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Cellular long-chain fatty acids' (LCFAs) uptake is a crucial physiological process that regulates cellular energy homeostasis. AMPK has been shown to modulate LCFAs uptake in several kinds of cells, but whether it exerts an impact on intestinal LCFAs uptake is not quite clear. In the current study, we found that AMPK reinforced LCFAs uptake in intestinal epithelial cells (IECs). Moreover, intestinal epithelium-specific AMPK deletion impaired intestinal LCFAs absorption and protected mice from high-fat diet-induced obesity. Mechanistically, we discovered that AMPK deletion reduced the CD36 protein level by upregulating Parkin-mediated polyubiquitination of CD36 in IECs. Furthermore, our results revealed that AMPK affected PARK2 (gene name of Parkin) mRNA stability in a YTHDF2-dependent manner through FTO-dependent demethylation of N 6 -methyladenosine (m 6 A). Besides, AMPK promoted the translocation of CD36 to the plasma membrane in IECs, but the inhibition of AKT signaling suppressed this effect, which also halted the accelerated fatty acid uptake induced by AMPK. These results suggest that AMPK facilitates the intestinal LCFAs uptake by upregulating CD36 protein abundance and promoting its membrane translocation simultaneously. Such findings shed light on the role of AMPK in the regulation of intestinal LCFAs uptake., (© 2020 Federation of American Societies for Experimental Biology.)

Diarrhea, such as steatorrhea, could result from fat absorption disorders, which could be caused by many factors, including Escherichia coli infection. However, it is not clear how E. coli affects fatty acid absorption in animals. Lipopolysaccharide (LPS), as one of the main pathogenic components of E. coli , is the main cause of the virulence of E. coli . Therefore, we used LPS to explore the underlying mechanism of E. coli that causes the inhibition of fatty acid absorption in the intestine. In this study, we found that LPS caused apoptosis of intestinal epithelial cells in mice. Further, caspase-3 activation caused the inhibition of fatty acid absorption in the intestinal porcine enterocyte cell line (IPEC-J2). However, direct treatment of LPS did not induce any significant change in fatty acid absorption in IPEC-J2. We then prepared conditioned medium of LPS-treated porcine macrophage cell line (3D4/2) for incubating IPEC-J2, as LPS initiates inflammation by activating immune cells. The conditioned medium decreased fatty acid absorption and caspase-3 activation in IPEC-J2. While inhibiting the activation of caspase-3 in IPEC-J2, conditioned medium no longer caused serious deficiency of fatty acid absorption. As IL-1β, IL-6, and TNF-α in conditioned medium increase significantly, IPEC-J2 was treated with IL-1β, IL-6, and TNF-α, respectively. Only TNF-α induced caspase-3 activation in IPEC-J2. Reducing the secretion of TNF-α in 3D4/2, there was no obvious activation of caspase-3 in IPEC-J2, and fatty acid absorption recovered effectively. Based on the above results, we hold the opinion that LPS does not suppress fatty acid absorption directly in the intestine, but may work on macrophages that secrete cytokines, such as TNF-α, inducing caspase-3 activation and finally leading to the inhibition of fatty acid absorption in intestine.

The molecular mechanisms underlying the cellular uptake of long-chain fatty acids and the regulation of this process have been debated in recent decades. Here, we established an intestinal barrier dysfunction model in mice and Caco2 cell line by Lipopolysaccharide (LPS), and evaluated the fatty acid uptake capacity of the intestine. We found that LPS stimulation restricted the absorption of long chain fatty acid (LCFA), while Cathelicidin-WA (CWA) pretreatment facilitated this physiological process. At the molecular level, our results demonstrated that the stimulatory effects of CWA on intestinal lipid absorption were dependent on cluster determinant 36 and fatty acid transport protein 4, but not fatty acid-binding protein. Further, an enhanced intestinal barrier was observed in vivo and in vitro when CWA alleviated the fatty acid absorption disorder induced by LPS stimulation. Mechanistically, peroxisome proliferator-activated receptor (PPAR-γ) signaling was considered as a key pathway for CWA to enhance LCFA absorption and barrier function. Treatment with a PPAR-γ inhibitor led to impaired intestinal barrier function and suppressed LCFA uptake. Moreover, once PPAR-γ signaling was blocked, CWA pretreatment could not maintain the stability of the intestinal epithelial cell barrier or LCFA uptake after LPS stimulation. Collectively, these findings suggested that PPAR-γ may serve as a target for specific therapies aimed at alleviating fatty acid uptake disorder, and CWA showed considerable potential as a new PPAR-γ agonist to strengthen intestinal barrier function against fatty acid malabsorption.

Bacterial infection causes nutrient malabsorption in small intestine. KR-32, a kind of synthetic antimicrobial peptide, has the bacteriostatic effect. In the present study, 2 experiments were designed to analyze the effects of KR-32 on fat absorption of piglets with or without Escherichia coli infection. In Exp. 1, 12 weaning piglets (21 d old) were allocated to 2 groups: piglets with an intraperitoneal (i.p.) injection of antimicrobial peptide KR-32 (APK) and piglets with an i.p. injection of an equivalent volume (1 mL) of phosphate-buffered saline (PBS) (CON-1). Results showed that after 7 d of growth, KR-32 did not significantly change growth performance and apparent total tract digestibility (ATTD) of feed nutrients of normal pigs. To confirm whether KR-32 affects those of enterotoxigenic Escherichia coli (ETEC) K88-challenged pigs, we performed Exp. 2, in which 18 piglets (28 d old) were divided into the following 3 groups: 1) piglets orally challenged with 1 × 1010 cfu ETEC K88 on day 1 followed by an i.p. injection of 0.6 mg/kg KR-32 (K88 + APK); 2) piglets orally challenged with 1 × 1010 cfu ETEC K88 on day 1 followed by an i.p. injection of an equivalent volume (1 mL) of PBS (K88); and 3) piglets with an oral administration of fresh Luria-Bertani broth (50 mL) followed by an i.p. injection of an equivalent volume of PBS (CON-2). Results showed that ETEC K88 challenge led to poor ADFI, ADG, and G:F in piglets; decreased ATTD of feed nutrients, especially CP and ether extract (EE); and intestinal morphology disorder. After i.p. injection of KR-32, ADG and ATTD of CP and EE were greatly increased, G:F was significantly reduced (P < 0.05), and, especially, ATTD of EE returned to a normal level compared with group CON-2. Fatty acid absorption also highly increased after KR-32 injection. Then we focused on fat digestion and fatty acid uptake. The pH in the intestine and pancreas lipase showed no difference among the 3 treatment groups, whereas fatty acid transporter protein 4 (FATP4) expression was remarkably improved (P < 0.05) and the epithelial barrier was recovered after i.p. injection of KR-32. In conclusion, KR-32, given to ETEC K88-challenged piglets, improved growth performance, ATTD of EE, fatty acid absorption, and intestinal morphology, which indicated that KR-32 was likely to improve the expression of FATP4 and by repairing the epithelial barrier, thereby alleviating fatty acid malabsorption., (© The Author(s) 2019. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

A better understanding of the molecular mechanism of intestinal fatty acid absorption could lead to novel approaches to treatment and prevention of fatty acid-related metabolic diseases. Although it is confirmed that absorption of long-chain fatty acids (LCFAs) decreases during the pathological processes, the genetic basis and molecular mechanisms remain largely unknown. N 6 -methyladenosine (m 6 A) is the most prevalent internal modification on eukaryotic mRNA. Recently, m 6 A has been found to play important roles in inflammation and antiviral responses. In this study, we show that deficiency of Mettl3, the core methyltransferase of m 6 A, exerts antimalabsorption of LCFA activity in vitro through inhibiting the inflammation response mediated by LPS. To substantiate this finding further, we found the levels of triglycerides were also sustained in cells with depleted Mettl3, which were cultured in Transwell to polarize with villus formation to simulate the situation in vivo. Mechanistically, depletion of Mettl3 decreases the m 6 A level of Traf6 mRNA, thereby its transcripts are entrapped in the nucleus, followed by the decreased expression of Traf6, leading to the suppression of NF-κB and MAPK signaling pathway. Thus, the inflammation response was suppressed, resulting in the sustained absorption of LCFA. Moreover, we found that ectopic expression of Traf6 largely abolishes the sustained absorption LCFA in Mettl3 depletion cells. Collectively, silencing Mettl3 could sustain LCFA absorption through blocking the TRAF6-dependent inflammation response. Our work uncovers a critical function of m 6 A methylation and provides insight into critical roles of Mettl3 in LCFA absorption and inflammatory disease., (Copyright © 2019 by The American Association of Immunologists, Inc.)

Dietary fatty acids have different effects on fat deposition in pigs. To clarify the underlying mechanisms of this difference, we compared the metabolism of palmitic (PAM, saturated), oleic (OLA, monounsaturated) and linoleic acid (LNA, polyunsaturated) in porcine adipocytes treated with 100 μM PAM, OLA or LNA. We observed that the adipocytes incubated with LNA accumulated more lipids compared with those treated with PAM and OLA. We then probed the metabolism of these fatty acids in porcine adipocytes by using isotope-labelled fatty acids. The results showed that 42% of the [1- 14 C] LNA, 34% of the [1- 14 C] PAM and 28% of the [1- 14 C] OLA were recovered in the cellular lipids. The gene expression analyses showed that LNA significantly increased the expression of adipogenesis- and oxidation-related genes including PPARγ, C/EBPα, ap2 and NRF1. In addition, the cells incubated with LNA showed a decreased Ser 112 phosphorylation in PPARγ compared to those incubated with PAM and OLA. Furthermore, when PPARγ Ser 112 phosphorylation was inhibited, no significant difference in the triacylglycerol contents in the adipocytes was observed. These results showed the dietary fatty acids had different metabolism pathways in porcine adipocytes, and LNA significantly promoted lipid accumulation, probably by regulating PPARγ phosphorylation in adipocytes.

To assess the effects of betaine on hepatic lipid accumulation and investigate the underlying mechanism, thirty-two male Sprague-Dawley rats weighing 100 (sd 2·50) g were divided into four groups, and started on one of four treatments: basal diet, basal diet with betaine administration, high-fat diet and high-fat diet with betaine administration. The results showed that no significant difference of body weight was found among experimental groups. Compared with high-fat diet-fed rats, a betaine supplementation decreased (P< 0·05) hepatic TAG accumulation induced by high-fat diet, which was also supported by hepatic histology results. Additionally, hepatic betaine-homocysteine methyltransferase concentration [corrected] as well as its mRNA abundance and lecithin level were found increased (P< 0·05) by betaine supplementation in both basal diet-fed rats and high-fat diet-fed rats. Betaine administration in high-fat diet-fed rats exhibited a higher (P< 0·05) concentration [corrected] of hepatic carnitine palmitoyltransferase 1 (CPT1) compared with high-fat diet-fed rats. High-fat diet inhibited (P< 0·05) the gene expression of hepatic PPARα and CPT1. However, betaine administration in high-fat diet-fed rats elevated (P< 0·05) the gene expression of PPARα and CPT1. Moreover, concentration, gene and protein expressions of hepatic fibroblast growth factor 21 (FGF21) were increased (P< 0·05) in response to betaine administration in high-fat diet group; meanwhile the gene expression of hepatic AMP-activated protein kinase was increased (P< 0·05) as well. The results suggest that betaine administration enhanced hepatic lipid export and fatty acid oxidation in high-fat diet-fed rats, thus effectively alleviating fat accumulation in the liver.

Obesity may result from altered fatty acid (FA) disposal. Altered FA distribution in obese individuals is poorly understood. Lean wild-type C57BL/6J and obese C57BL/6Job/ob mice received an oral dose of [1-(14)C]18:1n-9 (oleic acid), and the radioactivity in tissues was evaluated at various time points. The (14)C concentration decreased rapidly in gastrointestinal tract but gradually increased and peaked at 96 h in adipose tissue, muscle and skin in lean mice. The (14)C concentration was constant in adipose tissue and muscle of obese mice from 4 h to 168 h. (14)C-label content in adipose tissue was significantly affected by genotype, whereas muscle (14)C-label content was affected by genotype, time and the interaction between genotype and time. There was higher total (14)C retention (47.7%) in obese mice than in lean mice (9.0%) at 168 h (P<0.05). The (14)C concentrations in the soleus and gastrocnemius muscle were higher in obese mice than in lean mice (P<0.05). Perirenal adipose tissue contained the highest (14)C content in lean mice, whereas subcutaneous adipose tissue (SAT) had the highest (14)C content and accounted for the largest proportion of total radioactivity among fat depots in obese mice. More lipid radioactivity was recovered as TAG in SAT from obese mice than from lean mice (P<0.05). Gene expression suggested acyl CoA binding protein and fatty acid binding protein are important for FA distribution in adipose tissue and muscle. The FA distribution in major tissues was altered in ob/ob mice, perhaps contributing to obesity. Understanding the disparity in FA disposal between lean and obese mice may reveal novel targets for the treatment and prevention of obesity.

Cold exposure promotes glucose oxidation and modulates the lipid metabolism in adipose tissue, but it is still not fully clear whether cold exposure could affect meat quality and fatty acid metabolism in skeletal muscle of pig in vivo. Here, we kept finishing pigs under cold or room temperature overnight and determined the effects of cold exposure on meat quality, fatty acids composition and transcriptional changes in skeletal muscle of pigs. We found that cold exposure significantly reduced the meat colour24 h and pH24 h, without affecting carcass characteristics and other meat quality traits. Considerable changes were found in the proportions of individual fatty acids and the total content of saturated fatty acid, polyunsaturated fatty acids, monounsaturated fatty acid and n3-fatty acids. RNA-seq results showed upregulated fatty acid biosynthesis genes and downregulated mitochondrial beta-oxidation genes. The lipid metabolism in cold-treated longissimus dorsi muscle might be regulated by functions of the lipoprotein particle, the extracellular matrix, and the PPAR signaling pathways. Our study revealed the potential of cold exposure to regulate the lipid metabolism and fatty acid composition in skeletal muscle of farmed animals. [ABSTRACT FROM AUTHOR]

Background: Heat stress has negative effects on the intestinal health of humans and animals. However, the impact of heat stress on intestinal microbial and metabolic changes remains elusive. Here, we investigated the cecal microbial and metabolic profiles in mice in response to heat stress. Methods: The mouse heat stress model was constructed by simulating a high-temperature environment. Twenty mice were randomly assigned to two groups, the control group (CON, 25°C) and the heat treatment group (HS, 40°C from 13:00 to 15:00 every day for 7 days). Serum and cecal contents were collected from the mice for serum biochemical analysis, 16S rRNA high-throughput sequencing, and non-targeted metabolomics. Results: Both core body temperature and water intake were significantly increased in the HS group. Serum biochemical indicators were also affected, including significantly increased triglyceride and decreased low-density lipoprotein in the heat stress group. The composition and structure of intestinal microbiota were remarkably altered in the HS group. At the species level, the relative abundance of Candidatus Arthromitus sp. SFB-mouse-Japan and Lactobacillus murinus significantly reduced, while that of Lachnospiraceae bacterium 3-1 obviously increased after HS. Metabolomic analysis of the cecal contents clearly distinguished metabolite changes between the groups. The significantly different metabolites identified were mainly involved in the fatty acid synthesis, purine metabolism, fatty acid metabolism, cyanoamino acid metabolism, glyceride metabolism, and plasmalogen synthesis. Conclusion: In summary, high temperature disrupted the homeostatic balance of the intestinal microbiota in mice and also induced significant alterations in intestinal metabolites. This study provides a basis for treating intestinal disorders caused by elevated temperature in humans and animals and can further formulate nutritional countermeasures to reduce heat stress-induced damage. [ABSTRACT FROM AUTHOR]

Sufficient fatty acid (FA) uptake from jejunal lumen is closely associated with pediatric growth. Enterotoxigenic Escherichia coli (ETEC), which poses a big threat to young mammals' health, is also targeted on the jejunum, however, the effects on FA uptake is not understood yet. To explore the impacts of ETEC on the FA uptake ability of jejunum epithelial enterocytes during early life, we orally gavaged weaning piglets with ETEC K88 and found intestinal inflammation combined with compromised uptake of LCFA (C16:0, C18:0, C20:3, C20:4) except for C14:0 whose chain length is similar to medium chain fatty acid (MCFA). Furthermore, we observed reduced protein expression of TJs, fatty acid transport protein 4 (FATP4), peroxisome proliferator-activated receptor γ (PPARγ), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), and upregulated expression of p-PPARγ. In the in vitro study, we challenged polarized porcine intestine jejunum cell line IPEC-J2 with ETEC K88 and discovered similar results on intestinal barrier and expression of associated genes combined with morphological changes. Based on the constructed cellular model, we then determined lower uptake of BODIPY-labeled C16:0 without any difference in the uptake of BODIPY-labeled C12:0. The content of intracellular triglyceride which was mainly synthesized by LCFA concomitantly lowered down. Using gene knock down and overexpression, FATP4 was confirmed to be responsible for LCFA uptake. Moreover, ERK1/2 inhibitor U0126 and PPARγ antagonist T0070907 revealed ETEC could initiate cascaded phosphorylation of ERK1/2 and PPARγ resulting in hindered expression of FATP4. These results indicate ETEC challenge will cause dysfunction in FATP4-dependent LCFA uptake by phosphorylation of ERK1/2 and PPARγ. Furthermore, intestinal uptake of MCFA is in a FATP4-independent manner which is not easily disturbed by ETEC. [ABSTRACT FROM AUTHOR]

n-3 Long-chain PUFA up-regulate intestinal lipid metabolism. However, whether these metabolic effects of PUFA on intestine are mediated by AMP-activated protein kinase (AMPK) remains to be elucidated. To determine the effects of α-linolenic acid (ALA) on intestinal fatty acid (FA) metabolism and whether these effects were affected by AMPK deletion, mice deficient in the catalytic subunit of AMPKα1 or AMPKα2 and wild-type (WT) mice were fed either a high-fat diet (HF) or HF supplemented with ALA (HF-A). The results showed that ALA supplementation decreased serum TAG content in WT mice. ALA also increased mRNA expression of genes (carnitine palmitoyltransferase 1a, acyl-CoA oxidase 1, medium-chain acyl-CoA dehydrogenase, cytochrome P450 4A10 and pyruvate dehydrogenase kinase isoenzyme 4a) involved in intestinal lipid oxidation and mRNA expression of TAG synthesis-related genes (monoacylglycerol O-acyltransferase 2, diacylglycerol O-acyltransferases 1 and 2) in WT mice. Consistent with these, expression levels of phosphorylated AMPKα1 and AMPKα2 were also increased in WT mice after ALA addition. However, in the absence of either AMPKα1 or AMPKα2, ALA supplementation failed to increase intestinal lipid oxidation. In addition, no significant effects of either diet (HF and HF-A) or genotype (WT, AMPKα1–/– and AMPKα2–/–) on FA uptake in the intestine and faecal TAG output were observed. Our results suggest that AMPK is indispensable for the effects of ALA on intestinal lipid oxidation. [ABSTRACT FROM PUBLISHER]

Background: Supplementation of feed with long-chain fatty acids (LCFAs) during the grower and finisher phases has long been discussed as a growth promotion strategy in pigs, but its effects are inconsistent. The purpose of our study was to comprehensively evaluate its effects on the growth performance based on the average daily gain (ADG), average daily feed intake (ADFI) and gain: feed (G:F) ratio and to unveil the roles of the basal diet, LCFA concentration and LCFA saturation. Results: We searched the PubMed and Web of Science databases (articles published from Jan 1st, 2000, to Sep 30th, 2018; restricted to English) and compared LCFA-supplemented diets with control diets. We retrieved 2346 studies, 18 of which (1314 pigs, 26 records) were eligible for our analysis. We used a random-effects model to calculate the weighted mean differences (WMDs) and 95% confidence intervals (CIs). LCFA supplementation in the grower-finisher phase improved the ADG (WMD = 41.74 g/d, 95% CI: 8.81 to 74.66, P = 0.013) and G:F ratio (WMD = 0.019, 95% CI: 0.006 to 0.032, P = 0.003). For supplementation solely in the finisher phase, we found a similar performance in the ADG (WMD = 39.93 g/d, 95% CI: 26.48 to 53.38, P < 0.001) and G:F ratio (WMD = 0.019, 95% CI: 0.006 to 0.032, P < 0.001) but a reduction in the ADFI (WMD = − 83.863 g/d, 95% CI: − 156.157 to − 11.569, P = 0.023). Specifically, approximately 5% LCFA supplementation in the finisher phase had significant effects on the ADG (WMD = 51.385 g/d, 95% CI: 35.816 to 66.954, P < 0.001), ADFI (WMD = − 102.869 g/d, 95% CI: − 189.236 to − 16.502, P = 0.02) and G:F ratio (WMD = 0.028, 95% CI: 0.018 to 0.039, P < 0.001), whereas a concentration of approximately 1% exhibited no effects. Conclusions: Overall, regardless of the basal diet and saturation, LCFA supplementation greatly improves the growth performance of grower and finisher pigs, primarily by increasing the energy density. [ABSTRACT FROM AUTHOR]

Cultured fat is an important component of cell-cultured meat, which furnishes essential fatty acids and phospholipids, as well as being abundant in cholesterol. However, few studies have been on regulating the nutritional composition of cell-cultured meat, especially concerning the deposition of polyunsaturated fatty acids (PUFAs) and cholesterol. Here, we use sodium alginate-gelatin scaffolds to generate cultured fat, and find that phosphatidylcholine (PC) can promote the adipogenic differentiation of fibro-adipogenic progenitors (FAPs), accelerate lipid accumulation, and facilitate cultured fat production in the sodium alginate-gelatin 3D culture system. Interestingly, when PC is loaded into Euglena (Eg-PC) for co-culture, the triglycerides (TGs) content in fat is further increased. Multi-omics analysis reveals that PC treatment significantly alters the lipid composition of cultured fat produced by FAPs and increases the content of TGs, especially PUFAs (alpha-linolenic acid and linolenic acid). More importantly, PC treatment also reduces the total cholesterol content of cultured fat. This study provides innovative approaches for producing cultured fat with "high PUFAs and low cholesterol". [Display omitted] • Production of cultured fat using sodium alginate-gelatin composite hydrogel system. • PC promotes the adipogenic differentiation of fibro-adipogenic progenitors (FAPs). • Euglena-PC enhances the efficiency of PC in regulating FAPs differentiation. • PC contributes to cultured meat production with "high PUFAs and low cholesterol". • PC decreases cholesterol deposition by regulating HIF1A-Insig2-HMGCR pathway. [ABSTRACT FROM AUTHOR]

• The FMF contains probiotics and low-molecular nutrients, such as trichloroacetic acid–soluble protein, lactic acid, and unsaturated fatty acid. • FMF supplementation improved the growth performance in finishing pigs. • Pigs fed FMF diets improved meat quality parameters, ω-6 and ω-3 polyunsaturated fatty acids proportions, and antioxidant ability of pigs. This study was conducted to evaluate the effects of feeding fermented mixed feed (FMF) on the growth performance, meat quality, muscle fatty acids profile and antioxidant ability in finishing pigs. In experiment 1, six hundred pigs (Duroc × Landrace × Large White) were randomly distributed into 3 treatments with 4 replicates (50 pigs per replicate). Dietary treatments included a control (CON; basal diet), a basal diet + 5% FMF (5% FMF), and a basal diet + 10% FMF (10% FMF). After 39 days of the experiment, growth performance was evaluated. In experiment 2, a total of four hundred finishing pigs were randomly allocated into 4 dietary treatments consisting of four replicates per treatment and 25 pigs per replicate. Dietary treatments were a control (CON; basal diet), a basal diet + 2% FMF (2% FMF), a basal diet + 4% FMF (4% FMF), and a basal diet + 8% FMF (8% FMF). The duration of the experiment was 35d. At the end of the experiment, 48 pigs from 4 dietary treatments were slaughtered for the determination of carcass and meat quality parameters. In experiment 1, compared with CON, dietary supplementation with 10% FMF increased (P < 0.05) gain/feed ratio (G/F), whereas there was no significant difference in 5% FMF group. In experiment 2, the final body weight, average daily gain (ADG) and G/F were higher (P < 0.05) in 8% FMF group. Feeding 8% FMF increased (P < 0.05) loin muscle area, a* value, marbling score, intramuscular fat (IMF), and inosine-5′-monophosphate (IMP), and decreased (P < 0.05) the drip loss of the longissimus muscle (LM). The percentages of C18:1ω-9c, C18:2ω-6c, C18:3ω-3 and C20:4ω-6c in LM were increased (P < 0.05) in pigs fed 8% FMF diet. Furthermore, greater (P < 0.05) SOD and GSH-Px activities were observed in serum and LM of pigs in 8% FMF group in comparison with CON. Collectively, the present study suggested that dietary FMF supplementation improved the growth performance in finishing pigs. Moreover, pigs fed FMF diets improved carcass performance, meat quality parameters, unsaturated fatty acids proportions and antioxidant ability compared to those fed FMF unsupplemented diets. [ABSTRACT FROM AUTHOR]