scholarly journals Di(isononyl) cyclohexane-1,2-dicarboxylate (DINCH) Alters Transcriptional Profiles, Lipid Metabolism and Behavior in Zebrafish Larvae

2021 ◽  
Author(s):  
Noha Saad ◽  
Ceyhun Bereketoglu ◽  
Ajay Pradhan
Keyword(s):  
Lipid Metabolism ◽  
Developmental Stages ◽  
Cholesterol Biosynthesis ◽  
Animal Health ◽  
Aquatic Organisms ◽  
Acid Synthesis ◽  
Hatching Rate ◽  
Dependent Manner ◽  
Developmental Abnormalities ◽  
Expression Of Genes

Plasticizers are commonly used in different consumer goods and personal care products to provide flexibility, durability and elasticity to polymers. Due to their reported toxicity, the use of several plasticizers including phthalates has been regulated and/or banned from the market. Di(isononyl) cyclohexane-1,2-dicarboxylate (DINCH) is an alternative plasticizer that was introduced to replace toxic plasticizers. Increasing global demand and lack of information regarding toxicity and safety assessment of DINCH have raised the concern to human and animal health. Hence, in the present study, we investigated the adverse effects of DINCH (at concentrations ranging from 0.01 to 10 μM) in early developmental stages of zebrafish using different endpoints such as hatching rate, developmental abnormalities, lipid metabolism, behavior analysis and gene expression. We found that DINCH caused hatching delay in a dose-dependent manner and altered the expression of genes involved in stress response. Lipid staining using Oil Red O stain showed a slight lipid accumulation around the yolk, brain, eye and neck with increasing concentration. Genes associated with lipid metabolism such as fatty acid synthesis, β-oxidation, elongation, lipid transport were significantly altered by DINCH. Behavioral analysis of larvae demonstrated a distinct locomotor activity including distance and acceleration upon exposure to DINCH both in light and dark. Genes involved in cholesterol biosynthesis and homeostasis were also affected by DINCH indicating possible developmental neurotoxicity. The present data shows that DINCH could induce physiological and metabolic toxicity to aquatic organisms. Hence, further analyses and environmental monitoring on DINCH should be conducted to determine its safety and toxicity levels.

LIF and CNTF, which share the gp130 transduction system, stimulate hepatic lipid metabolism in rats

1996 ◽  
Vol 271 (3) ◽  
pp. E521-E528 ◽  
Author(s):  
K. Nonogaki ◽  
X. M. Pan ◽  
A. H. Moser ◽  
J. Shigenaga ◽  
I. Staprans ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Acid Synthesis ◽  
Interleukin 4 ◽  
Dependent Manner ◽  
Hepatic Triglyceride ◽  
Serum Triglycerides ◽  
Triglyceride Secretion

We determined the effects of leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) on lipid metabolism in intact rats. Administration of LIF and CNTF increased serum triglycerides in a dose-dependent manner with peak values at 2 h. The effects of LIF and CNTF on serum cholesterol were very small, and serum glucose was unaffected. Both LIF and CNTF stimulated hepatic triglyceride secretion, hepatic de novo fatty acid synthesis, and lipolysis. Pretreatment with phenylisopropyl adenosine, which inhibits lipolysis, partially inhibited LIF- and CNTF-induced hypertriglyceridemia. Interleukin-4, which inhibits cytokine-induced hepatic fatty acid synthesis, also partially inhibited LIF- and CNTF-induced hypertriglyceridemia. These results indicate that both lipolysis and de novo fatty acid synthesis play a role in providing fatty acids for the increase in hepatic triglyceride secretion. Neither indomethacin nor adrenergic receptor antagonists affected the hypertriglyceridemia. The combination of LIF plus CNTF showed no additive effects consistent with the action of both cytokines through the gp130 transduction system. Thus LIF and CNTF have similar effects on lipid metabolism; they join a growing list of cytokines that stimulate hepatic triglyceride secretion and may mediate the changes in lipid metabolism that accompany the acute phase response.

scholarly journals Postnatal activation of TLR4 in astrocytes promotes excitatory synaptogenesis in hippocampal neurons

2016 ◽  
Vol 215 (5) ◽  
pp. 719-734 ◽  
Author(s):  
Yi Shen ◽  
Huaping Qin ◽  
Juan Chen ◽  
Lingyan Mou ◽  
Yang He ◽  
...  
Keyword(s):  
Brain Development ◽  
Hippocampal Neurons ◽  
Developmental Stages ◽  
Primary Response ◽  
Synapse Development ◽  
Dependent Manner ◽  
Developmental Abnormalities ◽  
Extracellular Signal ◽  
Immune Challenges ◽  
Tlr4 Activation

Astrocytes are critical in synapse development, and their dysfunction in crucial developmental stages leads to serious neurodevelopmental diseases, including seizures and epilepsy. Immune challenges not only affect brain development, but also promote seizure generation and epileptogenesis, implying immune activation is one of the key factors linking seizures and epilepsy to abnormal brain development. In this study, we report that activating astrocytes by systemic lipopolysaccharide (LPS) challenges in the second postnatal week promotes excitatory synapse development, leading to enhanced seizure susceptibility in mice. Toll-like receptor 4 (TLR4) activation in astrocytes increased astrocytic extracellular signal–related kinase 1/2 (Erk1/2) and phospho-Erk1/2 levels in a myeloid differentiation primary response protein 88 (MyD88)–dependent manner. Constitutively activating Erk1/2 in astrocytes was sufficient to enhance excitatory synaptogenesis without activating TLR4. Deleting MyD88 or suppressing Erk1/2 in astrocytes rescued LPS-induced developmental abnormalities of excitatory synapses and restored the enhanced seizure sensitivity. Thus, we provide direct evidence for a developmental role of astrocytes in shaping a predisposition to seizure generation.

scholarly journals Central Resistin Regulates Hypothalamic and Peripheral Lipid Metabolism in a Nutritional-Dependent Fashion

Endocrinology ◽  
2008 ◽  
Vol 149 (9) ◽  
pp. 4534-4543 ◽  
Author(s):  
María J. Vázquez ◽  
C. Ruth González ◽  
Luis Varela ◽  
Ricardo Lage ◽  
Sulay Tovar ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Mrna Expression ◽  
Fatty Acid Synthase ◽  
De Novo ◽  
Acid Synthesis ◽  
Inhibitory Effect ◽  
De Novo Lipogenesis ◽  
Dependent Manner ◽  
Fed State

Evidence suggests that the adipocyte-derived hormone resistin (RSTN) directly regulates both feeding and peripheral metabolism through, so far, undefined hypothalamic-mediated mechanisms. Here, we demonstrate that the anorectic effect of RSTN is associated with inappropriately decreased mRNA expression of orexigenic (agouti-related protein and neuropeptide Y) and increased mRNA expression of anorexigenic (cocaine and amphetamine-regulated transcript) neuropeptides in the arcuate nucleus of the hypothalamus. Of interest, RSTN also exerts a profound nutrition-dependent inhibitory effect on hypothalamic fatty acid metabolism, as indicated by increased phosphorylation levels of both AMP-activated protein kinase and its downstream target acetyl-coenzyme A carboxylase, associated with decreased expression of fatty acid synthase in the ventromedial nucleus of the hypothalamus. In addition, we also demonstrate that chronic central RSTN infusion results in decreased body weight and major changes in peripheral expression of lipogenic enzymes, in a tissue-specific and nutrition-dependent manner. Thus, in the fed state central RSTN is associated with induced expression of fatty acid synthesis enzymes and proinflammatory cytokines in liver, whereas its administration in the fasted state does so in white adipose tissue. Overall, our results indicate that RSTN controls feeding and peripheral lipid metabolism and suggest that hepatic RSTN-induced insulin resistance may be mediated by central activation of de novo lipogenesis in liver.

scholarly journals Dietary protein intake affects expression of genes for lipid metabolism in porcine skeletal muscle in a genotype-dependent manner

2015 ◽  
Vol 113 (7) ◽  
pp. 1069-1077 ◽  
Author(s):  
Yingying Liu ◽  
Fengna Li ◽  
Lingyun He ◽  
Bie Tan ◽  
Jinping Deng ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lipid Metabolism ◽  
Dietary Protein ◽  
Protein Intake ◽  
Dependent Manner ◽  
Dietary Protein Intake ◽  
Lipogenic Genes ◽  
Expression Of Genes ◽  
Mini Pigs ◽  
Mrna Expression Levels

Skeletal muscle is a major site for the oxidation of fatty acids (FA) in mammals, including humans. Using a swine model, we tested the hypothesis that dietary protein intake regulates the expression of key genes for lipid metabolism in skeletal muscle. A total of ninety-six barrows (forty-eight pure-bred Bama mini-pigs (fatty genotype) and forty-eight Landrace pigs (lean genotype)) were fed from 5 weeks of age to market weight. Pigs of fatty or lean genotype were randomly assigned to one of two dietary treatments (low- or adequate-protein diet), with twenty-four individually fed pigs per treatment. Our data showed that dietary protein levels affected the expression of genes involved in the anabolism and catabolism of lipids in the longissimus dorsi and biceps femoris muscles in a genotype-dependent manner. Specifically, Bama mini-pigs had more intramuscular fat, SFA and MUFA, as well as elevated mRNA expression levels of lipogenic genes, compared with Landrace pigs. In contrast, Bama mini-pigs had lower mRNA expression levels of lipolytic genes than Landrace pigs fed an adequate-protein diet in the growing phase. These data are consistent with higher white-fat deposition in Bama mini-pigs than in Landrace pigs. In conclusion, adequate provision of dietary protein (amino acids) plays an important role in regulating the expression of key lipogenic genes, and the growth of white adipose tissue, in a genotype- and tissue-specific manner. These findings have important implications for developing novel dietary strategies in pig production.

scholarly journals Gene Expression Profiling in Wild-Type and PPAR-Null Mice Exposed to Perfluorooctane Sulfonate Reveals PPAR-Independent Effects

PPAR Research ◽  
2010 ◽  
Vol 2010 ◽  
pp. 1-23 ◽  
Author(s):  
Mitchell B. Rosen ◽  
Judith R. Schmid ◽  
J. Christopher Corton ◽  
Robert D. Zehr ◽  
Kaberi P. Das ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Ribosome Biogenesis ◽  
Cholesterol Biosynthesis ◽  
Perfluorooctane Sulfonate ◽  
Gene Profiling ◽  
Blood Levels ◽  
Wild Type ◽  
Altered Expression ◽  
Expression Of Genes ◽  
Independent Effects

Perfluorooctane sulfonate (PFOS) is a perfluoroalkyl acid (PFAA) and a persistent environmental contaminant found in the tissues of humans and wildlife. Although blood levels of PFOS have begun to decline, health concerns remain because of the long half-life of PFOS in humans. Like other PFAAs, such as, perfluorooctanoic acid (PFOA), PFOS is an activator of peroxisome proliferator-activated receptor-alpha (PPAR) and exhibits hepatocarcinogenic potential in rodents. PFOS is also a developmental toxicant in rodents where, unlike PFOA, its mode of action is independent of PPAR. Wild-type (WT) and PPAR-null (Null) mice were dosed with 0, 3, or 10 mg/kg/day PFOS for 7 days. Animals were euthanized, livers weighed, and liver samples collected for histology and preparation of total RNA. Gene profiling was conducted using Affymetrix 430_2 microarrays. In WT mice, PFOS induced changes that were characteristic of PPAR transactivation including regulation of genes associated with lipid metabolism, peroxisome biogenesis, proteasome activation, and inflammation. PPAR-independent changes were indicated in both WT and Null mice by altered expression of genes related to lipid metabolism, inflammation, and xenobiotic metabolism. Such results are similar to studies done with PFOA and are consistent with modest activation of the constitutive androstane receptor (CAR), and possibly PPAR and/or PPAR/. Unique treatment-related effects were also found in Null mice including altered expression of genes associated with ribosome biogenesis, oxidative phosphorylation, and cholesterol biosynthesis. Of interest was up-regulation ofCyp7a1, a gene which is under the control of various transcription regulators. Hence, in addition to its ability to modestly activate PPAR, PFOS induces a variety of PPAR-independent effects as well.

scholarly journals Lipid metabolism in Calanus finmarchicus is sensitive to variations in predation risk and food availability

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Elise Skottene ◽  
Ann M. Tarrant ◽  
Dag Altin ◽  
Rolf Erik Olsen ◽  
Marvin Choquet ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Predation Risk ◽  
Food Availability ◽  
Lipid Accumulation ◽  
Developmental Stages ◽  
Life Stage ◽  
Calanus Finmarchicus ◽  
Expression Of Genes ◽  
Food Conditions ◽  
Lipid Stores

AbstractLate developmental stages of the marine copepods in the genus Calanus can spend extended periods in a dormant stage (diapause) that is preceded by the accumulation of large lipid stores. We assessed how lipid metabolism during development from the C4 stage to adult is altered in response to predation risk and varying food availability, to ultimately understand more of the metabolic processes during development in Calanus copepods. We used RNA sequencing to assess if perceived predation risk in combination with varied food availability affects expression of genes associated with lipid metabolism and diapause preparation in C. finmarchicus. The lipid metabolism response to predation risk differed depending on food availability, time and life stage. Predation risk caused upregulation of lipid catabolism with high food, and downregulation with low food. Under low food conditions, predation risk disrupted lipid accumulation. The copepods showed no clear signs of diapause preparation, supporting earlier observations of the importance of multiple environmental cues in inducing diapause in C. finmarchicus. This study demonstrates that lipid metabolism is a sensitive endpoint for the interacting environmental effects of predation pressure and food availability. As diapause may be controlled by lipid accumulation, our findings may contribute towards understanding processes that can ultimately influence diapause timing.

Conjugated Linoleic Acid (t-10, c-12) Reduces Fatty Acid Synthesis de Novo, but not Expression of Genes for Lipid Metabolism in Bovine Adipose Tissue ex Vivo

Lipids ◽  
2013 ◽  
Vol 49 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Seong Ho Choi ◽  
David T. Silvey ◽  
Bradley J. Johnson ◽  
Matthew E. Doumit ◽  
Ki Yong Chung ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Linoleic Acid ◽  
Conjugated Linoleic Acid ◽  
Fatty Acid Synthesis ◽  
De Novo ◽  
Ex Vivo ◽  
Acid Synthesis ◽  
Expression Of Genes

scholarly journals High-Fructose Diet-Induced Metabolic Disorders Were Counteracted by the Intake of Fruit and Leaves of Sweet Cherry in Wistar Rats

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2638 ◽  
Author(s):  
Dziadek ◽  
Kopeć ◽  
Piątkowska ◽  
Leszczyńska
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Fatty Acid Synthesis ◽  
Wistar Rats ◽  
Sweet Cherry ◽  
Acid Synthesis ◽  
High Fructose Diet ◽  
Expression Of Genes ◽  
High Fructose ◽  
Freeze Dried

Numerous studies have indicated that the use of plants rich in bioactive compounds may reduce the risk of non-communicable diseases. The aim of this study was to investigate how the addition of fruit and leaves to high-fructose diet affects lipid metabolism, including the expression of genes involved in fatty acid synthesis and oxidation in the liver and adipose tissue, as well as oxidative stress and inflammation in Wistar rats. The animals were fed with AIN-93G diet, high fructose (HFr) diet, HFr diet with addition of 5% or 10% freeze-dried fruits, and HFr diet with addition of 1% or 3% freeze-dried leaves. The experiment lasted 12 weeks. The results showed that the intake of fruit and leaves of sweet cherry caused the improvement of the liver function, as well as beneficially affected lipid metabolism, among others, by regulating the expression of genes associated with fatty acid synthesis and β-oxidation. Additionally, they exhibited antioxidant and anti-inflammatory properties. In conclusion, the addition of fruit and leaves reduced the adverse changes arising from the consumption of high fructose diet. Therefore, not only commonly consumed fruits, but also leaves can be potentially used as functional foods. These findings may be helpful in prevention and treatment of the obesity-related metabolic diseases, especially cardiovascular diseases.

scholarly journals Dynamic characteristics of lipid metabolism in cultured granulosa cells from geese follicles at different developmental stages

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Shanyan Gao ◽  
Xiang Gan ◽  
Hua He ◽  
Shenqiang Hu ◽  
Yan Deng ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Granulosa Cells ◽  
Dynamic Characteristics ◽  
Developmental Stages ◽  
Lipid Synthesis ◽  
Follicular Development ◽  
Vital Role ◽  
Intracellular Lipids ◽  
Expression Of Genes

Abstract Previous studies have shown that lipid metabolism in granulosa cells (GCs) plays a vital role during mammalian ovarian follicular development. However, little research has been done on lipid metabolism in avian follicular GCs. The goal of the present study was to investigate the dynamic characteristics of lipid metabolism in GCs from geese pre-hierarchical (6–10 mm) and hierarchical (F4-F2 and F1) follicles during a 6-day period of in vitro culture. Oil red O staining showed that with the increasing incubation time, the amount of lipids accumulated in three cohorts of GCs increased gradually, reached the maxima after 96 h of culture, and then decreased. Moreover, the lipid content varied among these three cohorts, with the highest in F1 GCs. The qPCR results showed genes related to lipid synthesis and oxidation were highest expressed in pre-hierarchical GCs, while those related to lipid transport and deposition were highest expressed in hierarchical GCs. These results suggested that the amount of intracellular lipids in GCs increases with both the follicular diameter and culture time, which is accompanied by significant changes in expression of genes related to lipid metabolism. Therefore, it is postulated that the lipid accumulation capacity of geese GCs depends on the stage of follicle development and is finely regulated by the differential expression of genes related to lipid metabolism.

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