acetyl-CoA Carboxylase Activity Research Articles

Metabolomics and microbiome co-analysis reveals altered innate immune responses in Charybdis japonica following Aeromonas hydrophila infection

A comprehensive bioinformatics analysis was conducted to elucidate the innate immune response of Charybdis japonica following exposure to Aeromonas hydrophila. This study integrated metabolomics, 16S rRNA sequencing, and enzymatic activity data to dissect the immune mechanisms activated in response to infection. Infection with A. hydrophila resulted in an increased abundance of beneficial intestinal genera such as Photobacterium spp., Rhodobacter spp., Polaribacter spp., Psychrilyobacter spp., and Mesoflavibacter spp. These probiotics appear to suppress A. hydrophila colonization by competitively dominating the intestinal microbiota. Key metabolic pathways affected included fatty acid biosynthesis, galactose metabolism, and nitrogen metabolism, highlighting their role in the crab's intestinal response. Enzymatic analysis revealed a decrease in activities of hexokinase, phosphofructokinase, and pyruvate kinase, which are essential for energy homeostasis and ATP production necessary for stress responses. Additionally, reductions were observed in the activities of acetyl-CoA carboxylase and fatty acid synthase. Gene expression analysis showed downregulation in Peroxiredoxin 1 (PRDX1), Peroxiredoxin 2 (PRDX2), glutathione-S-transferase (GST), catalase (CAT), and glutathione (GSH), with concurrent increases in malondialdehyde (MDA) levels, indicating severe oxidative stress. This study provides insights into the molecular strategies employed by marine crabs to counteract bacterial invasions in their natural habitat.

Activation of hepatic acetyl-CoA carboxylase by S-nitrosylation in response to diet

Nitric oxide (NO), produced primarily by nitric oxide synthase enzymes, is known to influence energy metabolism by stimulating fat uptake and oxidation. The effects of NO on de novo lipogenesis (DNL), however, are less clear. Here we demonstrate that hepatic expression of endothelial nitric oxide synthase is reduced following prolonged administration of a hypercaloric high-fat diet. This results in marked reduction in the amount of S-nitrosylation of liver proteins including notably acetyl-CoA carboxylase (ACC), the rate-limiting enzyme in DNL. We further show that ACC S-nitrosylation markedly increases enzymatic activity. Diminished endothelial nitric oxide synthase expression and ACC S-nitrosylation may thus represent a physiological adaptation to caloric excess by constraining lipogenesis. Our findings demonstrate that S-nitrosylation of liver proteins is subject to dietary control and suggest that DNL is coupled to dietary and metabolic conditions through ACC S-nitrosylation.

The GPR40 novel agonist SZZ15-11 improves non-alcoholic fatty liver disease by activating the AMPK pathway and restores metabolic homeostasis in diet-induced obese mice.

Non-alcoholic fatty liver is the most common cause of chronic liver disease. GPR40 is a potential therapeutic target for energy metabolic disorders. GPR40 is a potential therapeutic target for energy metabolic disorders. SZZ15-11 is a newly synthesized GPR40 agonist. In this study, we estimate the potency of SZZ15-11 in fatty liver treatment. In vivo, diet-induced obese (DIO) mice received SZZ15-11 (50 mg/kg) and TAK875 (50 mg/kg) for 6 weeks. Blood glucose and lipid, hepatocyte lipid and liver morphology were analysed. In vitro, HepG2 cells and GPR40-knockdown HepG2 cells induced with 0.3 mM oleic acid were treated with SZZ15-11. Triglyceride and total cholesterol of cells were measured. At the same time, the AMPK pathway regulating triglycerides and cholesterol esters synthesis was investigated via western blot and quantitative polymerase chain reaction in both liver tissue and HepG2 cells. SZZ15-11 was found to not only attenuate hyperglycaemia and hyperlipidaemia but also ameliorate fatty liver disease in DIO mice. At the same time, SZZ15-11 decreased triglyceride and total cholesterol content in HepG2 cells. Whether examined in the liver of DIO mice or in HepG2 cells, SZZ15-11 upregulated AMPKα phosphorylation and then downregulated the expression of the cholesterogenic key enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase and inhibited acetyl-CoA carboxylase activity. Furthermore, SZZ15-11 promotes AMPK activity via [cAMP]i accumulation. This study confirmed that SZZ15-11, a novel GPR40 agonist, improves hyperlipidaemia and fatty liver, partially via Gs signalling and the AMPK pathway in hepatocytes.

Molecular cloning and gene expression of acc2 from grass carp (Ctenopharyngodon idella) and the regulation of glucose metabolism by ACCs inhibitor.

Acetyl-CoA carboxylase (ACC) catalyzes the carboxylation of acetyl-CoA to malonyl-CoA. Malonyl-CoA, which plays a key role in regulating glucose and lipid metabolism, is not only a substrate for fatty acid synthesis but also an inhibitor of the oxidation pathway. ACC exists as two isoenzymes that are encoded by two different genes. ACC1 in grass carp (Ctenopharyngodon idellus) has been cloned and sequenced. However, studies on the cloning, tissue distribution, and function of ACC2 in grass carp were still rare. The full-length cDNA of acc2 was 8537bp with a 7146bp open reading frame encoding 2381 amino acids. ACC2 had a calculated molecular weight of 268.209kDa and an isoelectric point of 5.85. ACC2 of thegrass carp shared the closest relationship with that of the common carp (Sinocyclocheilus grahami). The expressions of acc1 and acc2 mRNA were detected in all examined tissues. Theexpression level of acc1 was high in the brain and fat but absent in the midgut and hindgut. Theexpression level of acc2 in the kidney was significantly higher than inother tissues, followed by the heart, brain, muscle, and spleen. ACCs inhibitor significantly reduced the levels of glucose, malonyl-CoA, and triglyceride in hepatocytes. This study showed that the function of ACC2 was evolutionarily conserved from fish to mammals. ACCs inhibitor inhibited the biological activity of ACCs, and reduced fat accumulation in grass carp.

Knockdown of ACOT4 alleviates gluconeogenesis and lipid accumulation in hepatocytes

Acyl-CoA thioesterase 4 (ACOT4) has been reported to be related to acetyl-CoA carboxylase activity regulation; However, its exact functions in liver lipid and glucose metabolism are still unclear. Here, we discovered explored the regulatory roles of ACOT4 in hepatic lipid and glucose metabolism in vitro. We found that the expression level of ACOT4 was significantly increased in the hepatic of db/db and ob/ob mice as well as obese mice fed a high fat diet. Adenovirus-mediated overexpression of ACOT4 promoted gluconeogenesis and high-glucose/high-insulin-induced lipid accumulation and impaired insulin sensitivity in primary mouse hepatocytes, whereas ACOT4 knockdown notably suppressed gluconeogenesis and decreased the triglycerides accumulation in hepatocytes. Furthermore, ACOT4 knockdown increased insulin-induced phosphorylation of AKT and GSK-3β in primary mouse hepatocytes. Mechanistically, we found that upregulation of ACOT4 expression inhibited AMP-activated protein kinase (AMPK) activity, and its knockdown had the opposite effect. However, activator A769662 and inhibitor compound C of AMPK suppressed the impact of the change in ACOT4 expression on AMPK activity. Our data indicated that ACOT4 is related to hepatic glucose and lipid metabolism, primarily via the regulation of AMPK activity. In conclusion, ACOT4 is a potential target for the therapy of non-alcoholic fatty liver (NAFLD) and type 2 diabetes.

The acyl-acyl carrier protein thioesterases GmFATA1 and GmFATA2 are essential for fatty acid accumulation and growth in soybean.

Acyl-acyl carrier protein (ACP) thioesterases (FAT) hydrolyze acyl-ACP complexes to release FA in plastids, which ultimately affects FA biosynthesis and profiles. Soybean GmFATA1 and GmFATA2 are homoeologous genes encoding oleoyl-ACP thioesterases whose role in seed oil accumulation and plant growth has not been defined. Using CRISPR/Cas9 gene editing mutation of Gmfata1 or 2 led to reduced leaf FA content and growth defect at the early seedling stage. In contrast, no homozygous double mutants were obtained. Combined this indicates that GmFATA1 and GmFATA2 display overlapping, but not complete functional redundancy. Combined transcriptomic and lipidomic analysis revealed a large number of genes involved in FA synthesis and FA chain elongation are expressed at reduced level in the Gmfata1 mutant, accompanied by a lower triacylglycerol abundance at the early seedling stage. Further analysis showed that the Gmfata1 or 2 mutants had increased composition of the beneficial FA, oleic acid. The growth defect of Gmfata1 could be at least partially attributed to reduced acetyl-CoA carboxylase activity, reduced abundance of five unsaturated monogalactosyldiacylglycerol lipids, and altered chloroplast morphology. On the other hand, overexpression of GmFATA in soybean led to significant increases in leaf FA content by 5.7%, vegetative growth, and seed yield by 26.9%, and seed FA content by 23.2%. Thus, overexpression of GmFATA is an effective strategy to enhance soybean oil content and yield.

Selenium nanomaterials promoted ferredoxin and iron–sulfur protein synthesis and acetyl CoA carboxylase activity to improve the photosynthesis and fatty-acid synthesis in soybean

Herein, the effect of selenium engineered nanomaterials (Se ENMs) on soybean photosynthesis and fatty-acid synthesis by regulating ferredoxin (Fd) and iron–sulfur (Fe/S) protein synthesis and acetyl CoA carboxylase (ACC) activity was explored.

Effects of polyethylene terephthalate microplastics on cell growth, intracellular products and oxidative stress of Scenedesmus sp.

Polyethylene terephthalate (PET) has been widely utilized in the synthesis of textile materials and packaging of foods and beverages. In recent years, it has been commonly detected in the form of microplastics (MPs) in wastewater. However, the effects of PET MPs on microalgal intracellular products and their interrelationships have been poorly investigated. In this study, the microalgae Scenedesmus sp. Strain H-1 was exposed to PET MPs to explore their effects on the growth, intracellular products (such as lipids, carbohydrates, and proteins), and antioxidative defense systems of Scenedesmus sp. The results demonstrated that PET MPs significantly reduced Scenedesmus sp. cell growth, with a maximum inhibition rate of 38.25% in the 500 mg L−1 treatment group. PET MPs had negative effects on glucose and nitrate utilization rates and reduced intracellular carbohydrates, intracellular proteins, and photosynthetic pigments. Surprisingly, PET MPs reduced acetyl-CoA carboxylase activity but induced lipid accumulation in microalgae. In addition, PET MPs significantly decreased the essential linoleic acid concentration and increased the palmitic acid content, resulting in reduced biodiesel quality. PET MPs induced the production of reactive oxygen species and malondialdehyde as well as the activities of superoxide dismutase and catalase. The results of the PCA indicated that the response mechanism of Scenedesmus sp. to PET MPs exposure was synergistic. This study provides fundamental data on the impact of MPs on the intracellular products of microalgae.

A bacteria-derived tetramerized protein ameliorates nonalcoholic steatohepatitis in mice via binding and relocating acetyl-coA carboxylase

Increased de novo lipogenesis (DNL) is a major feature of nonalcoholic steatohepatitis (NASH). None of the drugs targeting the catalytic activity of acetyl-CoA carboxylase (ACC), the rate-limiting enzyme in the DNL process, have been approved by the FDA. Whether cytosolic ACC1 can be regulated spatially remains to be explored. Herein, we find that streptavidin (SA), which is a bacterium-derived tetrameric protein, forms cytosolic condensates and efficiently induces a spatial re-localization of ACC1 in liver cells, concomitant with inhibited lipid accumulation. Both SA tetrameric structure and multivalent protein interaction are required for condensate formation. Interestingly, the condensates are further characterized as gel-like membraneless organelle (SAGMO) and significantly restrict the cytosolic dispersion of ACC1 and fatty acid synthase. Notably, AAV-mediated delivery of SA partially blocks mouse liver DNL and ameliorates NASH without eliciting hypertriglyceridemia. In summary, our study shows that insulating lipogenesis-related proteins by SAGMO might be effective for NASH treatment.

Gibberellic acid (GA) role in acetyl-coA carboxylase enzyme regulation and in improving oil palm yield

Seaweed specifically, Sargassum sp. is known to contains a boosting hormone growth that has been promoted plant growth and yield due to the containing of auxin, gibberelic acid (GA) and cytokinine, and also some amino acids especially glutamic acid. Those composition could be used as an booster of palm oil production which related to acetyl co-A carboxylase activity (ACC). ACC is the rate determination step in fatty acid accumulation, and becomes active through dephosphorylation of some serine residues that induced by magnesium and glutamate. Moreover, ACC was regulated by AtWRI1 and AtWRI1-TCP4 interaction, a mechanism that allow fine-tuning of the oil biosynthetic pathway. In this research we conducted gene expression experiments, and molecular docking analyses to study the possible mechanism of seaweed composition stimulating oil accumulation in the oil palm. Further analysis was conducted to ensure whether the interaction between TCP4 and candidate inhibitors were able to phosphorylate TCP4 and decrease its activity. GA application resulted in the increase of oil accumulation in 1 month after application, although in the second month the oil accumulation showed decreasing. Increase of oil accumulation in the first month in line with the increase of the expression of ACC in 3rd and 5th weeks. Meanwhile, TCP4 showed decrease expression that resulted in the increase of the WRI1 in 5th week. From this result, it was indicated that GA application could block the TCP4, so it could not interact with WRI1, resulted in the expression of WRI1 and ACC. This interaction stimulates the oil accumulation in oil palm.

Gibberellic acid (GA) role in acetyl-coA carboxylase enzyme regulation and in improving oil palm yield

Seaweed specifically, Sargassum sp. is known to contains a boosting hormone growth that has been promoted plant growth and yield due to the containing of auxin, gibberelic acid (GA) and cytokinine, and also some amino acids especially glutamic acid. Those composition could be used as an booster of palm oil production which related to acetyl co-A carboxylase activity (ACC). ACC is the rate determination step in fatty acid accumulation, and becomes active through dephosphorylation of some serine residues that induced by magnesium and glutamate. Moreover, ACC was regulated by AtWRI1 and AtWRI1-TCP4 interaction, a mechanism that allow fine-tuning of the oil biosynthetic pathway. In this research we conducted gene expression experiments, and molecular docking analyses to study the possible mechanism of seaweed composition stimulating oil accumulation in the oil palm. Further analysis was conducted to ensure whether the interaction between TCP4 and candidate inhibitors were able to phosphorylate TCP4 and decrease its activity. GA application resulted in the increase of oil accumulation in 1 month after application, although in the second month the oil accumulation showed decreasing. Increase of oil accumulation in the first month in line with the increase of the expression of ACC in 3rd and 5th weeks. Meanwhile, TCP4 showed decrease expression that resulted in the increase of the WRI1 in 5th week. From this result, it was indicated that GA application could block the TCP4, so it could not interact with WRI1, resulted in the expression of WRI1 and ACC. This interaction stimulates the oil accumulation in oil palm.

Lycopene Alleviates the Adverse Effects of Feeding High-Lipid Diets to Hybrid Grouper (♀Epinephelus fuscoguttatus ×♂E. lanceolatus).

It has been found that high-lipid diets (HLDs) disrupt lipid metabolism in fish, leading to an excessive accumulation of lipids in various tissues of the fish body. The objective of this study was to investigate if the inclusion of lycopene (LCP) in an HLD may mitigate the adverse consequences of excessive dietary lipid intake in hybrid grouper (♀ Epinephelus fuscoguttatus × ♂ E. lanceolatus). The experimental design incorporated a control group (L0), which was administered a diet consisting of 42% protein and 16% lipid. The diets for groups L1, L2, and L3 were developed by augmenting the control diet with 100, 200, and 400 mg/kg LCP, respectively. The duration of the trial spanned a period of 42 days. The results of the study showed that the weight gain rate (WGR) and protein efficiency ratio (PER) of the three LCP treatment groups (L1, L2, and L3) tended to increase and then decrease, with a significant increase in WGR and PER in L2 (P < 0.05). Visceral somatic index and hepatic somatic index tended to decrease and then increase in all treatment groups, with a significant decrease in L2 (P < 0.05). In serum dietary LCP significantly reduced triglyceride (TG), total cholesterol (TC), and low-density lipoprotein (LDL) content and significantly increased high-density lipoprotein (HDL) content (P < 0.05). In the liver, dietary LCP reduced TC, TG, and very LDL levels and improved lipoprotein lipase, hepatic lipase, fatty acid (FA) synthetase, and acetyl-CoA carboxylase activities. The number and area of hepatic lipid droplets decreased significantly with increasing LCP content. In the liver, the addition of appropriate levels of LCP significantly upregulated lipoprotein lipase (lpl) and peroxisome proliferator-activated receptor α (pparα). In summary, dietary LCP improves growth and reduces lipid deposition in the liver of hybrid grouper by increasing lipolytic metabolism and decreasing FA synthesis. Under the experimental conditions, the fitted curve analysis showed that the recommended LCP additions to the high lipid diet for juvenile hybrid grouper were 200-300 mg/kg.

Different Dietary Sources of Selenium Alleviate Hepatic Lipid Metabolism Disorder of Heat-Stressed Broilers by Relieving Endoplasmic Reticulum Stress.

As global warming continues, the phenomenon of heat stress (HS) in broilers occurs frequently. The alleviating effect of different selenium (Se) sources on HS-induced hepatic lipid metabolism disorders in broilers remains unclear. This study compared the protective effects of four Se sources (sodium selenite; selenium yeast; selenomethionine; nano-Se) on HS-induced hepatic lipid metabolism disorder and the corresponding response of selenotranscriptome in the liver of broilers. The results showed that HS-induced liver injury and hepatic lipid metabolism disorder, which were reflected in the increased activity of serum alanine aminotransferase (ALT), the increased concentration of triacylglycerol (TG) and total cholesterol (TC), the increased activity of acetyl-CoA carboxylase (ACC), diacylglycerol O-acyltransferase (DGAT) and fatty acid synthase (FAS), and the decreased activity of hepatic lipase (HL) in the liver. The hepatic lipid metabolism disorder was accompanied by the increased mRNA expression of lipid synthesis related-genes, the decreased expression of lipidolysis-related genes, and the increased expression of endoplasmic reticulum (ER) stress biomarkers (PERK, IRE1, ATF6, GRP78). The dietary supplementation of four Se sources exhibited similar protective effects. Four Se sources increased liver Se concentration and promoted the expression of selenotranscriptome and several key selenoproteins, enhanced liver antioxidant capacity and alleviated HS-induced ER stress, and thus resisted the hepatic lipid metabolism disorders of broilers exposed to HS. In conclusion, dietary supplementation of four Se sources (0.3 mg/kg) exhibited similar protective effects on HS-induced hepatic lipid metabolism disorders of broilers, and the protective effect is connected to the relieving of ER stress.

Comparative metabolomics analysis investigating the impact of melatonin-enriched diet on energy metabolism in the crayfish, Cherax destructor.

Melatonin is a multifunctional bioactive molecule present in almost all organisms and has been gradually used in the aquaculture industry in recent years. Energy metabolism is an essential process for individuals to maintain their life activities; however, the process through which melatonin regulates energy metabolism in aquatic animals remains unclear. The present study aimed to conduct a comprehensive analysis of the regulatory mechanism of melatonin for energy metabolism in Cherax destructor by combining metabolomics analysis with the detection of the key substance content, enzymatic activity, and gene expression levels in the energy metabolism process after culturing with dietary melatonin supplementation for 8weeks. Our results showed that dietary melatonin increased the content of glycogen, triglycerides, and free fatty acids; decreased lactate levels; and promoted the enzymatic activity of pyruvate kinase (PK), malate dehydrogenase (MDH), and acetyl-CoA carboxylase. The results of gene expression analysis showed that dietary melatonin also increased the expression levels of hexokinase, PK, MDH, lactate dehydrogenase, lipase, and fatty acid synthase genes. The results of metabolomics analysis showed that differentially expressed metabolites were significantly enriched in lysine degradation and glycerophospholipid metabolism. In conclusion, our study demonstrates that dietary melatonin increased oxidative phosphorylation, improved glucose utilization, and promoted storage of glycogen and lipids in C. destructor. These lipids are used not only for energy storage but also to maintain the structure and function of cell membranes. Our results further add to the understanding of the mechanisms of energy regulation by melatonin in crustaceans.

Effects of dietary melatonin on growth performance, nutrient composition, and lipid metabolism of Pacific white shrimp (Penaeus vannamei)

The goal of this study was to investigate the effects of dietary melatonin (MT) on the growth physiology and lipid metabolism of Penaeus vannamei (P. vannamei). We prepared six experimental diets with varying MT levels (0 (control), 22.5, 41.2, 82.7, 165.1, 329.2 mg/kg) and fed six groups of shrimp with these diets for 2 months. The highest survival, body length growth rate, weight gain, and specific growth rates occurred in shrimp that were fed the diet containing 82.7 mg/kg MT, and the highest levels of docosahexaenoic acid (DHA) and arachidonic acid (ARA) were also found in this treatment group. Compared with the control group, there were no significant differences in moisture, crude protein, and ash contents in shrimp fed with MT, but the crude lipid content was significantly decreased in the high concentration MT supplemented group. Compared to the control group, shrimp fed 82.7 mg/kg MT had better morphology and structure of the hepatopancreas, whereas the hepatopancreas tissues were damaged in shrimp from the high dose MT groups. Analysis of lipid metabolism-related enzymes and genes in the hepatopancreas showed that dietary MT greatly decreased fatty acid synthase and acetyl-CoA carboxylase activities but increased carnitine palmitoyltransferase 1 activity. At the transcriptional level, dietary MT reduced hepatopancreas fat accumulation by upregulating lipid oxidation genes and downregulating lipid synthesis genes. A broken-line model revealed that the ideal MT concentration was in the range of 59.59–71.97 mg/kg. We found that MT supplementation improved P. vannamei growth performance, enhanced fatty acid β oxidation, and prevented fat deposition in the hepatopancreas.

Metabolic heterogeneity of tissue-resident macrophages in homeostasis and during helminth infection

Tissue-resident macrophage populations constitute a mosaic of phenotypes, yet how their metabolic states link to the range of phenotypes and functions in vivo is still poorly defined. Here, using high-dimensional spectral flow cytometry, we observe distinct metabolic profiles between different organs and functionally link acetyl CoA carboxylase activity to efferocytotic capacity. Additionally, differences in metabolism are evident within populations from a specific site, corresponding to relative stages of macrophage maturity. Immune perturbation with intestinal helminth infection increases alternative activation and metabolic rewiring of monocyte-derived macrophage populations, while resident TIM4+ intestinal macrophages remain immunologically and metabolically hyporesponsive. Similar metabolic signatures in alternatively-activated macrophages are seen from different tissues using additional helminth models, but to different magnitudes, indicating further tissue-specific contributions to metabolic states. Thus, our high-dimensional, flow-based metabolic analyses indicates complex metabolic heterogeneity and dynamics of tissue-resident macrophage populations at homeostasis and during helminth infection.

Effect of carbon and nitrogen concentrations on lipid accumulation and regulation of acetyl-CoA carboxylase in Papiliotrema laurentii.

Biodiesel is an interesting alternative to petroleum diesel as it is renewable, biodegradable, and has a low pollutant content. Yeast oils can be used for biodiesel production instead of edible oils, mitigating the use of arable land and water for biodiesel production. Maximum lipid accumulation is reached at 48h of cultivation by the oleaginous yeast Papiliotrema laurentii UFV-1. Nevertheless, the effects of carbon and nitrogen concentrations on lipid accumulation, as well as the regulation of lipid metabolism in this yeast are still not well-characterised. Therefore, this work evaluated the effects of carbon and nitrogen concentrations on the lipid accumulation in P. laurentti, the expression of the ACC gene, and the activity of the enzyme acetyl-CoA carboxylase (ACCase) in different carbon:nitrogen ratios (C:N) and glucose concentrations. The variation of ammonium sulfate concentration did not affect the growth and lipid accumulation in P. laurentii UFV-1. On the other hand, glucose concentration remarkably influenced biomass and lipid production by this yeast. Therefore, the carbon concentration is more important than the nitrogen concentration for lipid production by P. laurentii UFV-1. Importantly, the levels of both ACC gene expression and ACCase activity were maximum during the late-exponential growth phase and decreased after reaching the highest lipid contents, which was easier evidenced during the accumulation and maximum lipid levels. As such, the reduction of ACCase enzyme activity seems to be related to the decrease in the expression level of the ACC gene.

Dietary choline activates the Ampk/Srebp signaling pathway and decreases lipid levels in Pacific white shrimp (Litopenaeus vannamei)

An 8-week feeding trial was conducted in Pacific white shrimp (Litopenaeus vannamei) to evaluate the effects of dietary choline supplementation on choline transport and metabolism, hepatopancreas histological structure and fatty acid profile, and regulation of lipid metabolism. Six isonitrogenous and isolipidic diets were formulated to contain different choline levels of 2.91 (basal diet), 3.85, 4.67, 6.55, 10.70 and 18.90 g/kg, respectively. A total of 960 shrimp (initial weight, 1.38 ± 0.01 g) were distributed randomly into twenty-four 250-L cylindrical fiber-glass tanks, with each diet assigned randomly to 4 replicate tanks. The results indicated that dietary choline significantly promoted the deposition of choline, betaine and carnitine (P < 0.05). The diameters and areas of R cells, total lipid and triglyceride contents in hepatopancreas, and triglyceride and non-esterified fatty acid contents in hemolymph were negatively correlated with dietary choline level. The contents of functional fatty acids in hepatopancreas, the activity of acetyl-CoA carboxylase (Acc), and the mRNA expression of fas, srebp and acc were highest in shrimp fed the diet containing 4.67 g/kg choline, and significantly higher than those fed the diet containing 2.91 g/kg, the lowest level of choline (P < 0.05). The number of R cells, content of very low-density lipoprotein (VLDL), activities of carnitine palmitoyl-transferase (Cpt1), lipoprotein lipase and hepatic lipase, and the mRNA expression levels of cpt1, fabp, fatp, ldlr, and ampk in hepatopancreas increased significantly as dietary choline increased (P < 0.05). In addition, hepatopancreas mRNA expression levels of ctl1, ctl2, oct1, badh, bhmt, ck, cept, and cct were generally up-regulated as dietary choline level increased (P < 0.01). In conclusion, dietary choline promoted the deposition of choline and its metabolites by up-regulating genes related to choline transport and metabolism. Moreover, appropriate dietary choline level promoted the development of hepatopancreas R cells and maintained the normal accumulation of lipids required for development, while high dietary choline not only promoted hepatopancreas lipid export by enhancing VLDL synthesis, but also promoted fatty acid β-oxidation and inhibited de novo fatty acid synthesis by activating the Ampk/Srebp signaling pathway. These findings provided further insight and understanding of the mechanisms by which dietary choline regulated lipid metabolism in L. vannamei.

Different effects of dietary β-hydroxy-β-methylbutyrate on composition of fatty acid and free amino acid, and fatty metabolism in the different muscles of broilers

In the study, 336 broiler chickens were selected to explore dietary effects of different β-hydroxy-β-methylbutyrate (HMB) levels (0 (control), 0.05, 0.10, and 0.15%) on the compositions of fatty acids and free amino acids, and lipid metabolism in the different muscles of broilers. In the breast muscle, dietary HMB supplementation hardly affected the free amino acid composition (P > 0.05). Compared to the control group, dietary 0.10 and 0.15% HMB supplementation decreased the content of C18:1n9c and thus the monounsaturated fatty acid (MUFA), and dietary 0.15% HMB supplementation increased the sum of saturated fatty acids (SFA) (P < 0.05). Moreover, compared to the control group, dietary 0.05 and 0.10% HMB increased the mRNA expression of proliferator activated receptor-γ and the activity of fatty acid synthase (FAS), and dietary 0.10% HMB increased the acetyl-CoA carboxylase activity (P < 0.05). In the leg muscle, dietary 0.10 and 0.15% HMB increased the MUFA content and decreased the polyunsaturated fatty acid (PUFA) content, the PUFA to SFA ratio, the mRNA expression of sterol regulatory element binding proteins-1c, and the activities of acyl-CoA oxidase 1 and acetyl-CoA synthetase (P < 0.05). Moreover, dietary 0.10% HMB decreased the activities of hydroxy-3-methylglutaryl-CoA synthase 1 and FAS in comparison to the control group (P < 0.05). Dietary 0.05% HMB decreased the contents of essential amino acids and nonessential amino acids (NEAA), and dietary 0.15% HMB decreased the NEAA content (P < 0.05). In summary, dietary 0.10% HMB supplementation had superior efficiency on lipogenesis in the breast muscle of broilers. However, dietary HMB supplementation, especially at the level of 0.05 and 0.15%, decreased meat nutritional values and the lipogenesis in leg muscles.

Gentamicin resistance to Escherichia coli related to fatty acid metabolism based on transcriptome analysis.

Antibiotic overuse and misuse have promoted the emergence and spread of antibiotic-resistant bacteria. Increasing bacterial resistance to antibiotics is a major healthcare problem, necessitating elucidation of antibiotic resistance mechanisms. In this study, we explored the mechanism of gentamicin resistance by comparing the transcriptomes of antibiotic-sensitive and -resistant Escherichia coli. A total of 410 differentially expressed genes were identified, of which 233 (56.83%) were up-regulated and 177 (43.17%) were down-regulated in the resistant strain compared with the sensitive strain. Gene Ontology (GO) analysis classifies differential gene expression into three main categories: biological processes, cellular components, and molecular functions. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that the up-regulated genes were enriched in eight metabolic pathways, including fatty acid metabolism, which suggests that fatty acid metabolism may be involved in the development of gentamicin resistance in E. coli. This was demonstrated by measuring the acetyl-CoA carboxylase activity, plays a fundamental role in fatty acid metabolism, was increased in gentamicin-resistant E. coli. Treatment of fatty acid synthesis inhibitor, triclosan, promoted gentamicin-mediated killing efficacy to antibiotic-resistant bacteria. We also found that exogenous addition of oleic acid, which involved in fatty acid metabolism, reduced E. coli sensitivity to gentamicin. Overall, our results provide insight into the molecular mechanism of gentamicin resistance development in E. coli.