acetyl-CoA Carboxylase Activity Research Articles

Farnesoid X receptor (FXR) and G protein-coupled bile acid receptor 1 (TGR5) signaling pathways improved the hepatic lipid metabolism in hybrid grouper

In the present study, juvenile hybrid grouper (Epinephelus fuscoguttatus♀ × E. lanceolatus♂) were intraperitoneally injected with taurocholic acid (I-TCA), obeticholic acid (FXR agonist, I-T747), guggulsterone (FXR antagonist, I-TGU), SBI-115 (TGR5 antagonist, I-TSBI), and INT-777 (TGR5 agonist, I-T777), respectively. The results showed that the fish injected with 50 mg kg−1 TCA three times during a 144 h period exhibited significantly lower hepatic lipid accumulation, compared to other concentrations and periods. Compared to the I-TCA group, the I-T747 treatment significantly increased the activities of hepatic adipose triglyceride lipase (ATGL) and carnitine palmitoyltransferase 1 (CPT1), as well as the expression of lipolysis and fatty acid uptake genes, while significantly decreased the conten of hepatic crude lipid, the activity of CPT1, and the expression of lipogenesis genes. Meanwhile, the I-TGU treatment significantly increased hepatic lipid deposition and the expression of lipogenesis genes. Compared to the I-TCA group, the I-T777 treatment did not significantly affect the parameters related to lipid deposition, but it significantly decreased the activities of acetyl-CoA carboxylase (ACC), CPT1, and fatty acid synthase (FAS), while significantly increasing the activity of ATGL and the expression of lipolysis and fatty acid uptake-related genes. Meanwhile, the I-TSBI treatment significantly increased the hepatic lipid accumulation, the activities of ACC, CPT1 and FAS, and the expression of lipogenesis and lipogenic transcriptional factors genes. In conclusion, activation of the FXR protected against the hepatic lipid accumulation by enhancing the lipolysis, while inhibition of FXR or TGR5 induced the hepatic lipid accumulation by enhancing the lipogenesis in hybrid grouper.

Lipopolysaccharide and tyloxapol accelerate the development of atherosclerosis in mice.

The occurrence of atherosclerosis is closely related to inflammation and lipid metabolism disorder. It has been found that lipopolysaccharide (LPS) could induce inflammation, and tyloxapol (Ty) could induce hyperlipidemia. However, the effects of LPS and Ty on the development and mechanism of atherosclerosis have not been investigated thoroughly. To answer this question, we used assay kits to detect total cholesterol (TC), triglyceride (TG), and low-density lipoprotein (LDL) content to evaluate dyslipidemia. We used hematoxylin and eosin staining to evaluate the pathological structure of the aorta and liver, and then used Oil Red O staining to access lipid accumulation in the aortic wall. Subsequently, we used the alanine transaminase (ALT) kit to examine the liver injury. Finally, we used the Western blot experiment to measure proteins that regulate lipid metabolism. We found that the LPS + Ty group could increase the levels of TC, TG, and LDL in the serum and promote lipid accumulation in the aortic wall in mice. Moreover, our study showed that the LPS + Ty group induced pathological changes in hepatocytes and increased ALT content in mice. Significantly, we found that the LPS + Ty group could activate acetyl-CoA carboxylase, sterol regulatory element-binding protein-1c, and inhibit peroxisome proliferator-activated receptors α in mice. Therefore, we suppose that LPS and Ty aggravated the development of atherosclerosis by promoting hyperlipidemia and the disorder of lipid metabolism in mice. These findings are significant for the study of the pathogenesis of atherosclerosis and the selection of animal models.

Effects of sodium acetate on lipid metabolism, antioxidant capability and cell apoptosis of blunt snout bream ( Megalobrama amblycephala ) hepatocytes treated by sodium palmitate

The present study aimed to figure out whether high-fat diet could change the contents of SCFAs in the intestine and the effects of such changes on fatty liver diseases in Megalobrama amblycephala. The results showed that acetate concentration in the intestinal tissue and chyme of M. amblycephala was decreased when fish fed high-fat diet (10% dietary fat) than that fed normal diet (5% dietary fat). Then, effects of sodium acetate (SA) on lipid metabolism, antioxidant capability and apoptosis of M. amblycephala hepatocytes treated by sodium palmitate (SP) were elucidated. It was showed that SP significantly increased cell damages, lipid accumulation, oxidative stress and apoptosis (p < 0.05). SA could reduce cell damages by decreasing the aspartate aminotransferase (AST) activity (p < 0.05), attenuate oxidative stress through reducing intracellular oxygen species (ROS) and malondialdehyde (MDA) contents (p < 0.05), alleviate lipid accumulation by decreasing total cholesterol (TC) and non-esterified fatty acids (NEFA) contents (p < 0.05), along with down-regulating acetyl CoA carboxylase (ACC) activity and up-regulating carnitine palmitoyltransferase 1 (CPT-1) mRNA expression (p < 0.05). In addition, SA increased mitochondrial membrane potential and reduced cell apoptosis caused by SP treatment. Transmission electron microscopy found that the structures of karyotheca, endoplasmic reticulum and mitochondria in hepatocytes were badly damaged by SP and then repaired by SA. Our findings may provide new ideas and basis for high-fat diet and SCFAs (acetate) used in aquaculture practice.

Elevation of Fatty Acid Biosynthesis Metabolism Contributes to Zhongshengmycin Resistance in Xanthomonas oryzae.

Xanthomonas oryzae severely impacts the yield and quality of rice. Antibiotics are the most common control measure for this pathogen; however, the overuse of antibiotics in past decades has caused bacterial resistance to these antibiotics. The agricultural context is of particular importance as antibiotic-resistant bacteria are prevalent, but the resistance mechanism largely remains unexplored. Herein, using gas chromatography–mass spectrometry (GC–MS), we demonstrated that zhongshengmycin-resistant X. oryzae (Xoo-Rzs) and zhongshengmycin-sensitive X. oryzae (Xoo-S) have distinct metabolic profiles. We found that the resistance to zhongshengmycin (ZS) in X. oryzae is related to increased fatty acid biosynthesis. This was demonstrated by measuring the Acetyl-CoA carboxylase (ACC) activity, the expression levels of enzyme genes involved in the fatty acid biosynthesis and degradation pathways, and adding exogenous materials, i.e., triclosan and fatty acids. Our work provides a basis for the subsequent control of the production of antibiotic-resistant strains of X. oryzae and the development of coping strategies.

Transcriptome Analysis of Ostrinia furnacalis Female Pheromone Gland: Esters Biosynthesis and Requirement for Mating Success.

Female moths use sex pheromones to attract males, and corresponding regulatory mechanism underlying sex pheromone biosynthesis is species-dependent. However, the detailed mechanism involved in sex pheromone biosynthesis in Ostrinia furnacalis has not yet been fully addressed. In the present study, transcriptome sequencing of O. furnacalis pheromone glands screened a serials of candidate genes involved in sex pheromone biosynthesis. Our analysis showed that sex pheromone release in O. furnacalis females arrives its peak at the 2nd scotophase, consistent with its mating behavior. Pheromone biosynthesis-activating neuropeptide (PBAN) was confirmed to regulate sex pheromone biosynthesis, and Ca2+ is the secondary messenger of PBAN signaling in O. furnacalis. The functional analysis of candidate genes demonstrated that the decreased mRNA levels or activities of calcineurin (CaN) and acetyl-CoA carboxylase (ACC) led to significant decrease in sex pheromone production and female capability to attract males, as demonstrated by RNAi-mediated knockdown and pharmacological inhibitor assay. Most importantly, the activities of CaN and ACC depend on the activation of PBAN/PBANR/Ca2+. Furthermore, fatty-acyl reductase 14 was involved in PBAN-mediated sex pheromone biosynthesis. Altogether, our results demonstrated that PBAN regulates sex pheromone biosynthesis through PBANR/Ca2+/CaN/ACC pathway to promote sex pheromone biosynthesis in O. furnacalis and provided a reference for non-model organism to study neuropeptide signal transduction.

Ampk Activation Normalizes Myogenic Regulatory Gene Expression In The Skeletal Muscle Of Dystrophic Animals

Skeletal muscle regeneration is a highly orchestrated physiological process that is dependent on the myogenic capacity of muscle stem cells (MuSCs). Recent studies have demonstrated a regulatory role for adenosine monophosphate-activated protein kinase (AMPK) in acute myotrauma-induced MuSC fate. However, the precise function of AMPK during persistent muscle regeneration has yet to be investigated. PURPOSE: To evaluate MuSC biology in response to a novel AMPK agonist in a model of cyclical skeletal muscle degeneration and regeneration. METHODS: Dystrophic C57BL/10-mdx (mdx) animals were treated with a single dose (5 mpk) of the orally bioactive AMPK activator MK-8722 via gavage and were euthanized 3-, 6-, or 12-hours (hrs) post-administration. Wild-type (WT) mice were also obtained at 3 hrs post-MK-8722 treatment. WT and mdx animals treated with the vehicle (Veh) solution served as control groups. Skeletal muscles were harvested and processed for immunoblotting, qPCR, and immunofluorescence analyses. RESULTS: As expected, gene expression of the myogenic regulators paired box 7 (Pax7), myogenic factor 5 (Myf5), myoblast determination protein (MyoD), and myogenin (MyoG) in dystrophic mice was significantly higher (~3-6-fold) relative to their WT littermates. We also observed a greater (p < 0.05) number of MyoD+ myonuclei and active MuSCs (Pax7+/MyoD+ myonuclei) in muscles of mdx animals relative to the WT group. MK-8722 administration significantly elevated AMPK and downstream acetyl-CoA carboxylase activation status in WT and dystrophic muscles. Pax7 and MyoG gene expression was 6-fold lower (p < 0.05) 6 hrs following MK-8722 administration relative to their Veh controls and similar (p > 0.05) to their WT counterparts. Furthermore, preliminary analyses (n = 4-7) revealed statistical trends toward fewer MyoD+ myonuclei and activated MuSCs in MK-8722 treated mdx animals at 12 hrs post-treatment compared to the Veh group. CONCLUSIONS: The present study is the first to evaluate MuSC biology following a single dose of a new-generation AMPK activator in dystrophic skeletal muscle. Our results suggest that acute pharmacological targeting of AMPK delays MuSC activation in highly regenerative skeletal muscle and prefaces further investigation of the therapeutic value of AMPK agonists in muscular dystrophy.

MIG12 is involved in the LXR activation-mediated induction of the polymerization of mammalian acetyl-CoA carboxylase

Liver X receptors (LXR) α and β are a family of nuclear receptors that regulate lipogenesis by controlling the expression of the genes involved in the synthesis of fatty acids. MID1IP1, which encodes MIG12, is a target gene of LXR. MIG12 induces fatty acid synthesis by stimulating the polymerization-mediated activation of acetyl-CoA carboxylase (ACC). Here, we show that LXR's activation stimulates ACC polymerization in HepG2 cells by increasing the expression of MIG12. A knockdown of MID1IP1 abrogated the stimulation completely. The mutations of MIG12's leucine-zipper domain reduced the interaction between MIG12 and ACC, thus decreasing the MIG12's capacity to stimulate ACC polymerization. These results indicate that LXR's activation stimulates lipogenesis not only through the induction of the genes encoding lipogenic enzymes but also through MIG12's stimulation of ACC polymerization.

Neonatal Vitamin C and Cysteine Deficiencies Program Adult Hepatic Glutathione and Specific Activities of Glucokinase, Phosphofructokinase, and Acetyl-CoA Carboxylase in Guinea Pigs' Livers.

Premature neonates are submitted to an early-life oxidative stress from parenteral nutrition, which is vitamin C (VC) deficient and induces low endogenous levels of glutathione. The oxidative stress caused by these deficiencies may permanently affect liver glycolysis and lipogenesis. This study evaluates the short- and long-term effects of neonatal VC and cysteine deficient diets on redox and energy metabolism. Three-day-old Hartley guinea pigs from both sexes were given a regular or a deficient diet (VC, cysteine, or both) until week 1 of life. Half of the animals were sacrificed at this age, while the other half ate a complete diet until 12 weeks. Liver glutathione and the activity and protein levels of glucokinase, phosphofructokinase, and acetyl-CoA-carboxylase were measured. Statistics: factorial ANOVA (5% threshold). At 1 week, all deficient diets decreased glutathione and the protein levels of glucokinase and phosphofructokinase, while cysteine deficiency decreased acetyl-CoA-carboxylase levels. A similar enzyme level was observed in control animals at 12 weeks. At this age, VC deficiency decreased glutathione, while cysteine increased it. Acetyl-CoA-carboxylase protein levels were increased, which decreased its specific activity. Early-life VC and cysteine deficiencies induce neonatal oxidative stress and an adult-like metabolism, while predisposing to increased lipogenic rates during adulthood.

Postharvest effects of sodium nitroprusside treatment on membrane fatty acids of blueberry (vaccinium corymbosum, cv. Bluecrop) fruit

Fatty acid plays an important role in maintaining membrane structural integrity. This study was conducted to evaluate the effects of postharvest sodium nitroprusside (SNP) treatment on fatty acid metabolism of blueberry fruit. The fruit harvested from a blueberry plantation were immersed in 0.10 mmol L−1 SNP aqueous solution at 20 °C for 10 min used for research (20 ± 0.5 °C and 80% RH for 8 d). SNP-treated fruit maintained a higher relative content of unsaturated fatty acids, exhibited higher fruit firmness and lower decay incidence than control. The SNP treatment increased fruit nitric oxide content, acetyl CoA carboxylase activity and the expression levels of the key genes for fatty acid synthesis. In contrast, SNP treatment decreased lipoxygenase activity and malondialdehyde content. Therefore, the postharvest SNP treatment maintain the fruit quality during shelf life by its positive effect on fatty acids metabolism.

Increasing the Ascomycin Yield by Relieving the Inhibition of Acetyl/Propionyl-CoA Carboxylase by the Signal Transduction Protein GlnB.

Ascomycin (FK520) is a multifunctional antibiotic produced by Streptomyces hygroscopicus var. ascomyceticus. In this study, we demonstrated that the inactivation of GlnB, a signal transduction protein belonging to the PII family, can increase the production of ascomycin by strengthening the supply of the precursors malonyl-CoA and methylmalonyl-CoA, which are produced by acetyl-CoA carboxylase and propionyl-CoA carboxylase, respectively. Bioinformatics analysis showed that Streptomyces hygroscopicus var. ascomyceticus contains two PII family signal transduction proteins, GlnB and GlnK. Protein co-precipitation experiments demonstrated that GlnB protein could bind to the α subunit of acetyl-CoA carboxylase, and this binding could be disassociated by a sufficient concentration of 2-oxoglutarate. Coupled enzyme activity assays further revealed that the interaction between GlnB protein and the α subunit inhibited both the activity of acetyl-CoA carboxylase and propionyl-CoA carboxylase, and this inhibition could be relieved by 2-oxoglutarate in a concentration-dependent manner. Because GlnK protein can act redundantly to maintain metabolic homeostasis under the control of the global nitrogen regulator GlnR, the deletion of GlnB protein enhanced the supply of malonyl-CoA and methylmalonyl-CoA by restoring the activity of acetyl-CoA carboxylase and propionyl-CoA carboxylase, thereby improving the production of ascomycin to 390 ± 10 mg/L. On this basis, the co-overexpression of the β and ε subunits of propionyl-CoA carboxylase further increased the ascomycin yield to 550 ± 20 mg/L, which was 1.9-fold higher than that of the parent strain FS35 (287 ± 9 mg/L). Taken together, this study provides a novel strategy to increase the production of ascomycin, providing a reference for improving the yield of other antibiotics.

The response of Trypanosoma brucei to Exogenous Fatty Acids in Low Lipid Conditions

Trypanosoma brucei is an extracellular parasite that causes African Sleeping Sickness and is endemic to the sub-Saharan African region. The parasite's extracellular nature forces the parasite to adapt to its host's environment. One of the regulatory mechanisms is to regulate fatty acid synthesis enzymes in response to exogenous fatty acids. Our previous study showed that the insect-host procyclic form (PF) T. brucei regulates the activity and expression level of acetyl-CoA carboxylase (ACC) when grown in media containing different lipid levels. PF in low lipid media has an elevated ACC activity but lower ACC protein level than in high lipid media. We also observed that the addition of C18:0 to PF in low lipid media reduced ACC activity and increased growth rate, which showed an environmental response to the exogenous fatty acid level. Here, we observe the growth and the ACC level of low lipid-adapted PF T. brucei after treatment with fatty acids of different chain lengths. We did not observe a significant change in the ACC protein level. However, we observed significant growth differences with the addition of different fatty acids, and some of these effects were cell density-dependent. These data suggested that the addition of fatty acids changes ACC's activity and PF growth pattern in low lipid, but does not change PF's ACC expression level. Future studies will investigate whether different fatty acids regulate ACC activity by phosphorylation, allosteric regulation, or a combination of both mechanisms.

THE IMPACT OF ESSENTIAL OILS OF THE LAMIACEAE FAMILY AGAINST TYLENCHULUS SEMIPENETRANS USING MOLECULAR MODELING METHODS

Tylenchulus semipenetrans is an economically important plant-parasitic nematode occurring in all citrus-producing regions of the world and causing a disease called “slow decline”. Chemical nematicides commonly used in agriculture have ecotoxicological effects. As a control method, attention has been paid to bio-nematicides that do not exhibit harmful effects on the ecosystem. In this study we will carry out the in scilico experiments in order to find the most coherent Enzyme-Ligand complex to lead to the best inhibitors of Acetyl CoA Carboxylase in Citrus Tylenchulus semipenetrans nematode. “Acetyl CoA Carboxylase” enzyme responsible for fatty acid synthesis in Tylenchulus semipenetrans, its alteration disrupting the synthesis of the surface layer, this inhibitory action is based on essential oils of aromatic plants, taking as an example the Lamiaceae family, using natural compounds extract from essential oils of Salvia verbenaca, Lavandula stoechas, Rosmarinus officinalis, and Thymus ciliatus. This study revealed for the first time that ?-phellandrène from Salvia verbenaca gives the best docking scores compared to Biotine, the co-crystallized inhibitor of the Acetyl CoA Carboxylase, to spirotetramat as chemical insecticide already used against citrus nematode, and to the other complexes. After that, the Molecular Dynamics Simulation study showed a good result for the ?-phellandrène- Acetyl CoA Carboxylase docked complex, for that we can consider that ?-phellandrène extracted from Salvia verbenaca’s essential oil as a functional inhibitor of Acetyl CoA Carboxylase activities and it can be used as good bio-nematicides against Tylenchulus semipenetrans.

Malonyl coenzyme A decarboxylase deficiency with a novel mutation.

Malonyl-CoA, a product of acetyl-CoA carboxylase is a metabolic intermediate in lipogenic tissues that include liver and adipose tissue, where it is involved in the denovo fatty acid synthesis and elongation. Malonyl-CoA decarboxylase (MLYCD, E.C.4.1.1.9), a 55-kDa enzyme catalyses the conversion of malonyl-CoA to acetyl-CoA and carbon dioxide, thus providing a route for disposal of malonyl-CoA from mitochondria and peroxisomes, whereas in the cytosol, the malonyl-CoA pool is regulated by the balance of MLYCD and acetyl-CoA carboxylase activities. So far, 34 cases with different MLYCD gene defects comprising point mutations, stop codons, and frameshift mutations have been reported in the literature. Here, we describe the follow-up of a patient affected by malonic aciduria upon neonatal onset. Molecular analysis showed novel homozygous mutations in the MLYCD gene. Our findings expand the number of reported cases and add a novel variant to the repertoire of MLYCD mutations.

The Role of Sugar Signaling in Regulating Plant Fatty Acid Synthesis.

Photosynthates such as glucose, sucrose, and some of their derivatives play dual roles as metabolic intermediates and signaling molecules that influence plant cell metabolism. Such sugars provide substrates for de novo fatty acid (FA) biosynthesis. However, compared with the well-defined examples of sugar signaling in starch and anthocyanin synthesis, until recently relatively little was known about the role of signaling in regulating FA and lipid biosynthesis. Recent research progress shows that trehalose 6-phosphate and 2-oxoglutarate (2-OG) play direct signaling roles in the regulation of FA biosynthesis by modulating transcription factor stability and enzymatic activities involved in FA biosynthesis. Specifically, mechanistic links between sucrose non-fermenting−1–related protein kinase 1 (SnRK1)–mediated trehalose 6-phosphate (T6P) sensing and its regulation by phosphorylation of WRI1 stability, diacylglycerol acyltransferase 1 (DGAT1) enzyme activity, and of 2-OG–mediated relief of inhibition of acetyl-CoA carboxylase (ACCase) activity by protein PII are exemplified in detail in this review.

Polysaccharide-rich red algae (Gelidium amansii) hot-water extracts ameliorate the altered plasma cholesterol and hepatic lipid homeostasis in high-fat diet-fed rats.

We have demonstrated that red algae Gelidium amansii (GA) hot-water extract (GHE) is a polysaccharide-rich fraction, containing 68.54% water-soluble indigestible carbohydrate polymers; the molecular weight of major polysaccharide is 892. Here, we investigated the mechanisms of GHE on plasma and hepatic lipid metabolisms in high-fat (HF) diet-fed rats. Rats were divided into: normal diet group, HF-diet group, HF-diet+5% GHE group, and HF-diet+1% cholestyramine group. GHE supplementation for 8 weeks significantly decreased plasma cholesterol, LDL-C, and VLDL-C levels and increased the fecal triglyceride and bile acid excretion in HF diet-fed rats. GHE group has lower lipid contents in the liver and adipose tissues. GHE supplementation decreased the activities of acetyl-CoA carboxylase, fatty acid synthase, and HMG-CoA reductase in the livers. The levels of increased phosphorylated AMP-activated protein kinase (AMPK), peroxisome proliferator activated receptor (PPAR)-α, farnesoid-X receptor (FXR), low density lipoprotein receptor (LDLR), and cytochrome P450-7A1 (CYP7A1) protein expression, and the decreased PPAR-γ protein expression in the livers were observed in GHE group. These results suggest that GHE supplementation is capable of interfering in cholesterol metabolism and increasing hepatic LDLR and CYP7A1 expression to decrease blood cholesterol, and activating FXR and AMPK to inhibit lipogenic enzyme activities and reduce the hepatic lipid accumulation.

Flaxseed Oil and Heated Flaxseed Supplements Have Different Effects on Lipid Deposition and Ileal Microbiota in Albas Cashmere Goats.

Simple SummaryWith the grassland desertification intensified, pasture carrying capacity decreased, and grass seasonal changed, stall-feeding fattening has become an effective means to protect the natural environment. The stall-feeding fattening increased the cashmere goats’ weight but reduced the meat quality and increased the saturated fatty acids content in muscle and fat tissue of cashmere goats. Supplementing flaxseed and flaxseed oil rich-in linolenic acid (ALA) to diet to improve meat quality is an effective nutritional regulation means. Previous research results of our team showed that compared to diet supplemented with flaxseed oil, added flaxseed increased linoleic acid biohydrogenation by reducing the Ruminobacter relative abundance and increasing the relative abundance of Prevotellaceae_UCG-001 and Fretibacterium in rumen, protected ALA away from biohydrogenation, and more n-3 polyunsaturated fatty acids entered the post-intestinal tract. Based on the previous research, this study explored whether the ALA flowing into the posterior intestine can reduce fat deposition and blood lipid by affecting intestinal microbiota. The results showed that adding flaxseed grain to diet decreased the growth performance, lipid deposition, and blood lipid content of goats by regulating the blood lipid-related enzyme activity, which positively associated with [Eubacterium]_coprostanoligenes_group, but negatively associated with unclassified_f_Peptostreptococcaceae, Intestinibacter, and Ruminococcus_2.The present study investigated the effect of flaxseed grain or flaxseed oil on ileal microbiota and lipid deposition of cashmere goats. Sixty kid goats (average body weight 18.6 ± 0.1 kg) were allocated to three treatments, fed for 90 days, with control treatment: basal diet (CON, total-mixed ration), experimental treatment: basal diet with added flaxseed oil (LNO), experimental treatment: basal diet with added heated flaxseed grain (HLS). The final body weight, body weight gain, the weight of kidney fat, omental fat, tail fat, and fat tissue, the activity of fatty acid synthetase, acetyl-coa carboxylase, and malic dehydrogenase, and the relative abundance (RA) of unclassified_f_Peptostreptococcaceae and Intestinibacter were remarkably higher in the LNO treatment than in the HLS treatment, but the [Eubacterium]_coprostanoligenes_group RA showed the opposite result. The content of triglyceride, cholesterol, and low-density lipoprotein cholesterol were significantly higher in the CON and LNO treatments than in the HLS treatment, while the hormone-sensitive lipase activity and the non-esterified fatty acid content showed the opposite result. In conclusion, the flaxseed grain is more efficient than flaxseed oil in ameliorating the blood lipid profiles and it is a potential product for decreasing the lipid deposition of cashmere goats.

Attenuation pathways of erythromycin and biochemical responses related to algal growth and lipid synthesis in a microalga-effluent system

Microalgal cultivation in municipal wastewater treatment plants (WWTPs) can realize the coupling of wastewater treatment and microalgae energy utilization, however, the residual antibiotics in effluents from WWTPs affect the growth of microalgae. In this study, green alga (Scenedesmus obliquus) cells were inoculated into the effluents to ascertain the attenuation pathways of erythromycin (ERY) and the biochemical responses of microalga in a microalga-effluent system. Results showed that hydrolysis, photolysis, and biodegradation (including bioadsorption) cause the attenuation of ERY in a microalga-effluent system, and the biodegradation (including bioadsorption) has the greatest removal rate (reaching a maximum of 57.87%), followed by hydrolysis (reaching a maximum of 34.13%), and photolysis (less than 5%) after five days. The photosynthetic pigment contents in cells of microalga decreased the most (by 35.66% for chlorophyll a), and the production of ROS was stimulated (by 33.75%) after five-day exposure to ERY at an initial concentration of 100 μg/L. Meanwhile, the activity of ribulose-1,5-biphosphate carboxylase (RuBPCase) decreased by 55.65%, and the activity of acetyl-CoA carboxylase (ACCase) increased by 55.65%. The ROS level, photosynthetic pigment content, and RuBPCase activity were extremely significantly correlated with each other (P < 0.01), indicating that exposure to ERY changed those biochemical responses related to the rate of photosynthesis of microalga, inhibiting the growth thereof. On the other hand, exposure to ERY increased lipid production by microalga through the induced ACCase activity.

Comparative Treatment Efficiency and Fatty Acid Synthesis of Chlorella vulgaris: Immobilization Versus Co-cultivation

Microalgae consists a promising feedstock for biofuel production due to their high growth rates and lipid content. Microalgal wastewater remediation can achieve both organic matters removal and biodiesel production, leading to economic benefits. In this study, immobilized microalgae and algae-bacteria consortia were used to treat synthetic fracturing wastewater. Organic matter removal, biomass production and lipid synthesis by co-culture of Chlorella vulgaris and Bacillus bacteria were investigated in comparison with an algae immobilization system during the process. The chemical oxygen demand removal rate and lipid concentration of the co-culture were both lower than those of the immobilized C. vulgaris, while algal biomass under the two cultivation conditions was similar. The immobilized algae provided higher amount of fatty acids, especially mono-unsaturated fatty acids, than the algae-bacteria consortia. Most of the fuel properties of biodiesel produced in both immobilized and co-cultured C. vulgaris complied with the specifications for standard biodiesel. The comparative results of enzyme activity showed that immobilization can enhance the activity of acetyl-CoA carboxylase, the key enzyme for fatty acids synthesis, leading to the formation of more fatty acids and lipids. Furthermore, immobilization decreased the ADP-glucose pyrophosphorylase activity and inhibited starch formation. Immobilization favors lipid production and removal of organics by C. vulgaris.

Nitrogen starvation–induced oxidative stress relieves PII-mediated inhibition of acetyl-CoA carboxylase (ACCase) activity and signals enhanced lipid synthesis in Synechococcus PCC 7942

The present study shows the existence of PII-acetyl-CoA carboxylase interaction in the cyanobacterium Synechococcus sp. PCC 7942 and the possible adverse impact of nitrogen starvation on this interaction. The in silico and in vitro analysis of PII-acetyl-CoA carboxylase interaction revealed that the biotin carboxyl carrier protein subunit of acetyl-CoA carboxylase enzyme actually interacts with the T-loop of PII protein. However, exposure of the cyanobacterium to nitrogen-starved condition showed a higher expression and activity of acetyl-CoA carboxylase at the intracellular level which denoted the impairment of PII-acetyl-CoA carboxylase interaction. A similar stimulatory effect of nitrogen starvation has also been noticed in the PII mutant of Synechococcus PCC 7942. Further, the physiological study reflected that nitrogen starvation–caused reactive oxygen species generation in the wild-type and PII mutant strains and lipid was increased in both strains of Synechococcus sp. PCC 7942. Proteomic analysis showed the upregulation of glycogen synthase, biotin carboxylase, and antioxidative enzymes and the deregulation of proteins involved in photosynthesis, energy metabolism, and protein synthesis. Interestingly, enhanced accumulation of transcripts of few tricarboxylic acid cycle genes was also noticed in the wild type. Although oxidative stress and lipid production were enhanced in both the test strains under nitrogen starvation, the impacts were more prominent in the mutant strain. Our results suggest that the nitrogen starvation–induced oxidative stress possibly relieved the PII-mediated inhibition of acetyl-CoA carboxylase and led to increased lipid synthesis in Synechococcus PCC 7942.

Orexin system is expressed in avian liver and regulates hepatic lipogenesis via ERK1/2 activation

Orexins are originally characterized as orexigenic hypothalamic neuropeptides in mammals. Subsequent studies found orexin to be expressed and perform pleiotropic functions in multiple tissues in mammals. In avian (non-mammalian) species, however, orexin seemed to not affect feeding behavior and its physiological roles are poorly understood. Here, we provide evidence that orexin and its related receptors are expressed in chicken hepatocytes. Double immunofluorescence staining showed that orexin is localized in the ER, Golgi, and in the lysosomes in LMH cells. Brefeldin A treatment reduced orexin levels in the culture media, but increased it in the cell lysates. Administration of recombinant orexins upregulated the expression of orexin system in the liver of 9-day old chicks, but did not affect feed intake. Recombinant orexins increased fatty acid synthase (FASN) protein levels in chicken liver, activated acetyl-CoA carboxylase (ACCα), and increased FASN, ATP citrate lyase(ACLY), and malic enzyme (ME) protein expression in LMH cells. Blockade ERK1/2 activation by PD98059 attenuated these stimulating effects of orexin on lipogenic factors. Overexpression of ERK1/2 increased the expression of lipogenic genes, and orexin treatment induced the phosphorylated levels of ERK1/2Thr202/Tyr204, but not that of p38 Thr180/Tyr182 or JNK1/2 Thr183/Tyr185 in chicken liver and LMH cells. Taken together, this is the first report evidencing that orexin is expressed and secreted from chicken hepatocytes, and that orexin induced hepatic lipogenesis via activation of ERK1/2 signaling pathway.