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Background & Aims Lactate has recently been reported to accumulate in the livers of patients progressing from simple steatosis to non-alcoholic steatohepatitis (NASH). However, the underlying mechanism(s) of lactate accumulation and the role of lactate in the progression of non-alcoholic fatty liver disease (NAFLD) are essentially unknown. Methods We compared the acetylome in liver samples taken from healthy individuals, patients with simple steatosis and patients with NASH to identify potential targets of acetylation with a role in lactate metabolism. Interactions between the acetylated target and acetyltransferases were measured in multiple cell lines. An acetyltransferase inhibitor was injected into high-fat diet (HFD)-fed mice to determine the role of lactate on NAFLD progression in vivo. Results Hyperacetylation of lactate dehydrogenase B (LDHB) was found to be associated with lactate accumulation in NAFL and NASH livers in humans and mice. P300/CBP-associated factor (PCAF)-mediated acetylation of LDHB K82 was found to significantly decrease LDHB activity and impair hepatic lactate clearance, resulting in lactate accumulation. Acetylated LDHB induced lactate accumulation which exacerbated lipid deposition and inflammatory responses by activating histone hyperacetylation in HFD-induced NASH. The administration of embelin, a PCAF inhibitor, and the generation of an acetylation-deficient mutant of LDHB ameliorated NASH. Conclusion PCAF-dependent LDHB acetylation plays a key role in hepatic lipid accumulation and inflammatory responses by impairing lactate clearance; this process might be a potential therapeutic target for the treatment of NASH. Lay summary Lactate is known to accumulate in the livers of patients during the progression of non-alcoholic fatty liver disease (NAFLD); however, the underlying mechanism(s) of this accumulation and its importance in disease progression are unknown. Herein, we show that the acetylation of an enzyme involved in lactate metabolism leads to impaired lactate clearance and exacerbates NAFLD progression.

BACKGROUND Increased hepatic glycolysis and lipogenesis are characteristic of pregnancy. OBJECTIVES The present study aimed to investigate the mechanism of garcinol on the amelioration of hepatic pyruvate and triglyceride (TG) accumulation in mid-to-late pregnant rats. METHODS Forty Sprague-Dawley pregnant rats (aged 9 wk, n = 10/diet) were fed a basal diet (control) or that diet plus garcinol at 100 ppm (Low Gar), 300 ppm (Mid Gar), or 500 ppm (High Gar) for 14 d. The livers were processed for Western blotting analyses and measuring enzymatic activity and pyruvate and TG concentrations. Hepatocytes from other pregnant Sprague Dawley rats were transfected with P300/CBP associating factor (PCAF) short interfering (si)RNAs; hepatocytes from nonpregnant Sprague-Dawley rats with overexpression of PCAF were treated with garcinol (5 μM). The activity and acetylation of upstream stimulatory factor (USF-1) and glycolytic enzymes were analyzed. RESULTS Dietary garcinol significantly decreased (P

Disorder of hepatic glucose metabolism is the characteristic of late-pregnant sows. The purpose of our study was to look into the mechanism of garcinol on the improvement of hepatic gluconeogenic enzyme in late-pregnant sows. Thirty second- and third-parity sows (Duroc × Yorkshire × Landrace, n 10/diet) were fed a basal diet (control) or that diet supplemented with 100 mg/kg (Low Gar) or 500 mg/kg (High Gar) garcinol from day 90 of gestation to the end of farrowing. The livers were processed to measure enzymatic activity. Hepatocytes from pregnant sows were transfected with P300/CBP-associating factor (PCAF) small interfering RNA (siRNA) or treated with garcinol. Dietary garcinol had no effect on average daily feed intake, body weight (BW), backfat and BW gain of late-pregnant sows. Garcinol promoted plasma glucose levels in pregnant sows and newborn piglets. Garcinol up-regulated hepatic gluconeogenic enzyme expression and decreased PCAF activity. Garcinol had no effect on the expression of PPAR-γ co-activator 1α (PGC-1α) and Forkhead box O1 (FOXO1) but significantly increased their activity and decreased their acetylation in late-pregnant sows. Transfection of PCAF siRNA to hepatocytes of pregnant sows increased PGC-1α and FOXO1 activities. Furthermore, in hepatocytes of pregnant sows, garcinol treatment also up-regulated the activities of PGC-1α and FOXO1 and inhibited the acetylation of PGC-1α and FOXO1. Garcinol improves hepatic gluconeogenic enzyme expression in late-pregnant sows, and this may be due to the mechanism of down-regulating the acetylation of PGC-1α and FOXO1 induced by PCAF in isolated hepatocytes.

Weaning significantly alters hepatic aromatic amino acid (AAA) metabolism and physiological functions. However, less is known about the regulating mechanism of hepatic AAA metabolism after weaning. A total of 200 21-day-old piglets (Duroc &times, Landrace) were assigned randomly to the control group and the weaning group. In this study, weaning significantly decreased the concentration of phenylalanine, tryptophan, and tyrosine in piglet livers (p &lt, 0.05). Additionally, through the detection of liver AAA metabolites and metabolic enzyme activity, it was observed that hepatic tryptophan catabolism was enhanced, while that of phenylalanine was weakened (p &lt, 0.05). Intriguingly, acetyl-proteome profiling of liver from weaned piglets showed that weaning exacerbated the acetylation of phenylalanine hydroxylase (PAH) and the deacetylation of tryptophan 2,3-dioxygenase (TDO). Analysis of PAH and TDO acetylation in Chang liver cells showed that acetylation decreased the PAH activity, while deacetylation increased the TDO activity (p &lt, 0.05). Furthermore, metabolites of AAAs and the acetylation statuses of PAH and TDO in primary hepatocytes from weaned piglets were consistent with the results in vivo. These findings indicated that weaning altered the PAH and TDO activity by affecting the acetylation state of the enzyme in piglets&rsquo, &rsquo, livers. Lysine acetylation may be a potential regulatory mechanism for AAA metabolism in response to weaning.

Background The effects of dietary garcinol on diarrhea and intestinal barrier function associated with its modulation of gut microbiota in weaned piglets were investigated. Method One hundred forty four weaned piglets (Duroc × Yorkshire × Landrace) from 16 pens (9 piglets per pen) were randomly divided into four treatment groups: controls (CON) or those supplemented with 200 mg/kg (LOW), 400 mg/kg (MID), or 600 mg/kg (HIGH) diet garcinol. After 14-day trial, three piglets per pen were chosen to collect plasma, intestinal tissue and colonic digesta samples. Results We demonstrated for the first time that garcinol promoted growth performance, as increased average daily feed intake (ADFI) and decreased feed/gain ratio (F/G); and reduced diarrhea incidence (P P P P P Escherichia coli, and increased the growth of the beneficial bacteria Lactobacillus. Conclusion This work provides a fundamental basis for the future development of garcinol-functional food use for improving diarrhea and intestinal barrier function in weaned piglets and for understanding the biological effects of garcinol and its potential as a functional feed additive.

Hepatic metabolic syndrome is associated with inflammation, as inflammation stimulates the reprogramming of nutrient metabolism and hepatic mitochondria-generated acetyl-CoA, but how acetyl-CoA affects the reprogramming of nutrient metabolism, especially glucose and fatty acids, in the condition of inflammation is still unclear. Here, we used an acute inflammation model in which pigs were injected with lipopolysaccharide (LPS) and found that hepatic glycolysis and fatty acid oxidation are both promoted. Acetyl-proteome profiling of LPS-infected pigs liver showed that inflammatory stress exacerbates the acetylation of mitochondrial proteins. Both mitochondrial glutamate oxaloacetate transaminase 2 (GOT2) and malate dehydrogenase 2 (MDH2) were acetylated, and the malate-aspartate shuttle (MAS) activity was stimulated to maintain glycolysis. With the use of 13C-carbon tracing in vitro, acetyl-CoA was found to be mainly supplied by lipid-derived fatty acid oxidation rather than glucose-derived pyruvate oxidative decarboxylation, while glucose was mainly used for lactate production in response to inflammatory stress. The results of the mitochondrial experiment showed that acetyl-CoA directly increases MDH2 and, in turn, the GOT2 acetylation level affects MAS activity. Treatment with palmitate in primary hepatocytes from LPS-injected pigs increased the hepatic production of acetyl-CoA, pyruvate, and lactate; MAS activity; and hepatic MDH2 and GOT2 hyperacetylation, while the deficiency of long-chain acetyl-CoA dehydrogenase resulted in the stabilization of these parameters. These observations suggest that acetyl-CoA produced by fatty acid oxidation promotes MAS activity and glycolysis via nonenzymatic acetylation during the inflammatory stress response.

The liver is an important organ responsible for amino acids (AA) conversion, and catabolism. To investigate the metabolic characteristic of AA in liver, eighteen castrated male pigs (20±1 kg), implanted with arterial–portal–hepatic–mesenteric catheters, were fed three crude protein (CP) diets (14%, 17%, 20%) with six pigs per group. Blood was sampled for 7.5 h post-feeding. Hepatic tissue was sampled from additional fifteen pigs (three CP diets groups, 5 per group) on 3 h post-feeding. Portal vein plasma flow (PVPF), hepatic vein plasma flow (HVPF), hepatic cumulative net appearance and related gene expression were analyzed. There were no difference (P>0.05) for PVPF and HVPF among the three CP diets. Compared with the 20% CP diet, the 14% CP diet increased (P

This study was performed to determine if pyruvate, which acts as a critical intermediate in energy metabolism, can substitute the role of glutamate as a metabolic fuel and effectively reduce nitrogen excretion in pigs. First, the experiment in vitro was carried out to investigate the effects of culturing porcine small intestinal epithelial cell line with pyruvate on the oxidation. Then, barrows weighing 40 kg were used in the experiment investigating the changes of nitrogen balance in response to addition of pyruvate to low-protein diets. Last, barrows (40 kg), which were surgically fitted with permanent catheters in the mesenteric vein, portal vein, hepatic vein, and carotid artery, were used to investigate the effects of supplementing low-protein diets with calcium pyruvate on the net portal fluxes of amino acids (AAs) and the consumption of AAs in the liver. The results showed that culturing cells with sodium pyruvate significantly reduced the number of glutamate oxidation (P < 0.05). Addition of calcium pyruvate to low-protein diets significantly reduced urinary nitrogen excretion from 13.2 g/d (18.0% crude protein, CP) to 10.3 g/d (15.0% CP) or 7.80 g/d (13.5% CP) and total nitrogen excretion from 22.5 g/d (18.0% CP) to 17.8 g/d (15.0% CP) or 14.2 g/d (13.5% CP) (P < 0.05), without obviously negative effects on the nitrogen retention (P > 0.05). Addition of calcium pyruvate to low-protein diets significantly decreased essential AA consumption rate in the liver (P < 0.05). This diet modification reduced the net portal fluxes of NH(3), glycine, and alanine, as well as urea production rate in the liver (P < 0.05). The results indicated that pyruvate is an effective substitute for glutamate as a supplement in low-protein diets, reducing porcine nitrogen excretion and nitrogen consumption.

The liver is the central organ of glycolipid metabolism, which regulates the metabolism of lipids and glucose to maintain energy homeostasis upon alterations of physiological conditions. Researchers formerly focused on the phosphorylation of glucagon in controlling liver metabolism. Noteworthily, emerging evidence has shown glucagon could additionally induce acetylation to control hepatic metabolism in response to different physiological states. Through inducing acetylation of complex metabolic networks, glucagon interacts extensively with various energy-sensing factors in shifting from glucose metabolism to lipid metabolism during prolonged fasting. In addition, glucagon-induced acetylation of different energy-sensing factors is involved in the advancement of nonalcoholic fatty liver disease (NAFLD) to liver cancer. Here, we summarize the latest findings on glucagon to control hepatic metabolism by inducing acetylation of energy-sensing factors. Finally, we summarize and discuss the potential impact of glucagon on the treatment of liver diseases.

Excess ammonia is produced during fasting when amino acids are used for glucogenesis. Together with ureagenesis, glucogenesis occurs in periportal hepatocytes mediated mainly through the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). In vivo experiments showed that fasting strongly stimulated mice glucagon secretion, hepatic PGC-1α, sirtuin 3 (SIRT3) and sirtuin 5 (SIRT5) expression and ureagenesis enzymatic activity such as carbamoyl phosphate synthetase 1 (CPS1) and ornithine transcarbamoylase (OTC). Interestingly, 15N-labeled urea and 13C-labeled glucose production in wild-type mice were significantly increased compared with PGC-1α null mice by [15N,13C]alanine perfused liver. Glucagon significantly stimulated ureagenesis, expression of SIRT3, SIRT5 and the activities of CPS1 and OCT but did not stimulate PGC-1α silencing hepatocytes in mice periportal hepatocytes. Contrarily, PGC-1α overexpression significantly increased the expression of SIRT3, SIRT5 and the activities of CPS1 and OTC, but induced no significant changes in CPS1 and OTC expression. Morever, SIRT3 directly deacetylates and upregulates the activity of OTC, while SIRT5 deacetylates and stimulates the activity of CPS1. During fasting, PGC-1α facilitates ureagenesis in mouse periportal hepatocytes by deacetylating CPS1 and OTC modulated by mitochondrial deacetylase, SIRT3 and SIRT5. This mechanism may be relevant to ammonia detoxification and metabolic homeostasis in liver during fasting.

The present study was conducted in a one-factorial arrangement to determine the effects ofdl-2-hydroxy-4-methylthiobutyrate (dl-HMTB) on the first-pass intestinal metabolism of dietary methionine and its extra-intestinal availability. Barrows (n6; aged 35 d; weight 8·6 kg), implanted with arterial, portal, mesenteric and gastric catheters, were fed a diet containingdl-methionine (dl-MET) ordl-HMTB once hourly and infused intramesenterically with 1 %p-aminohippurate and intragastrically with [1-13C]methionine at 7·0 μmol/kg body weight per h. Arterial and portal blood samples were taken at hourly intervals until 6 h of tracer infusion and pigs was then killed for collection of muscle, intestine, liver and kidney samples. The net portal appearance of methionine, expressed as the fraction of ingested directly availablel-methionine, was higher (P dl-HMTB than in thedl-MET diet, and there was no difference (P = 0·26) in the fractional portal balance of [1-13C]methionine between the diets. [1-13C]methionine enrichment (tracer:tracee ratio; mol/100 mol amino acid) in the jejunum, arterial and portal plasma, liver, kidney and muscle was also not different (P>0·05) between the groups. Over the 6 h period after the start of feeding, the average concentration of citrulline both in the arterial and portal plasma was higher (P dl-HMTB than in thedl-MET group, and arterial plasma ornithine and taurine concentration was also higher (P dl-HMTB than in thedl-MET group. However, plasma urea concentration both in the arterial and portal vein was lower (P dl-HMTB than in thedl-MET group. These results suggested that the potential difference in the first-pass use of methionine by the intestine between thedl-HMTB anddl-MET diets might affect intestinal and systemic metabolism of other amino acids, which may provide new important insights into nutritional efficiency of different methionine sources.

The present study was designed to investigate the effect of dietary fish oil supplementation on piglet T helper cells (Th) polarization in relation to its impact on piglet serum interferon γ (IFN-γ) and interleukin 10 (IL-10) concentrations and splenic expression of Th1/Th2 characteristic genes. The diets of 18 gestating sows were supplemented with 7% lard (C) (n = 10) or 7% fish oil (T) (n = 8) from 10 d before parturition to weaning. At weaning, a split plot experiment was designed, 56 piglets, 28 each from sows fed with fish oil diet or lard diet, were divided into four groups of 7 replicates (one female and one castrated male per replicate) based on both sow diet during lactation and post-weaning piglet diet (C had 7% lard and T had 7% fish oil): CC, CT, TC, TT, and were fed the 7% fish oil or lard diet from day 35 to day 70. Serum concentrations of IFN-γ and IL-10, and Th1/Th2 related genes expression levels in spleen were measured and analyzed. The results showed that piglets fed with fish oil diet during post-weaning tended to have higher serum IFN-γ/IL-10 ratio (P = 0.09) than lard diet fed piglets. Lactation fish oil feeding increased splenic IL-12b, IL-12 receptor β2 (IL-12Rβ2), IL-2 and IFN-γ genes expression (P

The aim of the study was to investigate the effects of dietary linseed (rich in n-3 PUFA) on expression of inflammation-related genes and on growth performance of growing-finishing barrows. Two isoenergetic and isonitrogenous diets were formulated, one as the basal diet and the other containing 10% linseed. Twenty-four Landrace x Yorkshire barrows weighing 35 +/- 3.7 kg were randomly assigned to 1 of 4 treatment groups, with 6 pigs per group. During the entire experimental period of 90 d, these 4 groups of pigs were first fed the basal diet and then fed the linseed diet for 0, 30, 60, and 90 d before slaughter, respectively. Pig growth; messenger RNA (mRNA) expression of peroxisome proliferator-activated receptor-gamma (PPARgamma), IL-1beta0, IL-6, and tumor necrosis factor-alpha (TNF-alpha); and plasma concentrations of the 3 proinflammatory cytokines were measured and analyzed. Average daily feed intake did not differ among treatment groups (P > 0.05), but ADG (P < 0.05) and G:F (P < 0.01) responded quadratically to the duration of linseed diet feeding, and pigs in the 60-d treatment group had the greatest ADG and G:F. The mRNA expression of PPARgamma in loin muscle and spleen increased linearly (P < 0.01) with the duration of linseed diet feeding, whereas its expression in adipose tissue was not affected (P = 0.095). Tumor necrosis factor-alpha and IL-6 mRNA expression in muscle, adipose, and spleen, as well as serum concentration of TNF-alpha, decreased linearly (P < 0.01) with the duration of linseed diet feeding. Peroxisome proliferator-activated receptor-gamma mRNA abundance was negatively correlated with IL-1beta, IL-6, and TNF-alpha mRNA abundance both in muscle (R(2) = 0.63, P < 0.001) and in spleen (R(2) = 0.69, P < 0.001), and PPARgamma mRNA expression in spleen (R(2) = 0.59, P < 0.01) and muscle (R(2) = 0.52, P < 0.05) was negatively correlated with serum TNF-alpha concentration. There were also significant quadratic relations between ADG and expression of PPARgamma (P < 0.05) and splenic TNF-alpha (P < 0.05). These data suggest that intake of n-3 PUFA from the linseed diet led to significant decreases in the expression of proinflammatory cytokine genes, which may stimulate growth in growing-finishing barrows, at least in part, through a PPARgamma-dependent mechanism.

The aim of the study was to investigate the effect of duration of feeding linseed (rich in n -3 PUFA) on peroxisome proliferator-activated receptor γ (PPARγ) and tumor necrosis factor (TNF-α) gene expression, and muscle mass of growing–finishing barrows. Two isoenergetic and isonitrogenous diets were formulated, and one of which was the basal diet and another one was the linseed diet including linseed at the level of 10%. Twenty-four Landrace × Yorkshire barrows weighing 35 ± 3.7 kg were randomly assigned to four treatments with six individuals per treatment. Pigs in treatment 1 (T1) fed the control diet throughout the experimental period, while pigs in T2, T3 and T4 fed the control diet except for 30, 60, and 90 d prior to slaughter when the linseed diet were fed. The experiment was conducted for 90 days. The longissimus muscle mass and each muscle mass in the hind leg were weighted. PPARγ and TNF-α mRNA expression levels in muscle, spleen and adipose tissue, and plasma concentrations of TNF-α data were measured and analyzed. The results showed that the longissimus muscle mass, quadriceps femoris muscle mass and semitendinosus muscle mass increased linearly ( P longissimus muscle and spleen increased ( P P = 0.095). Duration of linseed addition linearly decreased ( P longissimus dorsi muscle , adipose and spleen, and serum concentration of TNF-α as well. The expression levels of PPARγ negatively correlated with the expression of TNF-α in muscle ( R 2 = 0.70, P R 2 R 2 = 0.77, P R 2 R 2 = 0.59, P R 2 R 2 = 0.52, P R 2 R 2 = 0.80, P R 2 R 2 = 0.87, P longissimus dorsi muscle mass. These data suggested that duration of feeding linseed diet lead to a linear decrease of TNF-α gene expression, which may increase the muscle mass in growing–finishing barrows, at least in part, through a PPARγ-dependent mechanism.

Overwhelming consensus emerges among countless evidences that obesity is characterized by a chronic low-grade inflammation in the adipose tissue (AT), which subsequently develops into a systemic inflammatory state contributing to obesity-associated diseases. N-3 Polyunsaturated fatty acids (n-3 PUFA), known as important modulators participating in inflammatory process, turn out to be an effective mitigating strategy dealing with local and systemic inflammation observed in obesity. Some of the effects of n-3 PUFA are brought about by regulation of gene expression through interacting with nuclear receptors and transcription factors; other effects are elicited by modulation of the amount and type of mediator derived from PUFAs. The metabolic effects of n-3 PUFA mainly result from their interactions with several organ systems, not limited to AT. Notably, the attenuation of inflammation in hard-hit AT, in turn, contributes to reducing circulating concentrations of proinflammatory cytokines and detrimental metabolic derivatives, which is beneficial for the function of other involved organs. The present review highlights a bridging mechanism between n-3 PUFA-mediated inflammation relief in AT and systemic benefits.

The present research was undertaken to determine the effects of EPA (20 : 5 n-3) and DHA (22 : 6 n-3) on chylomicron and VLDL synthesis and secretion by Caco-2 cells. Cells were incubated for 12 to 36 h with 400 μM OA, EPA, and DHA; then 36 h was chosen for further study because EPA and DHA decreased de novo triglycerides synthesis in a longer incubation compared with OA (P<0.01). Neither the uptake nor oxidation was different in response to the respective fatty acids (P>0.05). Compared with OA, intercellular and secreted nascent apolipoprotein B48 and B100 were decreased by EPA and DHA (P<0.01). Both DHA and EPA resulted in a lower secretion of chylomicron and VLDL (P<0.01). In contrast to OA, EPA and DHA were preferentially incorporated into phospholipids instead of triacylglycerols (P<0.01). These discoveries demonstrated that exposure of DHA and EPA reduced the secretion of chylomicron and VLDL partly by regulating the synthesis of TG and apoB.

The study was conducted to investigate whether dietary fish oil could influence growth of piglets via regulating the expression of proinflammatory cytokines. A split-plot experimental design was used with sow diet effect in the main plots and differing piglet diet effect in the subplot. The results showed that suckling piglets from fish oil fed dams grew rapidly (P<0.05) than control. It was also observed that these piglets had higher ADG, feed intake, and final body weight (P<0.05) during postweaning than those piglets from lard fed dams. Furthermore, there was a significant decrease (P<0.01) in the expression of interleukin 6 and tumor necrosis factor-αinlongissimus dorsimuscle. In contrast, there was a tendency (P<0.10) towards lower ADG and higher feed : gain in weaned piglets receiving fish oil compared with those receiving lard. Meanwhile, splenic proinflammatory cytokines expression was increased (P<0.01) in piglets receiving fish oil during postweaning period. The results suggested that 7% fish oil addition to sows' diets alleviated inflammatory response via decreasing the proinflammatory cytokines expression in skeletal muscle and accelerated piglet growth. However, 7% fish oil addition to weaned piglets' diets might decrease piglet growth via increasing splenic proinflammatory cytokines expression.

Previous evidence shows that the extensive catabolism of dietary essential amino acids (AA) by the intestine results in decreased availability of these AA for protein synthesis in extraintestinal tissues. This raises the possibility that extraintestinal availability of AA may be improved by supplying the animal with an AA source more of which can bypass the intestine. To test this hypothesis, six barrows (35-day-old, 8.6 +/- 1.4 kg), implanted with arterial, portal, and mesenteric catheters, were fed a DL-methionine (DL-MET) or DL-2-hydroxy-4-methylthiobutyrate (DL-HMTB) diet once hourly and infused intramesenterically with 1% p-amino hippurate. Although the directly available L-MET in DL-MET diet was about 1.2-fold that in DL-HMTB diet, the net portal appearance of L-MET was not different between the two diets. Compared with the low mRNA abundance and low activity of D-2-hydroxy acid dehydrogenase (D-HADH) and l-2-hydroxy acid oxidase (L-HAOX) in the intestine, the high mRNA abundance and high activity of D-AA oxidase (D-AAOX) indicated that the intestine had a relatively higher capacity of D-MET utilization than of dl-HMTB utilization to L-MET synthesis and its subsequent metabolism. However, in contrast to the much lower D-AAOX activity (nmol/g tissue) in the stomach than in the liver and kidney, both d-HADH and L-HAOX activity in the stomach was comparable with those in the liver and/or kidney, indicating the substantial capacity of the stomach to convert DL-HMTB to L-MET. Collectively, the difference in distribution of activity and mRNA abundance of D-AAOX, D-HADH, and L-HAOX in the piglets may offer a biological basis for the similar portal appearance of L-MET between DL-MET and DL-HMTB diets, and thus may provide new important insights into nutritional efficiency of different L-MET sources.

To determine whether portal plasma flow (PPF) and net portal appearance of amino acids (AA) could be affected by 2-hydroxy-4-methylthiobutyrate (HMB), six barrows (35-day-old, 8.6+/-1.4 kg), implanted with arterial, portal and mesenteric catheters, were fed a DL-methionine (as the control) or HMB-supplemented diet once hourly and infused intramesenterically with 1% p-amino hippurate. PPF was numerically 9% higher (P=0.09) in HMB-fed pigs than in controls over a 4-6 h period. Compared with controls, pigs fed the HMB diet had increased (P

The aim of the study was to investigate the effect of n-3 PUFA enrichment in longissimus muscle on intramuscular fat (IMF) content and expression of related genes in growing-finishing barrows. Two isoenergetic, isonitrogenous and isolipidic diets were formulated: one was basal diet and the other contained 10% linseed. Twenty-four Landrace x NewDamLine barrows weighing 35 +/- 3.7 kg were randomly assigned to four treatment groups with six pigs per group. During the whole experimental period of 90 days, all groups were first fed the basal diet and then the linseed diet for 0, 30, 60, and 90 days before slaughter, respectively. Meat quality, fatty acid composition, and expression of genes involved in adipogenesis in longissimus muscle were measured and analyzed. The IMF content increased linearly (P < 0.05) as the linseed diet feeding time prolonged. Meanwhile, n-3 PUFA content and expression of peroxisome proliferator-activated receptor delta (PPARdelta), PPARgamma, adipocyte fatty acid-binding protein (aP2) and lipoprotein lipase (LPL) increased linearly (P < 0.01) as well, while the expression of wingless related MMTV integration site 10b (Wnt10b) linearly decreased (P < 0.01). Furthermore, significant (P < 0.01) quadratic or linear relation was observed between n-3 PUFA enrichment and expression of these genes, while significant (P < 0.01) quadratic or linear relation was observed between the expression of PPARgamma, aP2 or Wnt10b and IMF content. These data show that enhancing n-3 PUFA enrichment in muscle leads to significant increase in IMF content. A possible explanation is due to alterations in the expression of genes involved in adipogenesis, however this will need to be confirmed by protein and enzyme activity studies.