Obesity is defined as increased adiposity, which leads to metabolic disease. The growth of adipose tissue depends on its capacity to expand through hyperplasia or hypertrophy, in order to buffer energy surplus. Also, during the establishment of obesity, adipose tissue expansion reflects adipose lipid metabolism (lipogenesis and/or lipolysis). It is well known that dietary factors can modify lipid metabolism promoting or preventing the development of metabolic abnormalities that concur with obesity. Trans-palmitoleic acid (TP), a biomarker of dairy consumption, has been associated with reduced adiposity in clinical studies. Thus, we aimed to evaluate the effect of TP over adiposity and lipid metabolism-related genes in a rodent model of diet-induced obesity (DIO). To fulfil this aim, we fed C57BL/6 mice with a Control or a High-Fat diet, added with or without TP (3 g/kg diet), during 11 weeks. Body weight and food intake were monitored, fat pads were weighted, histology of visceral adipose tissue was analysed and lipid metabolism-related gene expression was explored by qPCR. Results show that TP consumption prevented weight gain induced by high-fat diet, reduced visceral adipose tissue weight and adipocyte size, while increasing the expression of lipolytic molecules. In conclusion, we show for the first time that TP influences adipose tissue metabolism, specifically lipolysis, resulting in decreased adiposity and reduced adipocyte size in a DIO mice model.

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome, ranging from simple steatosis to non-alcoholic steatohepatitis (NASH) particularly among chronic consumers of added sugar-rich diets. However, the impact of early consumption of such diets on NAFLD onset and progression is unclear. Thus, this study sought to characterise metabolic factors involved in NAFLD progression in young mice fed with a high-sucrose diet (HSD). Male Swiss mice were fed HSD or regular chow (CTR) from weaning for up to 60 or 90 days. Obesity development, glucose homeostasis and serum biochemical parameters were determined at each time-point. At day 90, mice were euthanised and white adipose tissue (WAT) collected for lipolytic function assessment and liver for histology, gene expression and cytokines quantification. At day 60, HSD mice presented increased body mass, hypertriglyceridemia, peripheral insulin resistance (IR) and simple steatosis. Upon 90 days on diet, WAT from HSD mice displayed impaired insulin sensitivity, which coincided with increased fasting levels of glucose and free fatty acids (FFA), as well as NAFLD progression to NASH. Transcriptional levels of lipogenic genes, particularly stearoyl-CoA desaturase-1, were consistently increased, leading to hepatic leukocyte infiltration and pro-inflammatory cytokines spillover. Therefore, our dataset supports IR triggering in the WAT as a major factor for dysfunctional release of FFA towards portal circulation and consequent upregulation of lipogenic genes and hepatic inflammatory onset, which decisively concurred for NAFLD-to-NASH progression in young HSD-fed mice. Notwithstanding, this study forewarns against the early introduction of dietary sugars in infant diet, particularly following breastfeeding cessation.

In this research paper we filter and verify miRNAs which may target silent information regulator homolog 2 (SIRT2) gene and then describe the mechanism whereby miRNA-212 might regulate lipogenic genes in mammary epithelial cell lines via targeting SIRT2. Bioinformatics analysis revealed that the bovine SIRT2 gene is regulated by three miRNAs: miR-212, miR-375 and miR-655. The three miRNAs were verified and screened by qRT-PCR, western blot, and luciferase multiplex verification techniques and only miR-212 was shown to have a targeting relationship with SIRT2. The results of co-transfecting miR-212 and silencing RNA (siRNA) showed that by targeting SIRT2, miR-212 can regulate the expression of fatty acid synthetase (FASN) and sterol regulatory element binding factor 1 (SREBP1) but not peroxisome proliferator-activated receptor gamma (PPARγ). Measurement of triglyceride (TAG) content showed that miR-212 increased the fat content of mammary epithelial cell lines. The study indicates that miR-212 could target and inhibit the expression of the SIRT2 gene to promote lipogenesis in mammary epithelial cell lines.

N-Carbamylglutamate (NCG) has been shown to enhance arginine synthesis and improve growth performance in animals. However, the effect of NCG on body fat deposition remains unknown. This study examined the effects of NCG on body fat deposition and evaluated the potential mechanisms involved. Rex rabbits (3 months old) were assigned to one of four dietary groups and supplemented with NCG at the following different concentrations in a feeding trial that lasted 67 d: 0 (control), 0·04, 0·08, and 0·12 %. NCG supplementation increased serum concentrations of arginine and proline by activating intestinal carbamoylphosphate synthase-І at the posttranscriptional level. Final body weights and growth performance were not affected by dietary NCG levels. However, NCG-treated rabbits had lower perirenal and subcutaneous fat percentages, serum TAG content, and hepatic fatty acid synthase (FAS) activity and increased NO synthase activity and serum levels of NO, growth hormone (GH), and insulin-like growth factor 1 (IGF-1). There were significant positive correlations between TAG content and perirenal fat percentage, as well as FAS activity and perirenal fat percentage, but significant negative correlations between TAG and NO levels, and FAS activity and IGF-1 level in rabbits after NCG treatment. NCG supplementation did not affect hepatic health indicators, except for serum ammonia concentrations, which were decreased in NCG-treated rabbits. Our results suggest that NCG can serve as a dietary supplement to reduce unfavourable fat deposition through inhibiting hepatic lipogenesis in animals since it appears to have no negative effects on growth performance or hepatic health.

Trans-10, cis-12 conjugated linoleic acid (CLA) decreases milk fat synthesis in lactating sows and involves, at least in part, the down-regulation of lipogenic genes. The objective was to evaluate the effect of CLA on milk composition and lipogenic gene expression. Twenty multiparous sows were randomly assigned to one of the two treatments for 18 d (from day 7 to day 25 of lactation): (1) control (no CLA added) and (2) 1 % of CLA mixed into the ration. CLA treatment decreased milk fat and protein content by 20 % (P = 0·004) and 11 % (P = 0·0001), respectively. However, piglet weight did not differ between treatments (P = 0·60). Dietary CLA increased the concentration of SFA in milk fat by 16 % (P < 0·0001) and decreased MUFA by 17·6 % (P < 0·0001). In the mammary gland, CLA reduced gene expression of acetyl-CoA carboxylase-α by 37 % (P = 0·003), fatty acid synthase by 64 % (P = 0·002), stearoyl-CoA desaturase 1 by 52 % (P = 0·003), lipoprotein lipase by 26 % (P = 0·03), acyl glycerol phosphate acyltransferase 6 by 15 % (P = 0·02) and diacylglycerol acyltransferase 1 by 27 % (P = 0·02), whereas the expression of fatty acid binding protein 3 was not altered by CLA treatment (P = 0·09). Mammary expression of casein-β and α-lactalbumin was reduced by CLA by 68 % (P = 0·0004) and 62 % (P = 0·005), respectively. Additionally, CLA had no effect on the expression of lipogenic genes evaluated in adipose tissue. In summary, CLA reduced milk fat content without negatively affecting litter performance and it affected mammary expression of genes involved in all lipogenic pathways studied.

An oral starch administration trial was used to evaluate glucose homoeostasis in grass carp (Ctenopharyngodon idella) and Chinese longsnout catfish (Leiocassis longirostris Günther). Fish were administered with 3 g of a water and starch mixture (with 3:2 ratio) per 100 g body weight after fasting for 48 h. Fish were sampled at 0, 1, 3, 6, 12, 24 and 48 h after oral starch administration. In grass carp, plasma levels of glucose peaked at 3 h but returned to baseline at 6 h. However, in Chinese longsnout catfish, plasma glucose levels peaked at 6 h and returned to baseline at 48 h. The activity of intestinal amylase was increased in grass carp at 1 and 3 h, but no significant change in Chinese longsnout catfish was observed. The activity of hepatic glucose-6-phosphatase fell significantly in grass carp but change was not evident in Chinese longsnout catfish. The expression levels and enzymic activity of hepatic pyruvate kinase increased in grass carp, but no significant changes were observed in the Chinese longsnout catfish. Glycogen synthase (gys) and glycogen phosphorylase (gp) were induced in grass carp. However, there was no significant change in gys and a clear down-regulation of gp in Chinese longsnout catfish. In brief, compared with Chinese longsnout catfish, grass carp exhibited a rapid increase and faster clearance rate of plasma glucose. This effect was closely related to significantly enhanced levels of digestion, glycolysis, glycogen metabolism and glucose-induced lipogenesis in grass carp, as well as the inhibition of gluconeogenesis.

The purpose of this study was to investigate potential mechanisms involved in fat deposition promoted by dietary lysine deficiency, particularly intramuscular fat (IMF), and differential responses between fatty and lean pigs. Carcass traits and lipogenic enzyme activities and gene expression levels in muscles and adipose tissue were investigated in Iberian (fatty) and Landrace × Large White (LDW) pigs under identical feeding level (based on body weight (BW)) and management conditions. Twenty-eight barrows of 10 kg initial BW, 14 per breed, were fed two isoproteic (200 g CP /kg DM) and isocaloric (14.7 MJ metabolizable energy/kg DM) diets with identical composition except for the lysine content (1.09% for diet adequate in lysine and 0.52% for diet deficient in lysine). At a BW of 25 kg, pigs were slaughtered. Compared with pigs fed the lysine-adequate diet, in both genotypes lysine-deficient diet led to lower carcass protein concentration, lower relative proportions of leaner components (loin, ham and shoulder; P < 0.01), and higher carcass fatty components and carcass lipid concentration (P < 0.001). Irrespective of diet, the activity and gene expression of lipogenic enzymes (fatty acid synthase (FAS), malic enzyme (ME) and glucose-6-phosphate dehydrogenase (G6PDH)) were greater in Iberian than in LDW pigs, particularly in adipose tissue where transcriptional regulators involved in the control of adipogenesis and lipogenesis were also upregulated in Iberian animals. In backfat tissue, there was a small decrease induced by or no effects of lysine-deficient diet on the activity and gene expression of lipogenic enzymes, nor in gene expression levels of upstream regulators of lipogenesis and adipogenesis. In longissimus muscle, the activity of FAS, G6PDH and ME increased with lysine deficiency in both genotypes (P < 0.01) and an upregulation of gene expression of lipogenic enzymes was specifically observed in Iberian pigs (P < 0.05 to P < 0.001). In biceps femoris muscle of lysine-deficient pigs, the activity of FAS and ME enzymes increased, ME1 gene was upregulated (added to FASN gene in the case of Iberian pigs; P < 0.01 to P < 0.001) and PPARA gene was downregulated (P < 0.05). The results show that in both fatty and lean pigs, the effect of lysine deficiency on lipid metabolism was tissue-specific, with an activation of lipogenesis in longissimus and biceps femoris muscle but no apparent stimulation in backfat adipose tissue. Suitable feeding protocols including lysine-deficient diets should be designed for each pig type in order to increase intramuscular lipids without penalizing the growth of lean carcass components.

In utero exposure to the ubiquitous plasticizer, bisphenol A (BPA) is associated with offspring obesity. As adipogenesis is a critical factor contributing to obesity, we determined the effects of in vivo maternal BPA and in vitro BPA exposure on newborn adipose tissue at the stem-cell level. For in vivo studies, female rats received BPA before and during pregnancy and lactation via drinking water, and offspring were studied for measures of adiposity signals. For in vitro BPA exposure, primary pre-adipocyte cell cultures from healthy newborns were utilized. We studied pre-adipocyte proliferative and differentiation effects of BPA and explored putative signal factors which partly explain adipose responses and underlying epigenetic mechanisms mediated by BPA. Maternal BPA-induced offspring adiposity, hypertrophic adipocytes and increased adipose tissue protein expression of pro-adipogenic and lipogenic factors. Consistent with in vivo data, in vitro BPA exposure induced a dose-dependent increase in pre-adipocyte proliferation and increased adipocyte lipid content. In vivo and in vitro BPA exposure promotes the proliferation and differentiation of adipocytes, contributing to an enhanced capacity for lipid storage. These findings reinforce the marked effects of BPA on adipogenesis and highlight the susceptibility of stem-cell populations during early life with long-term consequence on metabolic homeostasis.

The present review will present the recent published results and discuss the main effects of nutrients, mainly fatty acids, on the expression of genes involved in lipid metabolism. In this sense, the review focuses in two phases: prenatal life and finishing phase, showing how nutrients can modulate gene expression affecting marbling and fatty acid profile in meat from ruminants. Adiposity in ruminants starts to be affected by nutrients during prenatal life when maternal nutrition affects the differentiation and proliferation of adipose cells enhancing the marbling potential. Therefore, several fetal programming studies were carried out in the last two decades in order to better understand how nutrients affect long-term expression of genes involved in adipogenesis and lipogenesis. In addition, during the finishing phase, marbling becomes largely dependent on starch digestion and glucose metabolism, being important to create alternatives to increase these metabolic processes, and modulates gene expression. Different lipid sources and their fatty acids may also influence the expression of genes responsible to encode enzymes involved in fat tissue deposition, influencing meat quality. In conclusion, the knowledge shows that gene expression is a metabolic factor affecting marbling and fatty acid profile in ruminant meat and diets and their nutrients have direct effect on how these genes are expressed.

Feeding a high concentrate (HC) diet is a widely used strategy for supporting high milk yields, yet it may cause certain metabolic disorders. This study aimed to investigate the changes in milk production and hepatic metabolism in goats fed different proportions of concentrate in the diet for 10 weeks. In total, 12 mid-lactating goats were randomly assigned to an HC diet (65% concentrate of dry matter, n=6) or a low concentrate (LC) diet (35% concentrate of dry matter, n=6). Compared with LC, HC goats produced greater amounts of volatile fatty acids and produced more milk and milk lactose, fat and protein (P<0.01). HC goats showed a greater concentration of ATP, NAD, plasma non-esterified fatty acids and hepatic triglycerides than LC goats (P<0.05). Real-time PCR results showed that messenger RNA (mRNA) expression of gluconeogenic genes, namely, glucose-6-phosphatase, pyruvate carboxylase and phosphoenolpyruvate carboxykinase were significantly up-regulated and accompanied greater gluconeogenic enzyme activities in the liver of HC goats. Moreover, the expression of hepatic lipogenic genes including sterol regulatory element-binding protein 1c, fatty acid synthase and diacylglycerol acyltransferase mRNA was also up-regulated by the HC diet (P<0.05). HC goats had greater hepatic phosphorylation of AMP-activated protein kinase than LC (P<0.05). Furthermore, histone-3-lysine-27-acetylation contributed to this elevation of gluconeogenic gene expression. These results indicate that lactating goats fed an HC diet for 10 weeks produced more milk, which was associated with up-regulated gene expression and enzyme activities involved in hepatic gluconeogenesis and lipogenesis.

The aim of this study was to investigate the effects of trans-fatty acids (TFA) on liver and serum TAG regulation in mice fed diets containing different proportions of n-3, n-6 and n-9 unsaturated fatty acids (UFA) from olive (O), maize (C) or rapeseed (R) oils partially substituted or not with TFA (Ot, Ct and Rt, respectively). Male CF1 mice were fed (30 d) one of these diets. The effects of the partial substitution (1 %, w/w) of different UFA with TFA on the activity and expression of hepatic enzymes involved in lipogenesis and fatty acids oxidation were evaluated, as well as their transcription factor expressions. Some of the mechanisms involved in the serum TAG regulation, hepatic VLDL rich in TAG (VLDL-TAG) secretion rate and lipoprotein lipase (LPL) activity were assessed. In liver, TFA induced an increase in TAG content in the Ot and Rt groups, and this effect was associated with an imbalance between lipogenesis and β-oxidation. In the Ot group, exacerbated lipogenesis may be one of the mechanisms responsible for the liver steatosis induced by TFA, whereas in Rt it has been related to a decreased β-oxidation, compared with their respective controls. The enhanced hepatic VLDL-TAG secretion in the Ot and Rt groups was compensated with a differential removal of TAG by LPL enzyme in extrahepatic tissues, leading to unchanged serum TAG levels. In brief, the effects of low levels of TFA on liver and serum TAG regulation in mice depend on the dietary proportions of n-3, n-6 and n-9 UFA.

Serum α1-acid glycoprotein (AGP) is elevated during late gestation and at birth in the pig and rapidly declines postnatally. In contrast, the pig is born with minimal lipid stores in the adipose tissue, but rapidly accumulates lipid during the first week. The present study examined if AGP can affect adipose tissue metabolism in the neonatal pig. Isolated cell cultures or tissue explants were prepared from dorsal subcutaneous adipose tissue of preweaning piglets. Porcine AGP was used at concentrations of 0, 100, 1000 and 5000 ng/ml medium in 24 h incubations. AGP reduced the messenger RNA (mRNA) abundance of the lipogenic enzymes, malic enzyme (ME), fatty acid synthase and acetyl coA carboxylase by at least 40% (P<0.001). The activity of ME and citrate lyase were also reduced by AGP (P<0.05). Glucose oxidation was reduced by treatment with 5000 ng AGP/ml medium (P<0.05). The 14C-glucose incorporation into fatty acids was reduced by ~25% by AGP treatment for 24 h with 1000 ng AGP/ml medium (P<0.05). The decrease in glucose metabolism by AGP appears to function through an inhibition in insulin-mediated glucose oxidation and incorporation into fatty acids. This was supported by the analysis of the mRNA abundance for sterol regulatory element-binding protein (SREBP), carbohydrate regulatory element-binding protein (ChREBP) and insulin receptor substrate 1 (IRS1), which all demonstrated reductions of at least 23% in response to AGP treatment (P<0.05). These data demonstrate an overall suppression of lipogenesis due to AGP inhibition of lipogenic gene expression in vitro, which the metabolic data and SREBP, ChREBP and IRS1 gene expression analysis suggest is through an inhibition in insulin-mediated events. Second, these data suggest that AGP may contribute to limiting lipogenesis within adipose tissue during the perinatal period, as AGP levels are highest for any serum protein at birth.

This study was designed to determine whether methyl-β-cyclodextrin (MCD) can substitute for albumin in incubation medium for neonatal swine adipose tissue explants, or whether MCD affects metabolism and cytokine expression. Subcutaneous adipose tissue explants (100 ± 10 mg) were prepared from 21-day-old pigs. Explants were incubated in medium 199 supplemented with 25 mM HEPES, 1.0 nM insulin at 37°C. The medium also contained bovine serum albumin (BSA) or MCD at 0%, 0.05%, 0.1%, 0.2% or 0.3%. Tissue explants were treated with these media for 1 h and then switched to the same basal incubation medium containing 0.05% BSA. Explants were removed from basal medium at 2 or 8 h of incubation, and real-time PCR was performed to assess expression of tumor necrosis α (TNF) and interleukin 6 (IL6), acetyl CoA carboxylase (ACAC) and fatty acid synthase (FASN). Alternatively, rates of 14C-glucose oxidation and lipogenesis were monitored ± insulin (100 nM), following MCD treatment. Incubation with BSA had minimal effects on gene expression or adipose tissue metabolism, only producing a doubling in TNF mRNA abundance (P < 0.01). Treatment with MCD increased TNF mRNA abundance by eightfold (P < 0.009), whereas IL6 gene expression increased a 100-fold (P < 0.001) with a suppression in ACAC and FASN expression (P < 0.01). This was paralleled by MCD inhibition of insulin-stimulated glucose oxidation and lipogenesis (P < 0.001). Addition of a TNF antibody to the incubation medium alleviated this inhibition of insulin-stimulated glucose metabolism by ∼30% (P < 0.05).

The effects of varying dietary digestible protein (DP) and digestible energy (DE) content on performance, nutrient retention efficiency and the de novo lipogenesis of DP origin were examined in triplicate groups of gilthead sea bream (Sparus aurata), fed nine extruded experimental diets. In order to trace the metabolic fate of dietary protein, 1·8 % fishmeal was replaced with isotope-labelled whole protein (>98 % 13C). The experiment was divided into a growth period lasting 89 d, growing fish from approximately 140 to 350 g, followed by a 3 d period feeding isotope-enriched diets. Isotope ratio MS was applied to quantify the 13C enrichment of whole-body lipid from dietary DP. Between 18·6 and 22·4 % of the carbon derived from protein was recovered in the lipid fraction of the fish, and between 21·6 and 30·3 % of the total lipid deposited could be attributed to dietary protein. DP retention was significantly improved by reductions in dietary DP:DE ratio, while the opposite was true for apparent digestible lipid retention. Both overall DE retention and whole-body proximate composition of whole fish were largely unaffected by dietary treatments, while feed conversion ratios were significantly improved with increasing dietary energy density. The present study suggests that gilthead sea bream efficiently utilises dietary nutrients over a wide range of DP:DE ratios and energy densities. In addition, they appear to endeavour a certain body energy status rather than maximising growth, which in the present trial was apparent from inherently high de novo lipogenesis originating from DP.

Coumarin is a natural compound abundant in plant-based foods such as citrus fruits, tomatoes, vegetables and green tea. Although coumarin has been reported to exhibit anti-coagulant, anti-inflammation and cholesterol-lowering properties, the effect of coumarin on hepatic lipid metabolism remains unclear. In the present study, we evaluated the ability of coumarin to protect against hepatic steatosis associated with a high-fat diet (HFD) and investigated potential mechanisms underlying this effect. C57BL/6J mice were fed a normal diet, HFD and HFD containing 0·05 % courmarin for 8 weeks. The present results showed that coumarin reduced weight gain and abdominal fat mass in mice fed the HFD for 8 weeks (P< 0·05). Coumarin also significantly reduced the HFD-induced elevation in total cholesterol, apoB, leptin and insulin (P< 0·05). In the liver of HFD-fed mice, coumarin significantly reduced total lipids, TAG and cholesterol (38, 22 and 9 % reductions, respectively; P< 0·05), as well as lipid droplet number and size. Additionally, thiobarbituric acid-reactive substance levels, as an indicator of hepatic steatosis, were attenuated by coumarin (P< 0·05). Finally, coumarin suppressed the HFD-induced up-regulation in fatty acid synthase (FAS) activity, and the expression of sterol regulatory element-binding protein-1, FAS, acetyl-CoA carboxylase 1, PPARγ and CCAAT/enhancer-binding protein-α in the liver. Taken together, these results demonstrate that coumarin could prevent HFD-induced hepatic steatosis by regulating lipogenic gene expression, suggesting potential targets for preventing hepatic steatosis.

Divergent selection of chickens for low or high abdominal fat (AF) but similar BW at 63 days of age was undertaken in 1977. The selection programme was conducted over seven successive generations. The difference between lines was then maintained constant at about twice the AF in the fat line as in the lean line. The aims of the first studies on these divergent chicken lines were to describe the growth, body composition and reproductive performance in young and adult birds. The lines were then used to improve the understanding of the relationship between fatness and energy and protein metabolism in the liver, muscle and adipose tissues, as well as the regulation of such metabolism at hormonal, gene and hypothalamic levels. The effects on muscle energy metabolism in relation to meat quality parameters were also described. This paper reviews the main results obtained with these lines.

The effects of replacing a digestible energy source from fat (fish oil) with carbohydrate (wheat starch) on performance, glycogenesis and de novo lipogenesis was examined in triplicate groups of juvenile gilthead sea bream (Sparus aurata), fed four extruded experimental diets. In order to trace the metabolic fate of dietary starch, 0·7 % wheat starch was replaced with isotope-labelled starch (>98 % 13C). Fish were fed the experimental diets for three consecutive 10 d periods, and isotope ratio MS was applied to quantify 13C enrichment of liver and whole-body glycogen and lipid pools over the three feeding periods. Glycogenesis originating from dietary starch accounted for up to 68·8 and 38·8 % of the liver and whole-body glycogen pools, respectively, while up to 16·7 % of the liver lipid could be attributed to dietary starch. Between 5 and 8 % of dietary starch carbon was recovered in whole-body lipid, and estimated deposition rates of de novo synthesised lipid originating from starch ranged from 18·7 to 123·7 mg/kg biomass per d. Dietary treatments did not significantly affect growth, feed performance or body composition of the fish, while the hepatosomatic index and glycogen content of whole fish and livers correlated directly with dietary starch inclusion level. The study suggests that gilthead sea bream efficiently synthesises glycogen from both dietary starch and endogenous sources. In contrast, lipogenesis from carbon derived from starch seems to play a minor role in overall lipid synthesis and deposition under the specified experimental conditions.

Gene expression profiles of bovine longissimus muscle as affected by dietary n-3 v.n-6 fatty acid (FA) intervention were analysed by microarray pre-screening of >3000 muscle biology/meat quality-related genes as well as subsequent quantitative RT-PCR gene expression validation of genes encoding lipogenesis-related transcription factors (CCAAT/enhancer-binding protein β, sterol regulatory element-binding transcription factor 1), key-lipogenic enzymes (acetyl-CoA carboxylase α (ACACA), fatty acid synthase (FASN), stearoyl-CoA desaturase (SCD)), lipid storage-associated proteins (adipose differentiation-related protein (ADFP)) and muscle biology-related proteins (cholinergic receptor, nicotinic, α1, farnesyl diphosphate farnesyl transferase 1, sema domain 3C (SEMA3C)). Down-regulation of ACACA (P = 0·00), FASN (P = 0·09) and SCD (P = 0·02) gene expression upon an n-3 FA intervention directly corresponded to reduced SFA, MUFA and total FA concentrations in longissimus muscle, whereas changes in ADFP (P = 0·00) and SEMA3C (P = 0·05) gene expression indicated improved muscle function via enhanced energy metabolism, vasculogenesis, innervation and mediator synthesis. The present study highlights the significance of dietary n-3 FA intervention on muscle development, maintenance and function, which are relevant for meat quality tailoring of bovine tissues and modulating animal production-relevant physiological processes.

The aim of the study was to examine the effect of a linseed diet on meat quality and on lipogenesis in rabbits. Twelve rabbits were fed a control or a linseed diet. There was no diet effect on growth, food consumption, carcass characteristics and meat ultimate pH and colour. Feeding the linseed diet increased the n-3 polyunsaturated fatty acids (PUFA) levels in perirenal and interscapular fats, in the Longissimus dorsi muscle and in the liver. The linseed diet produced lower linoleic acid/α-linolenic acid ratios in adipose tissues and in the Longissimus dorsi muscle, but not in the liver. Diet did not affect lipogenic enzyme activities in the Longissimus dorsi muscle, whereas the linseed diet decreased the lipogenic potential in perirenal and interscapular fats, and in the liver. Feeding rabbits with a high n-3 PUFA diet led to a decrease in the oxidative stability of perirenal fat and the Longissimus dorsi muscle, and to an inhibition of stearoyl-CoA-desaturase activity in liver and in adipose tissues, but not in muscle.

Non-alcoholic fatty liver disease (NAFLD) is one of the most common manifestations of chronic liver disease worldwide. The aim of the present study was to assess the effect of resveratrol on liver fat accumulation, as well as on the activity of those enzymes involved in lipogenesis and fatty acid oxidation in fa/fa Zucker rats. A total of thirty rats were assigned to three experimental groups and orally treated with resveratrol for 6 weeks, or without resveratrol (C: control group; RSV15 group: 15 mg/kg body weight per d; RSV45 group: 45 mg/kg body weight per d). Liver histological analysis was performed by microscopy. Levels of hepatic carnitine palmitoyltransferase-Ia (CPT-Ia), acyl-coenzyme A oxidase (ACO), fatty acid synthase, glucose-6-phosphate dehydrogenase and malic enzyme were assessed by spectrophotometry, and acetyl-CoA carboxylase was assessed by radiometry. Commercial kits were used to determine serum TAG, NEFA, total HDL and non-HDL-cholesterol, glycerol, ketonic bodies, glucose, insulin, adiponectin, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP), hepatic TAG, thiobarbituric acid reactive substrates, GSH (GSSG) and superoxide dismutase. Resveratrol reduced liver weight and TAG content. It did not modify the activity of lipogenic enzymes but it did increase CPT-Ia and ACO activities. NEFA and ALP were reduced in both resveratrol-treated groups. AST/GOT was reduced only by the lowest dose. ALT/GPT, TAG and adiponectin remained unchanged. Resveratrol reduced liver oxidative stress. This study demonstrates that resveratrol can protect the liver from NAFLD by reducing fatty acid availability. Moreover, resveratrol also protects liver from oxidative stress.