scholarly journals Diet Regulation of Long-Chain PUFA Synthesis: Role of Macronutrients, Micronutrients, and Polyphenols on Δ-5/Δ-6 Desaturases and Elongases 2/5

2020 ◽  
Author(s):  
Melissa Gonzalez-Soto ◽  
David M Mutch
Keyword(s):  
Dietary Fats ◽  
Mrna Levels ◽  
Micronutrient Deficiencies ◽  
Chain Pufa ◽  
Increased Risk ◽  
Marine Products ◽  
Disease Risks ◽  
Dietary Components ◽  
Long Chain

ABSTRACT Deficiencies in the n–3 (ω-3) long-chain PUFAs (LC-PUFAs) EPA and DHA are associated with increased risk for the development of numerous diseases. Although n–3 LC-PUFAs can be obtained by consuming marine products, they are also synthesized endogenously through a biochemical pathway regulated by the Δ-5/Δ-6 desaturase and elongase 2/5 enzymes. This narrative review collates evidence from the past 40 y demonstrating that mRNA expression and activity of desaturase and elongase enzymes are influenced by numerous dietary components, including macronutrients, micronutrients, and polyphenols. Specifically, we highlight that both the quantity and the composition of dietary fats, carbohydrates, and proteins can differentially regulate desaturase pathway activity. Furthermore, desaturase and elongase mRNA levels and enzyme activities are also influenced by micronutrients (folate, vitamin B-12, vitamin A), trace minerals (iron, zinc), and polyphenols (resveratrol, isoflavones). Understanding how these various dietary components influence LC-PUFA synthesis will help further advance our understanding of how dietary patterns, ranging from caloric excesses to micronutrient deficiencies, influence disease risks.

Nutritional Contributions to the CNS Pathophysiology of HIV-1 Infection and Implications for Treatment

CNS Spectrums ◽  
2000 ◽  
Vol 5 (4) ◽  
pp. 61-72 ◽  
Author(s):  
Teri T. Baldewicz ◽  
Pim Brouwers ◽  
Karl Goodkin ◽  
Adarsh M. Kumar ◽  
Mahendra Kumar
Keyword(s):  
Disease Progression ◽  
Causative Factor ◽  
Nutritional Deficiencies ◽  
Micronutrient Deficiencies ◽  
Increased Risk ◽  
Immunodeficiency Virus ◽  
Nutritional Deficits ◽  
Hiv 1

AbstractNutritional deficiencies are commonplace in patients with human immunodeficiency virus type 1 (HIV-1) infection, and recent research has indicated that nutritional factors may play an important role in the pathogenesis of HIV-1 disease. Although nutritional deficiencies are unlikely to be the primary causative factor in disease progression, they may contribute to cognitive dysfunction, neurologic abnormalities, mood disturbance, and immune dysregulation associated with HIV-1 infection. Furthermore, deficiencies of specific micronutrients have been associated with increased risk of HIV-1–associated mortality. This article will briefly summarize the role of macronutrient deficiency, the interactions of specific micronutrient deficiencies with neuropsychiatrie functioning, and the role of these factors in HIV-1 disease progression. Since recent research has shown that normalization of many nutritional deficits and supplementation beyond normal levels are associated with improvements in neuropsychiatrie functioning, potential treatment implications will also be discussed.

scholarly journals A28 CHARACTERIZING THE ROLE OF NR4A1 IN THE REGULATION OF INTESTINAL SMOOTH MUSCLE CELL PHENOTYPE AND FUNCTION

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 147-148
Author(s):  
H E Szczepanski ◽  
K L Flannigan ◽  
B Mainoli ◽  
L Alston ◽  
J Lee ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Negative Feedback ◽  
Muscle Hypertrophy ◽  
Phenotypic Switching ◽  
Cell Phenotype ◽  
Stricture Formation ◽  
Mrna Levels ◽  
Tissue Remodelling ◽  
Increased Risk

Abstract Background Intestinal fibrosis and stricture formation are common complications of Crohn’s disease (CD). Recently, smooth muscle hypertrophy/hyperplasia have gained greater recognition as a driver of stricture formation, rather than an increase in fibrosis alone. Despite advances in treatment of CD, current therapies do little to prevent or reverse strictures. NR4A1 is an orphan nuclear receptor that is anti-fibrotic in non-intestinal systems and exhibits anti-proliferative effects in smooth muscle cells (SMCs). NR4A1 gene variants have been associated with increased risk of IBD, however, mechanisms regulating NR4A1 expression and its role in intestinal SMC function have not been investigated. Aims To characterize the role of NR4A1 presence and activation in modulating intestinal SMC phenotype. Methods Primary intestinal SMCs were isolated from Nr4a1+/+and Nr4a1-/-mice. A commercially sourced human primary intestinal SMC line was also used. Mass spectrometry identified proteomic differences between Nr4a1+/+and Nr4a1-/-SMCs. To assess the role of NR4A1 in regulating SMC growth, basal and platelet-derived growth factor-BB (PDGF-BB)-induced proliferation were quantified. NR4A1 activation was induced by selective agonists, cytosporone B (Csn-B) and 6-mercaptopurine (6-MP). Cellular respirometry was used to determine metabolism in Nr4a1+/+and Nr4a1-/-SMCs. Expression of NR4A1 and phenotypic switching mediators were assessed by qPCR. Immunofluorescence was used to assess contractile markers and cell morphology. Results Proteomic analysis revealed increased expression of proteins related to the cell cycle, metabolism, and extracellular matrix synthesis in Nr4a1-/-SMCs. Nr4a1+/+SMCs upregulated proteins involved in smooth muscle contraction and was supported by higher mRNA levels of myocardin and lower Krüppel-like factor 4. Nr4a1-/-cells were more proliferative compared to Nr4a1+/+cells under basal conditions. Treating human intestinal SMCs with Csn-B attenuated proliferation induced by PDGF-BB. Similar effects were observed in Nr4a1+/+SMCs, however, the anti-proliferative effect of Csn-B was absent in Nr4a1-/-cells. Nr4a1-/-SMCs had higher maximal respiration, spare respiratory capacity, and glycolysis. NR4A1 expression was rapidly induced by Csn-B/6-MP and PDGF-BB, the latter suggesting a potential negative feedback mechanism to control mitogen-induced SMC proliferation. Conclusions Our results suggest that NR4A1 is a regulator of intestinal SMC proliferation, bioenergetics, and phenotype. Its induction by mitogens may contribute to a negative feedback loop to control smooth muscle growth. These data support targeting NR4A1 to treat excessive smooth muscle hypertrophy/hyperplasia that contributes to tissue remodelling observed in fibrostenotic CD. Funding Agencies CCC, CIHR

scholarly journals PUFA-derived endocannabinoids: an overview

2013 ◽  
Vol 72 (4) ◽  
pp. 451-459 ◽  
Author(s):  
Maria Grazia Cascio
Keyword(s):  
Cannabinoid Receptors ◽  
Endocannabinoid System ◽  
Significant Progress ◽  
Intracellular Space ◽  
Step Process ◽  
Intracellular Degradation ◽  
Chain Pufa ◽  
Pathological Conditions ◽  
Long Chain

Following on from the discovery of cannabinoid receptors, of their endogenous agonists (endocannabinoids) and of the biosynthetic and metabolic enzymes of the endocannabinoids, significant progress has been made towards the understanding of the role of the endocannabinoid system in both physiological and pathological conditions. Endocannabinoids are mainly n-6 long-chain PUFA (LCPUFA) derivatives that are synthesised by neuronal cells and inactivated via a two-step process that begins with their transport from the extracellular to the intracellular space and culminates in their intracellular degradation by hydrolysis or oxidation. Although the enzymes responsible for the biosynthesis and metabolism of endocannabinoids have been well characterised, the processes involved in their cellular uptake are still a subject of debate. Moreover, little is yet known about the roles of endocannabinoids derived from n-3 LCPUFA such as EPA and DHA. Here, I provide an overview of what is currently known about the mechanisms for the biosynthesis and inactivation of endocannabinoids, together with a brief analysis of the involvement of the endocannabinoids in both food intake and obesity. Owing to limited space, recent reviews will be often cited instead of original papers.

scholarly journals Modulation of aquaporin gene expression by n-3 long-chain PUFA lipid structures in white and brown adipose tissue from hamsters

2018 ◽  
Vol 120 (10) ◽  
pp. 1098-1106 ◽  
Author(s):  
Paula A. Lopes ◽  
Rute Martins ◽  
Inês Vieira da Silva ◽  
Marta S. Madeira ◽  
José A. M. Prates ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Differential Expression ◽  
Mrna Levels ◽  
Chain Pufa ◽  
Epa And Dha ◽  
Brown Adipose ◽  
Long Chain ◽  
Lipid Structures

AbstractEPA (20 : 5n-3) and DHA (22 : 6n-3) fatty acids have weight-reducing properties with physiological activity depending on their molecular structure – that is, as TAG or ethyl esters (EE). Aquaporins (AQP) are membrane protein channels recognised as important players in fat metabolism, but their differential expression in white adipose tissue (WAT) and brown adipose tissue (BAT), as well as their modulation by dietary n-3 long-chain PUFA (LCPUFA) such as EPA and DHA, has never been investigated. In this study, the transcriptional profiles of AQP3, AQP5, AQP7 and selected lipid markers of WAT (subcutaneous and visceral) and BAT (interscapular) from hamsters fed diets containing n-3 LCPUFA in different lipid structures such as fish oil (FO, rich in EPA and DHA in the TAG form) and FO-EE (rich in EPA and DHA in the EE form) were used and compared with linseed oil (LSO) as the reference group. A clear effect of fat depot was observed for AQP3 and leptin (LEP), with the lowest values of mRNA found in BAT relative to WAT. The opposite occurred for PPARα. AQP7 was affected by diet, with FO-fed hamsters having higher mRNA levels compared with LSO-fed hamsters. The relative gene expression of AQP5, adiponectin (ADIPO), GLUT4 and PPARγ was influenced by both fat tissue and diet. Taken together, our results revealed a differential expression profile of AQP and some markers of lipid metabolism in both WAT and BAT in response to feeding n-3 LCPUFA in two different structural formats: TAG v. EE.

Postprandial Activation of Coagulant Factor VII by Long-chain Dietary Fatty Acids

1996 ◽  
Vol 76 (03) ◽  
pp. 369-371 ◽  
Author(s):  
T A B Sanders ◽  
G J Miller ◽  
Tamara de Grassi ◽  
Najat Yahia
Keyword(s):  
Fatty Acids ◽  
Dietary Fatty Acids ◽  
Factor Vii ◽  
Fat Intake ◽  
Long Chain Fatty Acids ◽  
Postprandial Lipaemia ◽  
Increased Risk ◽  
Coagulant Activity ◽  
Long Chain Triglycerides ◽  
Long Chain

SummaryFactor VII coagulant activity (FVIIc) is associated with an increased risk of fatal ischaemic heart disease (IHD). Several reports have suggested that dietary fat intake or hypertriglyceridaemia are associated with elevated levels of FVII. This study demonstrates that an intake of long-chain fatty acids sufficient to induce postprandial lipaemia in healthy subjects leads to a substantial elevation in both FVIIc and the concentration of FVII circulating in the activated form. Such an increase in FVIIc could not be induced by medium-chain triglycerides. These results suggest that the consumption of a sufficient amount of long-chain triglycerides to induce postprandial lipaemia induces the activation of FVII.

Vitamin A: dietologist’s position

2020 ◽  
pp. 49-57
Author(s):  
S. V. Orlova ◽  
E. A. Nikitina ◽  
L. I. Karushina ◽  
Yu. A. Pigaryova ◽  
O. E. Pronina
Keyword(s):  
Immune Response ◽  
Urinary Tract ◽  
Gastrointestinal Tract ◽  
Vitamin A ◽  
Developed Countries ◽  
Therapeutic Practice ◽  
The Past ◽  
Increased Risk ◽  
Mucous Membranes

Vitamin A (retinol) is one of the key elements for regulating the immune response and controls the division and differentiation of epithelial cells of the mucous membranes of the bronchopulmonary system, gastrointestinal tract, urinary tract, eyes, etc. Its significance in the context of the COVID‑19 pandemic is difficult to overestimate. However, a number of studies conducted in the past have associated the additional intake of vitamin A with an increased risk of developing cancer, as a result of which vitamin A was practically excluded from therapeutic practice in developed countries. Our review highlights the role of vitamin A in maintaining human health and the latest data on its effect on the development mechanisms of somatic pathology.

Myocardial Noncompaction

2018 ◽  
Vol 69 (8) ◽  
pp. 2209-2212
Author(s):  
Alexandru Radu Mihailovici ◽  
Vlad Padureanu ◽  
Carmen Valeria Albu ◽  
Venera Cristina Dinescu ◽  
Mihai Cristian Pirlog ◽  
...  
Keyword(s):  
Ventricular Arrhythmias ◽  
Specific Treatment ◽  
Left Ventricular ◽  
Left Ventricular Noncompaction ◽  
Ventricular Noncompaction ◽  
Genetic Transmission ◽  
Asymptomatic Patients ◽  
Increased Risk ◽  
Patients With Heart Failure

Left ventricular noncompaction is a primary cardiomyopathy with genetic transmission in the vast majority of autosomal dominant cases. It is characterized by the presence of excessive myocardial trabecularities that generally affect the left ventricle. In diagnosing this condition, echocardiography is the gold standard, although this method involves an increased risk of overdiagnosis and underdiagnosis. There are also uncertain cases where echocardiography is inconclusive, a multimodal approach is needed, correlating echocardiographic results with those obtained by magnetic resonance imaging. The clinical picture may range from asymptomatic patients to patients with heart failure, supraventricular or ventricular arrhythmias, thromboembolic events and even sudden cardiac death. There is no specific treatment of left ventricular noncompaction, but the treatment is aimed at preventing and treating the complications of the disease. We will present the case of a young patient with left ventricular noncompactioncardiomyopathy and highlight the essential role of transthoracic echocardiography in diagnosing this rare heart disease.

Semi-Quantitative Ultrasonographic Evaluation of NAFLD

2020 ◽  
Vol 26 (32) ◽  
pp. 3915-3927 ◽  
Author(s):  
Stefano Ballestri ◽  
Claudio Tana ◽  
Maria Di Girolamo ◽  
Maria Cristina Fontana ◽  
Mariano Capitelli ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Imaging Techniques ◽  
Metabolic Complications ◽  
Nonalcoholic Fatty Liver ◽  
Non Invasive ◽  
Increased Risk ◽  
Risk Of Progression ◽  
Progressive Liver Disease

: Nonalcoholic fatty liver disease (NAFLD) embraces histopathological entities ranging from the relatively benign simple steatosis to the progressive form nonalcoholic steatohepatitis (NASH), which is associated with fibrosis and an increased risk of progression to cirrhosis and hepatocellular carcinoma. NAFLD is the most common liver disease and is associated with extrahepatic comorbidities including a major cardiovascular disease burden. : The non-invasive diagnosis of NAFLD and the identification of subjects at risk of progressive liver disease and cardio-metabolic complications are key in implementing personalized treatment schedules and follow-up strategies. : In this review, we highlight the potential role of ultrasound semiquantitative scores for detecting and assessing steatosis severity, progression of NAFLD, and cardio-metabolic risk. : Ultrasonographic scores of fatty liver severity act as sensors of cardio-metabolic health and may assist in selecting patients to submit to second-line non-invasive imaging techniques and/or liver biopsy.

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