Changes in Fatty Acid Dietary Profile Affect the Brain–Gut Axis Functions of Healthy Young Adult Rats in a Sex-Dependent Manner

Dietary modifications, including those affecting dietary fat and its fatty acid (FA) composition, may be involved in the development of brain–gut axis disorders, with different manifestations in males and females. Our aim was to evaluate the impact of three purified diets with different FA composition on the brain–gut axis in rats of both sexes. Male and female Wistar rats fed a cereal-based standard diet from weaning were used. At young adult age (2–3 months old), animals were divided into three groups and treated each with a different refined diet for 6 weeks: a control group fed on AIN-93G diet containing 7% soy oil (SOY), and two groups fed on AIN-93G modified diets with 3.5% soy oil replaced by 3.5% coconut oil (COCO) or 3.5% evening primrose oil (EP). Different brain–gut axis parameters were evaluated during 4–6 weeks of dietary intervention. Compared with SOY diet (14% saturated FAs, and 58% polyunsaturated FAs), COCO diet (52.2% saturated FAs and 30% polyunsaturated FAs) produced no changes in brain functions and minor gastrointestinal modifications, whereas EP diet (11.1% saturated FAs and 70.56% polyunsaturated FAs) tended to decrease self-care behavior and colonic propulsion in males, and significantly increased exploratory behavior, accelerated gastrointestinal transit, and decreased cecum and fecal pellet density in females. Changes in FA composition, particularly an increase in ω-6 polyunsaturated FAs, seem to facilitate the development of brain–gut axis alterations in a sex-dependent manner, with a relatively higher risk in females.

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Effects of full-time v. part-time grazing on seasonal changes in milk coagulation properties and fatty acid composition

Journal of Dairy Research ◽

10.1017/s0022029921000169 ◽

2021 ◽

pp. 1-6

Author(s):

Franziska S. Akert ◽

Michael Kreuzer ◽

Carmen Kunz ◽

Beat Reidy ◽

Joel Berard

Keyword(s):

Fatty Acid ◽

Seasonal Variations ◽

Milk Fat ◽

Seasonal Effects ◽

Full Time ◽

Fa Composition ◽

Part Time ◽

Milk Coagulation ◽

The Impact ◽

Feeding Systems

Abstract For this research communication our objective was to investigate to what extent milk coagulation properties and milk fatty acid (FA) composition were affected by different feeding systems, season and their interaction. Eighteen cows in total were subjected to one of three different feeding system treatments: full-time grazing or part-time grazing combined with indoor feeding of fresh grass with low or high concentrate supplementation. Milk was sampled in spring, summer and autumn. Milk coagulation time was 15.0, 19.0 and 17.7 min, coagulation dynamics 1.67, 3.41 and 1.79 min, and curd firmness 52.7, 32.4 and 47.0 mm in spring, summer and autumn, respectively. Thus, milk coagulation properties of the milk were lower during summer. There were strong seasonal effects on milk FA proportions, but there were not always changes with progressing season, or changes were different with respect to the impact of the feeding systems (system × season interaction). The milk fat was favourably rich in oleic acid, conjugated linoleic acid and α-linolenic acid and had a low n-6/n-3 fatty acid ratio in all systems. Factors like seasonal variations in grass composition and the energy balance of the cows were considered relevant for the milk FA composition. Overall, seasonal variations in milk quality were less pronounced with part-time grazing with fresh grass indoors as compared to full-time grazing without concentrate.

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Effect of almond consumption on the serum fatty acid profile: a dose–response study

British Journal Of Nutrition ◽

10.1017/s0007114514001640 ◽

2014 ◽

Vol 112 (7) ◽

pp. 1137-1146 ◽

Cited By ~ 19

Author(s):

Stephanie Nishi ◽

Cyril W. C. Kendall ◽

Ana-Maria Gascoyne ◽

Richard P. Bazinet ◽

Balachandran Bashyam ◽

...

Keyword(s):

Fatty Acid ◽

Risk Score ◽

Percentage Change ◽

Control Group ◽

Dependent Manner ◽

Serum Fatty Acid ◽

Full Dose ◽

Fa Composition ◽

Chd Risk ◽

Half Dose

Consumption of almonds has been shown to be associated with a decreased risk of CHD, which may be related to their fatty acid (FA) composition. However, the effect of almond consumption on the serum FA composition is not known. Therefore, in the present study, we investigated whether almond consumption would alter the serum FA profile and risk of CHD, as calculated using Framingham's 10-year risk score, in a dose-dependent manner in hyperlipidaemic individuals when compared with a higher-carbohydrate control group using dietary interventions incorporating almonds. A total of twenty-seven hyperlipidaemic individuals consumed three isoenergetic (mean 1770 kJ/d) supplements during three 1-month dietary phases: (1) full-dose almonds (50–100 g/d); (2) half-dose almonds with half-dose muffins; (3) full-dose muffins. Fasting blood samples were obtained at weeks 0 and 4 for the determination of FA concentrations. Almond intake (g/d) was found to be inversely associated with the estimated Framingham 10-year CHD risk score (P= 0·026). In both the half-dose and full-dose almond groups, the proportions of oleic acid (OA) and MUFA in the TAG fraction (half-almond: OA P= 0·003; MUFA P= 0·004; full-almond: OA P< 0·001; MUFA P< 0·001) and in the NEFA fraction (half-almond: OA P= 0·01; MUFA P= 0·04; full-almond: OA P= 0·12; MUFA P= 0·06) increased. The estimated Framingham 10-year CHD risk score was inversely associated with the percentage change of OA (P= 0·011) and MUFA (P= 0·016) content in the TAG fraction. The proportions of MUFA in the TAG and NEFA fractions were positively associated with changes in HDL-cholesterol concentrations. Similarly, the estimated Framingham 10-year CHD risk score was inversely associated with the percentage change of OA (P= 0·069) and MUFA content in the NEFA fraction (P= 0·009). In conclusion, the results of the present study indicate that almond consumption increases OA and MUFA content in serum TAG and NEFA fractions, which are inversely associated with CHD lipid risk factors and overall estimated 10-year CHD risk.

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NG2 glia regulate brain innate immunity via TGF-β2/TGFBR2 axis

BMC Medicine ◽

10.1186/s12916-019-1439-x ◽

2019 ◽

Vol 17 (1) ◽

Cited By ~ 6

Author(s):

Shu-zhen Zhang ◽

Qin-qin Wang ◽

Qiao-qiao Yang ◽

Huan-yu Gu ◽

Yan-qing Yin ◽

...

Keyword(s):

Innate Immunity ◽

Diphtheria Toxin ◽

Transforming Growth Factor ◽

Critical Role ◽

Normal Brain ◽

Sequencing Analysis ◽

Brain Functions ◽

Lps Challenge ◽

The Impact ◽

The Brain

Abstract Background Brain innate immunity is vital for maintaining normal brain functions. Immune homeostatic imbalances play pivotal roles in the pathogenesis of neurological diseases including Parkinson’s disease (PD). However, the molecular and cellular mechanisms underlying the regulation of brain innate immunity and their significance in PD pathogenesis are still largely unknown. Methods Cre-inducible diphtheria toxin receptor (iDTR) and diphtheria toxin-mediated cell ablation was performed to investigate the impact of neuron-glial antigen 2 (NG2) glia on the brain innate immunity. RNA sequencing analysis was carried out to identify differentially expressed genes in mouse brain with ablated NG2 glia and lipopolysaccharide (LPS) challenge. Neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice were used to evaluate neuroinflammatory response in the presence or absence of NG2 glia. The survival of dopaminergic neurons or glial cell activation was evaluated by immunohistochemistry. Co-cultures of NG2 glia and microglia were used to examine the influence of NG2 glia to microglial activation. Results We show that NG2 glia are required for the maintenance of immune homeostasis in the brain via transforming growth factor-β2 (TGF-β2)-TGF-β type II receptor (TGFBR2)-CX3C chemokine receptor 1 (CX3CR1) signaling, which suppresses the activation of microglia. We demonstrate that mice with ablated NG2 glia display a profound downregulation of the expression of microglia-specific signature genes and remarkable inflammatory response in the brain following exposure to endotoxin lipopolysaccharides. Gain- or loss-of-function studies show that NG2 glia-derived TGF-β2 and its receptor TGFBR2 in microglia are key regulators of the CX3CR1-modulated immune response. Furthermore, deficiency of NG2 glia contributes to neuroinflammation and nigral dopaminergic neuron loss in MPTP-induced mouse PD model. Conclusions These findings suggest that NG2 glia play a critical role in modulation of neuroinflammation and provide a compelling rationale for the development of new therapeutics for neurological disorders.

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Regulatory Roles of Bone in Neurodegenerative Diseases

Frontiers in Aging Neuroscience ◽

10.3389/fnagi.2020.610581 ◽

2020 ◽

Vol 12 ◽

Author(s):

Zhengran Yu ◽

Zemin Ling ◽

Lin Lu ◽

Jin Zhao ◽

Xiang Chen ◽

...

Keyword(s):

Stem Cells ◽

Neurodegenerative Diseases ◽

The Elderly ◽

Lymphoid Organ ◽

The Body ◽

Hematopoietic Stem ◽

Brain Functions ◽

And Function ◽

The Impact ◽

The Brain

Osteoporosis and neurodegenerative diseases are two kinds of common disorders of the elderly, which often co-occur. Previous studies have shown the skeletal and central nervous systems are closely related to pathophysiology. As the main structural scaffold of the body, the bone is also a reservoir for stem cells, a primary lymphoid organ, and an important endocrine organ. It can interact with the brain through various bone-derived cells, mostly the mesenchymal and hematopoietic stem cells (HSCs). The bone marrow is also a place for generating immune cells, which could greatly influence brain functions. Finally, the proteins secreted by bones (osteokines) also play important roles in the growth and function of the brain. This article reviews the latest research studying the impact of bone-derived cells, bone-controlled immune system, and bone-secreted proteins on the brain, and evaluates how these factors are implicated in the progress of neurodegenerative diseases and their potential use in the diagnosis and treatment of these diseases.

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Chemerin-induced macrophages pyroptosis in fetal brain tissue leads to cognitive disorder in offspring of diabetic dams

Journal of Neuroinflammation ◽

10.1186/s12974-019-1573-6 ◽

2019 ◽

Vol 16 (1) ◽

Cited By ~ 1

Author(s):

Zhaoxia Liang ◽

Luyang Han ◽

Dianjianyi Sun ◽

Yanmin Chen ◽

Qi Wu ◽

...

Keyword(s):

Cognitive Impairment ◽

Brain Tissue ◽

Abdominal Cavity ◽

Behavioral Changes ◽

Dependent Manner ◽

Diabetes In Pregnancy ◽

The Impact ◽

The Brain ◽

In Pregnancy ◽

Brain Tissues

Abstract Background Chemerin is highly expressed in the serum, placenta tissue, and umbilical cord blood of diabetic mother; however, the impact of chemerin on cognitive disorders of offspring from mothers with diabetes in pregnancy remains unclear. Methods A diabetic phenotype in pregnant mice dams was induced by streptozocin (STZ) injection or intraperitoneal injection of chemerin. Behavioral changes in offspring of diabetic dams and nondiabetic controls were assessed, and changes in chemerin, two receptors of chemerin [chemerin receptor 23 (ChemR23) and chemokine (C-C motif) receptor-like 2 (CCRL2)], macrophages, and neurons in the brain tissue were studied to reveal the underlying mechanism of the behavioral changes. Results Chemerin treatment mimicked the STZ-induced symptom of maternal diabetes in mice along with the altered behavior of offspring in the open field test (OFT) assay. In the exploring process for potential mechanism, the brain tissues of offspring from chemerin-treated dams were observed with an increase level of macrophage infiltration and a decrease number of neuron cells. Moreover, an increased level of NOD-like receptor family pyrin domain containing 3 (NLRP3) and apoptosis-associated speck-like (Asc) protein as well as pyroptosis [characterized by increased active caspase-1 content and secretion of cytokines such as interleukin (IL) 1 beta (IL-1β) and IL-18] more activated in macrophages is also observed in the brain of these diabetic dam’s offspring, in the presence of ChemR23. In vitro, it was found that pyroptosis activation was increased in macrophages separated from the abdominal cavity of normal mice, after chemerin treatment. However, depletion of CCRL2 decreased the level of chemerin in the brain tissues of diabetic dams’ offspring; depletion of ChemR23 decreased macrophage pyroptosis, and depletion of either receptor reversed chemerin-mediated neurodevelopmental deficits and cognitive impairment of offspring of diabetic pregnant dams. Conclusions Chemerin induced diabetic pregnant disease and CCRL2 were required to enrich chemerin in the brain of offspring. Aggregation of chemerin could lead to macrophage recruitment, activation of pyroptosis, the release of inflammatory cytokines, a decrease in the number of neurons, and cognitive impairment in offspring in a ChemR23-dependent manner. Targeting CCRL2 and/or ChemR23 could be useful for treating neuropsychological deficits in offspring of dams with diabetes in pregnancy.

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The Role of Dietary Antioxidants in the Pathogenesis of Neurodegenerative Diseases and Their Impact on Cerebral Oxidoreductive Balance

Nutrients ◽

10.3390/nu12020435 ◽

2020 ◽

Vol 12 (2) ◽

pp. 435 ◽

Cited By ~ 4

Author(s):

Anna Winiarska-Mieczan ◽

Ewa Baranowska-Wójcik ◽

Małgorzata Kwiecień ◽

Eugeniusz R. Grela ◽

Dominik Szwajgier ◽

...

Keyword(s):

Neurodegenerative Diseases ◽

Negative Impact ◽

Functional Disorders ◽

Brain Functions ◽

Diet Supplements ◽

The Impact ◽

The Brain ◽

All Diseases

Neurodegenerative diseases are progressive diseases of the nervous system that lead to neuron loss or functional disorders. Neurodegenerative diseases require long-term, sometimes life-long pharmacological treatment, which increases the risk of adverse effects and a negative impact of pharmaceuticals on the patients’ general condition. One of the main problems related to the treatment of this type of condition is the limited ability to deliver drugs to the brain due to their poor solubility, low bioavailability, and the effects of the blood-brain barrier. Given the above, one of the main objectives of contemporary scientific research focuses on the prevention of neurodegenerative diseases. As disorders related to the competence of the antioxidative system are a marker in all diseases of this type, the primary prophylactics should entail the use of exogenous antioxidants, particularly ones that can be used over extended periods, regardless of the patient’s age, and that are easily available, e.g., as part of a diet or as diet supplements. The paper analyzes the significance of the oxidoreductive balance in the pathogenesis of neurodegenerative diseases. Based on information published globally in the last 10 years, an analysis is also provided with regard to the impact of exogenous antioxidants on brain functions with respect to the prevention of this type of diseases.

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Brain Physiology and Pathophysiology in Mental Stress

ISRN Physiology ◽

10.1155/2013/806104 ◽

2013 ◽

Vol 2013 ◽

pp. 1-23 ◽

Cited By ~ 14

Author(s):

Karim Alkadhi

Keyword(s):

Signal Transduction ◽

Learning And Memory ◽

Mental Stress ◽

Negative Effects ◽

Functional Changes ◽

Brain Physiology ◽

Brain Functions ◽

Brain Structure And Function ◽

The Impact ◽

The Brain

Exposure to various forms of stress is a common daily occurrence in the lives of most individuals, with both positive and negative effects on brain function. The impact of stress is strongly influenced by the type and duration of the stressor. In its acute form, stress may be a necessary adaptive mechanism for survival and with only transient changes within the brain. However, severe and/or prolonged stress causes overactivation and dysregulation of the hypothalamic pituitary adrenal (HPA) axis thus inflicting detrimental changes in the brain structure and function. Therefore, chronic stress is often considered a negative modulator of the cognitive functions including the learning and memory processes. Exposure to long-lasting stress diminishes health and increases vulnerability to mental disorders. In addition, stress exacerbates functional changes associated with various brain disorders including Alzheimer’s disease and Parkinson’s disease. The primary purpose of this paper is to provide an overview for neuroscientists who are seeking a concise account of the effects of stress on learning and memory and associated signal transduction mechanisms. This review discusses chronic mental stress and its detrimental effects on various aspects of brain functions including learning and memory, synaptic plasticity, and cognition-related signaling enabled via key signal transduction molecules.

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Current Paradigms to Explore the Gut Microbiota Linkage to Neurological Disorders

EMJ Neurology ◽

10.33590/emjneurol/20-00068 ◽

2020 ◽

pp. 68-79

Author(s):

Varruchi Sharma ◽

Atul Sankhyan ◽

Anshika Varshney ◽

Renuka Choudhary ◽

Anil K. Sharma

Keyword(s):

Gut Microbiota ◽

Neurological Disorders ◽

Brain Function ◽

Intervention Strategy ◽

Neurological Complications ◽

Communication Link ◽

Brain Functions ◽

Current Review ◽

The Impact ◽

The Brain

It has been suggested that an intricate communication link exists between the gut microbiota and the brain and its ability to modulate behaviour of an individual governing homeostasis. Metabolic activity of the microbiota is considered to be relatively constant in healthy individuals, despite differences in the composition of microbiota. The metabolites produced by gut microbiota and their homeostatic balance is often perturbed as a result of neurological complications. Therefore, it is of paramount importance to explore the link between gut microbiota and brain function and behaviour through neural, endocrine, and immune pathways. This current review focusses on the impact of altered gut microbiota on brain functions and how microbiome modulation by use of probiotics, prebiotics, and synbiotics might prove beneficial in the prevention and/or treatment of neurological disorders. It is important to carefully understand the complex mechanisms underlying the gut–brain axis so as to use the gut microbiota as a therapeutic intervention strategy for neurological disorders.

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Use of Active Salmon-Lecithin Nanoliposomes to Increase Polyunsaturated Fatty Acid Bioavailability in Cortical Neurons and Mice

International Journal of Molecular Sciences ◽

10.3390/ijms222111859 ◽

2021 ◽

Vol 22 (21) ◽

pp. 11859

Author(s):

Elodie Passeri ◽

Kamil Elkhoury ◽

Maria Camila Jiménez Garavito ◽

Frédéric Desor ◽

Marion Huguet ◽

...

Keyword(s):

Fatty Acid ◽

Docosahexaenoic Acid ◽

Cortical Neurons ◽

Particle Surface ◽

Standard Diet ◽

Omega 3 ◽

Rat Embryo ◽

Negative Particle ◽

Age Related ◽

The Brain

Omega-3 polyunsaturated fatty acids (n-3 PUFAs) play an important role in the development, maintenance, and function of the brain. Dietary supplementation of n-3 PUFAs in neurological diseases has been a subject of particular interest in preventing cognitive deficits, and particularly in age-related neurodegeneration. Developing strategies for the efficient delivery of these lipids to the brain has presented a challenge in recent years. We recently reported the preparation of n-3 PUFA-rich nanoliposomes (NLs) from salmon lecithin, and demonstrated their neurotrophic effects in rat embryo cortical neurons. The objective of this study was to assess the ability of these NLs to deliver PUFAs in cellulo and in vivo (in mice). NLs were prepared using salmon lecithin rich in n-3 PUFAs (29.13%), and characterized with an average size of 107.90 ± 0.35 nm, a polydispersity index of 0.25 ± 0.01, and a negative particle-surface electrical charge (−50.4 ± 0.2 mV). Incubation of rat embryo cortical neurons with NLs led to a significant increase in docosahexaenoic acid (DHA) (51.5%, p < 0.01), as well as palmitic acid, and a small decrease in oleic acid after 72 h (12.2%, p < 0.05). Twenty mice on a standard diet received oral administration of NLs (12 mg/mouse/day; 5 days per week) for 8 weeks. Fatty acid profiles obtained via gas chromatography revealed significant increases in cortical levels of saturated, monounsaturated, and n-3 (docosahexaenoic acid,) and n-6 (docosapentaenoic acid and arachidonic acid) PUFAs. This was not the case for the hippocampus or in the liver. There were no effects on plasma lipid levels, and daily monitoring confirmed NL biocompatibility. These results demonstrate that NLs can be used for delivery of PUFAs to the brain. This study opens new research possibilities in the development of preventive as well as therapeutic strategies for age-related neurodegeneration.

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Impact of temperature on the expression of Kennedy Pathway genes in developing soybean seeds

Canadian Journal of Plant Science ◽

10.4141/cjps-2014-261 ◽

2015 ◽

Vol 95 (1) ◽

pp. 87-101 ◽

Cited By ~ 2

Author(s):

Amy J. M. McNaughton ◽

Barry J. Shelp ◽

Istvan Rajcan

Keyword(s):

Fatty Acid Composition ◽

Fatty Acid ◽

Acid Composition ◽

Quantitative Polymerase Chain Reaction ◽

Soybean Seeds ◽

Dependent Manner ◽

Oil Storage ◽

Kennedy Pathway ◽

Soybean Genotypes ◽

The Impact

McNaughton, A. J. M., Shelp, B. J. and Rajcan, I. 2015. Impact of temperature on the expression of Kennedy Pathway genes in developing soybean seeds. Can. J. Plant Sci. 95: 87–101. The main oil storage molecule, triacylglycerol (TAG), can be created by the Kennedy Pathway. The objective of this study was to determine the impact of growing temperature on the expression of the Kennedy Pathway genes, glycerol-3-phosphate acyltransferase (G3PAT), lysophosphatidic acid acyltransferase (LPAAT), and diacylglycerol acyltransferase 1 (DGAT1), in developing seed of four soybean genotypes with altered fatty acid composition using quantitative polymerase chain reaction. The three growing temperatures were: high, 30°C day/25°C night; normal, 25°C day/20°C night; and low, 20°C day/15°C night. The expression of G3PAT steadily declined following 15 d after flowering (DAF), suggesting that it is likely to be more highly expressed earlier in development than was measured in the study. As a result, the expression of G3PAT did not correspond to fatty acid accumulation. LPAAT expression coincided with accumulation of oleic acid (18:1∆9) and linolenic acid (18:3∆9,12,15) in a temperature-dependent manner. The expression of DGAT1 corresponded to accumulation of linoleic acid (18:2∆9,12), which varied among the soybean genotypes, indicating a genotypic effect on the expression of DGAT1. This study suggests that the expression of the acyltransferase enzymes of the Kennedy Pathway influences the fatty acid composition in seed of four altered fatty acid soybean genotypes.

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