconut oil in plant-based cheese systems while maintaining good functional properties and improving the sustainability and health benefits of the final product.

Effects of fatty acid chain length on structure and in vitro enzymatic digestibility of type 5 resistant starch

SummaryThe effects of saturated fatty acids with different chain lengths (C12, C14, C16, C18) on the structure and digestibility of type 5 resistant starch (RS5s) were investigated. The complexing index (CI), structure, phase transition temperature, digestibility and evaluation glycemic index (eGI) values of RS5s were determined. High‐amylose corn starch VII (HA7) ‐ myristic acid (MA) complex had the highest CI value (41.1%), relative crystallinity (40.4%) and 1047 cm−1/1022 cm−1 (1.0), smallest full width at half maximum (fwhm) of the band at 480 cm−1 (16.4), indicating that RS5 with 14‐carbon saturated fatty acids was more easily to form V‐type crystal complexes with amylose, and the long‐range and short‐range molecular orderliness was the best. With the increase of the carbon chain (12 ~ 18), The peak temperature (Tp) of the complexes gradually increased from the HA7‐lauric acid (LA) complex (112.8 °C) to HA7‐stearic acid (SA) complex (119.1 °C). The content of slow digestible starch (SDS) and eGI values gradually decreased (P &lt; 0.05), and the content of resistant starch (RS) significantly increased (P &lt; 0.05). These results indicated fatty acid chain length and long‐range molecular orderliness were the main factors affecting the digestibility of RS5s.

Effect of Saturated Fatty Acids on the Antiwear and Rheological Properties of Olive Oil

The study determines the effect of saturated fatty acids (coconut oil) on the rheological and tribological properties of olive oil. The olive oil is blended with different proportions of coconut oil (10%, 20%, 30%, 40%, and 50%) and the different properties (flow behaviour and antiwear) are studied on Anton Paars rheometer and Four-ball tester respectively. The study reveals that the blends depict Newtonian behaviour with a decrease in the dynamic viscosity of the olive oil. Also, WSD decreases at a higher proportion of coconut oil in the blends with an improvement of 10.74% at a 50:50 ratio. The blending of two oils for the enhancement of the lubrication properties of biolubricants can prove beneficial in making them a suitable replacement for mineral oils.

Acute effects of prior dietary fat ingestion on postprandial metabolic responses to protein and carbohydrate co-ingestion in overweight and obese men: A randomised crossover trial

Obesity and insulin resistance are associated with an impaired sensitivity to anabolic stimuli such as dietary protein (anabolic resistance). Omega-3 polyunsaturated fatty acids (n-3 PUFA) may be protective against the deleterious effects of saturated fatty acids (SFA) on insulin resistance. However, the contribution of excess fat consumption to anabolic and insulin resistance and the interaction between SFA and n-3 PUFA is not well studied. The primary aim of this study was to investigate the effects of an oral fat pre-load, with or without the partial substitution of SFA with fish oil (FO)-derived n-3 PUFA, on indices of insulin and anabolic sensitivity in response to subsequent dietary protein and carbohydrate (dextrose) co-ingestion. Eight middle-aged males with overweight or obesity (52.8±2.0yr, BMI 31.8±1.4kg·m-2) ingested either an SFA, or isoenergetic SFA and FO emulsion (FO), or water/control (Con), 4h prior to a bolus of milk protein and dextrose. Lipid ingestion (in particular FO) impaired the early postprandial uptake of branched chain amino acids (BCAA) into the skeletal muscle in response to protein and dextrose, and attenuated the peak glycaemic response, but was not accompanied by differences in whole body (Matsuda Index: Con: 4.66±0.89, SFA: 5.10±0.94 and FO: 4.07±0.59) or peripheral (forearm glucose netAUC: Con: 521.7±101.7; SFA: 470.2±125.5 and FO: 495.3±101.6μmol·min-1·100g lean mass·min [t=240-420min]) insulin sensitivity between visits. Postprandial whole body fat oxidation was affected by visit (P=0.024) with elevated rates in SFA and FO, relative to Con (1.85±0.55; 2.19±0.21 and 0.65±0.35kJ·h-1·kg-1 lean body mass, respectively), however muscle uptake of free fatty acids (FFA) was unaffected. Oral lipid preloads, consisting of SFA and FO, impair the early postprandial BCAA uptake into skeletal muscle, which occurs independent of changes in insulin sensitivity. ClinicalTrials.gov Identifier NCT03146286.

Upregulation of 4-Hydroxynonenal Contributes to the Negative Effect of n-6 Polyunsaturated Fatty Acid on Alcohol-Induced Liver Injury and Hepatic Steatosis.

The present study aimed to investigate the effects of saturated fatty acids (SFA) and n-6 polyunsaturated fatty acids (PUFA) on alcoholic liver disease (ALD) and the underlying mechanisms. C57BL/6J male mice were randomly fed a corn oil or palm oil diet (rich in n-6 PUFA and SFA, respectively) with or without ethanol for four weeks (n = 10/group). A series of experiments in vitro with AML-12 hepatocyte were conducted to better elucidate the potential mechanisms underlying the phenomenon observed in animals. Compared with palm oil, corn oil aggravated alcohol-induced liver injury and hepatic steatosis, indicated by a histological analysis and significant elevations of plasma alanine aminotransferase and hepatic triacylglycerol (TG) level. Apoptosis-associated proteins in the ASK1-JNK pathway were significantly enhanced in the liver of mice from the corn oil + ethanol group than in the palm oil + ethanol group. The corn oil + ethanol diet also inhibited the activation of both AMPK and downstream protein acetyl-CoA carboxylase (ACC) and promoted the SREBP-1c expression, subsequently accelerating lipid synthesis. In addition, 4-hydroxynonenal (4-HNE) levels in plasma and liver were significantly upregulated in response to corn oil + ethanol feeding. Interestingly, the in vitro study showed that 4-HNE significantly attenuated cell viability, elevated the expression of cleaved-caspase 3 protein and TG level, and regulated key molecules in ASK1-JNK and AMPK pathways in a dose-dependent manner. In conclusion, the n-6 PUFA diet showed a negative effect on alcohol-induced liver injury and steatosis. It might be related to the upregulation of 4-HNE and subsequent changes of proteins, namely, ASK1, JNK, AMPK, ACC, and SREBP-1c.

Effects of Emulsifiers on Engineering and Microstructural Properties of HPMC/Shellac Composite Films

Hydroxypropyl methylcellulose/Shellac-based Composite (HPMC/Sh composite) is produced from oil/water emulsion. The emulsifiers are necessarily used to stabilize and enhance the dispersion of this emulsion. This study conducted the experiments to evaluate effects of saturated fatty acids of lauric acid (LA), stearic acid (SA) and unsaturated fatty acid of oleic acid (OA) to the sensory, mechanical properties and microstructure of the HPMC/Sh emulsion. In which, the saturated fatty acids were used in mixtures with the ratios of shellac : emulsifier at 20 : 1, 10 : 1, and 5 : 1. On the other hand, the unsaturated fatty acid was used in mixtures with the ratio of shellac : emulsifier at 1 : 5, 1 : 10, and 1 : 20. The emulsifiers increased the dispersion and effective interaction of the polymers causing the emulsion formation become more stable and finer particle size. In addition, the films had smooth surfaces without unfractured, flexible and elastic.

Effects of palmitic acid and eicosapentaenoic acid on angiogenesis of porcine vascular endothelial cells.

Restricted placental angiogenesis is an important cause of intrauterine growth retardation in piglets. During pregnancy, sow obesity can result in an increase in placental lipid deposition, subsequently inhibiting placental angiogenesis and fetal development. However, the effect of different types of fatty acids on placental angiogenesis is still unclear. Trophoblast cells and vascular endothelial cells constitute two important types of placental tissue. In this study, we used palmitic acid (C16:0) and eicosapentaenoic acid (C20:5, n‐3), respectively, to treat porcine trophectoderm cells (pTr2) and porcine iliac artery endothelial cells (PIEC) to study the effects of saturated fatty acids and n‐3 polyunsaturated fatty acids (PUFAs) on placental angiogenesis in vitro. We found that C16:0 caused significant cytotoxicity in pTr2 and PIEC (p < 0.01) and inhibited the proliferation and migration of PIEC (p < 0.01), whereas C20:5 treatment exhibited very low cytotoxicity and minimal inhibition of cellular proliferation. Meanwhile, a low concentration of C16:0 had no effect on the tube formation in PIEC, whereas C20:5 significantly promoted tube formation of PIEC (p < 0.01). These results suggested that saturated fatty acids and n‐3 PUFAs had different effects on placental angiogenesis. As essential functional fatty acid, n‐3 PUFA might be effective measure in alleviating the placental lipotoxicity caused by sow obesity during pregnancy.

Functional characterization of two alpha beta hydrolase domain (ABHD) genes associated with lipid accumulation in Ctenopharyngodon idella kidney (CIK) cells

Members of the α/β-hydrolase domain (ABHD) protein family have emerged as novel potential regulators of lipid metabolism and signal transduction. In this study, two ABHD genes (ABHD4 and ABHD5, named CiABHD4 and CiABHD5) were identified and characterized in Ctenopharyngodon idella. The ORF of CiABHD4 cDNA was 1101 bp (MK645600), and encode 366 amino acids. The ORF of CiABHD5 cDNA was 1035 bp (KP325482), and encode 344 amino acids. Phylogenetic analysis showed that the CiABHD4 and CiABHD5 were all closely clustered with the fish ABHD4 and ABHD5 subcluster. Both CiABHD4 and CiABHD5 in Ctenopharyngodon idella were highly expressed in liver. Moreover, we compared the effect of saturated fatty acids (palmitic acid, PA), monounsaturated fatty acids (oleic acid, OA) and polyunsaturated fatty acids (Docosahexaenoic acid, DHA) on CiABHD4 and CiABHD5 expression, and found that PA significantly induce expression of CiABHD4 and CiABHD5, but OA and DHA significantly increased lipid droplet (LD) formation in L8824 and CIK cells. Furthermore, inhibition of ER stress or IRE1α significantly alleviated CiABHD4 and CiABHD5 expression induced by PA, indicating that ER stress or IRE1α pathway was involved in PA-induced CiABHD4 and CiABHD5 expression. Subcellular localization analysis indicated that CiABHD4 and CiABHD5 proteins were differentially distributed in COS7 cells. In addition, the overexpression of CiABHD4 or CiABHD5 increased the significant expression of ATGL genes, and decrease lipid accumulation induced by the OA/PA combination in COS7 cells. We also demonstrated that CiABHD5 does not directly interact with ATGL by Co-IP assay. Taken together, our results suggested that CiABHD4 and CiABHD5 were induced by PA through ER stress, and play essential roles in lipid accumulation by regulating ATGL expression in Ctenopharyngodon idella.

A STUDY ON CLASSIFICATION OF INHIBITORS OF FATTY ACID TRANSPORT PROTEIN-2 IN CELL

Inhibition of uptake of fatty acids in non-adipose tissues seems an attractive mechanism for treatment of lipotoxicity, dyslipidemia and other elements related to metabolic syndrome and obesity. Fatty acid transport proteins (FATPs) are bifunctional proteins involved in the uptake and activation of fatty acids by esterication with coenzyme A. To date, only inhibitors specic to FATP1 and FATP4 have been identied. Here we characterize a FATP2-specic fatty acid uptake inhibitor, CB5. Identied in a high throughput screening in yeast transformed with humanFATP2, CB5 is effective in inhibiting the uptake of fatty acid at low micro-molar ranges in cell lines that are models for intestines, liver, muscle, pancreas and adipose tissue with varying potencies. Inhibition was also specic for long and very-long chain fatty acids and not for medium chain fatty acids, which are transported by diffusion. Finally, CB5 was effective in protecting the cell lines that are models for liver and pancreas and primary liver cells from lipotoxic effects of saturated fatty acid, palmitic acid. High throughput screening also identied clozapine and chlorpromazine, atypical antipsychotics drugs, as inhibitors of FATP2-mediated fatty acid uptake in yeast system. However, atypical antipsychotics were ineffective in inhibiting the uptake of FAanalog C1-BODIPY-C12 in HepG2 cells. They were also ineffective in protecting HepG2 cells from the lipotoxic effects generated by saturated fatty acid compared to CB5 that exhibited protection to the cells, demonstrating that they are not effective inhibitors of fatty acid transport compared with CB5.

The omega‐3 sparing effect of saturated fatty acids: A reason to reconsider common knowledge of fish oil replacement

The omega‐3 sparing effect of saturated fatty acids: A reason to reconsider common knowledge of fish oil replacement

Oleate Ameliorates Palmitate-Induced Impairment of Differentiative Capacity in C2C12 Myoblast Cells

A common observation in metabolic disorders and aging is the elevation of free fatty acids, which can form ectopic fat deposition and result in lipotoxicity. Ectopic fat deposition of skeletal muscle has been recognized as an important component of aging, frailty and sarcopenia. Previous studies have suggested that lipotoxicity caused by free fatty acids mainly stemmed from saturated fatty acids and decreased unsaturated/ saturated fatty acid ratio in serum are also observed among metabolic disorder patients. However, the different effects of saturated fatty acids and unsaturated fatty acids on skeletal muscle are not fully differentiative capacity of C2C12 myoblasts by affecting Pax7, MyoD and MyoG, which are master regulators of lineage specification and the myogenic program. Then, oleate (OA), a monounsaturated fatty acid, were added to culture medium together with PA. Results showed that OA could ameliorate the impairment of differentiative capacity in C2C12 myoblast cells. In addition, we found PI3K/Akt signaling pathway played an important role during the process by RNA-sequencing and bioinformatics analysis. The positive effect of OA on myoblast differentiative capacity disappeared if PI3K inhibitor LY294002 was added. In conclusion, our study showed that PA could destroy differentiative capacity of C2C12 myoblasts by affecting the expression of Pax7, MyoD and MyoG, and OA could improve this impairment through PI3K /Akt signaling pathway.

PSVI-14 Effects of saturated fatty acids of 6 to 12 carbons in length on spoilage microbes, zoonotic pathogens and antimicrobial resistant bacteria in air exposed corn silage

Abstract Aerobic exposure of silage during the feed-out phase promotes growth of spoilage as well as pathogenic and multi-drug resistant (MDR) microbes which can risk infection of food-producing animals and the foods they produce. Livestock producers are interested in finding effective yet environmentally friendly interventions to preserve the nutritional value of these spoiled feedstuffs. We investigated the antimicrobial activity of 6 to 12 carbon-containing saturated fatty acids (C6, C8, C10 or C12) added (0.03 g) individually or as 1:1 mixtures of C6:C8:C10:C12 or C8:C10 to 4 g of overnight exposed silage suspended in 10 mL water. Net changes in colony counts, determined as the difference between counts measured after 0 and 24 h aerobic incubation (22oC) of untreated and treated silage suspensions (n = 3/treatment), were subjected to an analysis of variance. Populations of wild-type total aerobes and experimentally-inoculated MDR-Staphylococcus aureus were unaffected by treatment (P &amp;gt; 0.05), decreasing on average (± SD) 0.64 ± 0.40 and 1.09 ± 0.39 log10 CFU/g silage, respectively. Treatment effects (P &amp;lt; 0.05) were observed against experimentally-inoculated Listeria monocytogenes, with the C8:C10 mix decreasing this foodborne pathogen by 0.64 log10 CFU/g compared to a 0.95 log10/g increase in controls. Indigenous yeast and mold, considered responsible for spoilage, were decreased 2.12 and 3.07 log10 CFU/g by the C8 and C8:C10 treatments compared to 0.40 log10 CFU/g increase in controls. Indigenous lactic acid bacteria, considered beneficial, were decreased most potently by the C8 and C8:C10 treatments compared to controls (1.28, 0.66 and 0.37 log10 CFU/g, respectively). Indigenous enterococci decreased in all incubations, including controls (3.03 log10 CFU/g), compared to 4.69 to 5.03 log10 CFU/g decreases in C6, C8, C10, C12 and C8:C10 treatments. Results reveal that some fatty acid treatments inhibited pathogenic and spoilage microbes, yet treatment optimization is needed to avoid adverse effects against beneficial microbes.

Oxidised metabolites of the omega-6 fatty acid linoleic acid activate dFOXO.

Obesity-induced inflammation, or meta-inflammation, plays key roles in metabolic syndrome and is a significant risk factor in diabetes and cardiovascular disease. To investigate causal links between obesity, meta-inflammation, and insulin signaling we established a Drosophila model to determine how elevated dietary fat and changes in the levels and balance of saturated fatty acids (SFAs) and polyunsaturated fatty acids (PUFAs) influence inflammation. We observe negligible effect of saturated fatty acid on inflammation but marked enhancement or suppression by omega-6 and omega-3 PUFAs, respectively. Using combined lipidomic and genetic analysis, we show omega-6 PUFA enhances meta-inflammation by producing linoleic acid-derived lipid mediator 9-hydroxy-octadecadienoic acid (9-HODE). Transcriptome analysis reveals 9-HODE functions by regulating FOXO family transcription factors. We show 9-HODE activates JNK, triggering FOXO nuclear localisation and chromatin binding. FOXO TFs are important transducers of the insulin signaling pathway that are normally down-regulated by insulin. By activating FOXO, 9-HODE could antagonise insulin signaling providing a molecular conduit linking changes in dietary fatty acid balance, meta-inflammation, and insulin resistance.

Maternal high fat diet consumption reduces liver alpha7 nicotinic cholinergic receptor expression and impairs insulin signalling in the offspring

The activation of nicotinic acetylcholine receptor α7 subunit (α7nAChR) has been associated to anti-inflammatory response in macrophages. High-fat diet (HFD) consumption during pregnancy and lactation impairs the cholinergic anti-inflammatory pathway in liver and white adipose tissue of offspring. In order to evaluate the relationship between damage in the cholinergic anti-inflammatory pathway and insulin resistance (IR) development, the liver of offspring of obese dams was investigated. Additionally, the capacity of α7nAChR activation to reduce IR induced by saturated fatty acid was investigated in hepatoma cell line. Initially, female mice were subjected to either standard chow (SC) or HFD during pregnancy and lactation period. After weaning, only male offspring from HFD dams (HFD-O) and SC dams (SC-O) were fed with the SC diet. Hepatic α7nAChR expression was downregulated, and hepatic TNF-α, IL-1β, and pIKK level, but not pJNK, were elevated in the HFD-O compared to SC-O mice. Besides, hepatic expression of TNF-α in response to lipopolysaccharide (LPS) was higher in HFD-O than SC-O mice. Insulin-stimulated phosphorylation of the AKT was lower in HFD-O compared to SC-O. Additionally, insulin-stimulated phosphorylation of the AKT in KOα7Alb-Cre mice fed HFD was lower than WT mice fed HFD. In hepatoma cell line, palmitate increased IL-6 and TNF-α expressions and pJNK level. These effects were accompanied by reduced capacity of insulin to stimulate AKT phosphorylation. PNU or nicotine reduced cytokine expression and JNK activation, but improved insulin resistance induced by palmitate. Our results suggest that maternal obesity impairs hepatic α7nAChR expression and AKT phosphorylation in the offspring. In vitro studies suggest that α7nAChR activation has potential to reduce deleterious effect of saturated fatty acids on insulin signalling.

Effects of saturated fatty acids on skeletal muscle differentiation in an intrauterine hyperglycemic environment

Effects of saturated fatty acids on skeletal muscle differentiation in an intrauterine hyperglycemic environment

Fatty acid regio-specificity of triacylglycerol molecules may affect plasma lipid responses to dietary fats\u2014a randomised controlled cross-over trial

Background/ObjectivesHypercholesterolaemic effects of saturated fatty acids (SFA) may be influenced not only by the chain length, but also by their specific location within the triacylglycerol (TAG) molecule. We examined the hypothesis that dietary fats rich in SFA, but containing mostly unsaturated fatty acids in the sn-2 position with most SFA in sn-1 and -3 (palm olein [PO] and cocoa butter [CB]) will have similar serum lipid outcomes to unsaturated olive oil (OO).Subjects/MethodsThirty-eight participants (20–40 yr, 18.5– ≤ 27.5 kg/m2) completed a 4-week randomised 3 × 3 crossover feeding intervention, preceded by 2-week run-in and separated by 2-week washout periods. Background diet contained 35 percentage of total energy (%E) fat, 18%E protein, 48%E carbohydrates, differing in test fats only (palm olein (PO), CB, OO; 20%E). Total cholesterol (TC)/high density lipoprotein cholesterol (HDL-C) ratio and related variables; TC, HDL-C, low density lipoprotein cholesterol (LDL-C), TAG, apoA1, ApoB, ApoA1 (apolipoprotein A1)/ApoB (apolipoprotein B), lipoprotein (a) (Lp(a)), NEFA, LDL sub-fractions, were assessed pre- and post-intervention. Data were analysed using mixed effects longitudinal models with a P-value < 0.05 considered significant.ResultsChanges in plasma fatty acids (P < 0.05) confirmed compliance; C18:1 increased with OO compared to PO and CB; C16:0 decreased with OO and C18:0 increased following CB. No differences were seen for TC/HDL-C (mean [95%CI] change for PO, 0.08[0.00, 0.15] mmol/L; CB, 0.06 [−0.05, 0.16] mmol/L; and OO, −0.01 [−0.15, 0.13] mmol/L; P = 0.53] or any other parameter including LDL sub-fractions. OO decreased IDL-A compared to PO (−2.2 [−4.31, −0.21] mg/dL, P = 0.03).ConclusionIn healthy young participants, plasma lipid responses to PO and CB, enriched in SFA but having primarily unsaturated fatty acid in the sn-2 position of TAG, did not differ from OO.

"Insulin-like" effects of palmitate compromise insulin signalling in hypothalamic neurons.

Saturated fatty acids are implicated in the development of metabolic diseases, including obesity and type 2 diabetes. There is evidence, however, that polyunsaturated fatty acids can counteract the pathogenic effects of saturated fatty acids. To gain insight into the early molecular mechanisms by which fatty acids influence hypothalamic inflammation and insulin signalling, we performed time-course experiments in a hypothalamic cell line, using different durations of treatment with the saturated fatty acid palmitate, and the omega-3 polyunsaturated fatty acid, docosahexaenoic acid (DHA). Western blot analysis revealed that palmitate elevated the protein levels of phospho(p)AKT in a time-dependent manner. This effect is involved in the pathogenicity of palmitate, as temporary inhibition of the PI3K/AKT pathway by selective PI3K inhibitors prevented the palmitate-induced attenuation of insulin signalling. Similar to palmitate, DHA also increased levels of pAKT, but to a weaker extent. Co-administration of DHA with palmitate decreased pAKT close to the basal level after 8h, and prevented the palmitate-induced reduction of insulin signalling after 12h. The monounsaturated fatty acid oleate had a similar effect on the palmitate-induced attenuation of insulin signalling, the polyunsaturated fatty acid linoleate had no effect. Measurement of the inflammatory markers pJNK and pNFκB-p65 revealed tonic elevation of both markers in the presence of palmitate alone. DHA alone transiently induced elevation of pJNK, returning to basal levels by 12h treatment. Co-administration of DHA with palmitate prevented palmitate-induced inflammation after 12h, but not at earlier timepoints.