NDLI: Metabolic syndrome: a brain disease.

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Year: 2012 Volume: 90 Issue: 12

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Year: 2012 Volume: 90 Issue: 9

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Up-regulation of myocardial connexin-43 in spontaneously hypertensive rats fed red palm oil is most likely implicated in its anti-arrhythmic effects.

Attenuation of endothelin-1-induced PKB and ERK1/2 signaling, as well as Egr-1 expression, by curcumin in A-10 vascular smooth muscle cells.

High cholesterol diet effects on ischemia-reperfusion injury of the heart.

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The ability of phosphodiesterase-5 inhibitors sildenafil and ordonafil to reverse L-NAME induced cardiac hypertrophy in the rabbit: possible role of calcineurin and p38.

Cardiorespiratory and metabolic responses associated with children's physical activity during self-paced games.

Dual influence of spontaneous hypertension on membrane properties and ATP production in heart and kidney mitochondria in rat: effect of captopril and nifedipine, adaptation and dysadaptation.

The acutely occluded left main coronary artery culprit in cardiogenic shock and initial percutaneous coronary intervention: a substudy of the Manitoba 'no option' left main PCI registry.

Metabolic syndrome: a brain disease.

Protective effects of dexrazoxane against acute ischaemia/reperfusion injury of rat hearts.

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Year: 2012 Volume: 90 Issue: 2

Year: 2012 Volume: 90 Issue: 1

Metabolic syndrome: a brain disease.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Singh, Ram B. Gupta, Siddharth Dherange, Parinita De Meester, Fabien Wilczynska, Agnieszka Alam, Shaan E. Pella, Daniel Wilson, Douglas W.
Description	Country affiliation: Poland Author Affiliation: Singh RB ( The TsimTsoum Institute, Krakow, Silesia, Poland. rbs@tsimtsoum.net)
Abstract	Recent research indicates an association between brain dysfunction and the pathogenesis of metabolic syndrome. To investigate this, we created a Medline search (up to December 2011) of articles in PubMed. The results indicated that refined carbohydrates, saturated and total fat, high levels of ω-6 fatty acids, and low levels of ω-3 fatty acids and other long chain polyunsaturated fatty acids (PUFA), all in conjunction with sedentary behaviour and mental stress can predispose to inflammation. Increased sympathetic activity, with increased secretion of catecholamine, cortisol, and serotonin can cause oxidative stress, which may damage the arcuate nucleus as well as the hypothalamus and macrophages, and the liver may release pro-inflammatory cytokines. These, in conjunction with an underlying deficiency in long chain PUFA, may damage the arcuate nucleus as well as neuropeptide-Y and pro-opiomelanocortin neurons and insulin receptors in the brain, especially during fetal life, infancy, and childhood, resulting in their dysfunction. Of the fatty acids in the brain, 30%-50% are long chain PUFA, which are incorporated in the cell membrane phospholipids. Hence, ω-3 fatty acids, which are also known to enhance parasympathetic activity and increase the secretion of anti-inflammatory cytokines interleukin (IL)-4 and IL-10 as well as acetylcholine in the hippocampus, may be protective. Therefore, treatment with ω-3 fatty acids may be applied for the prevention of metabolic syndrome.
File Format	HTM / HTML
ISSN	00084212
e-ISSN	12057541
Journal	Canadian Journal of Physiology and Pharmacology
Issue Number	9
Volume Number	90
Language	English
Publisher	Canadian Science Publishing
Publisher Date	2012-09-01
Publisher Place	Canada
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Pharmacology Brain Diseases Metabolism Metabolic Syndrome X Aging Psychology Appetite Regulation Physiology Arcuate Nucleus Of Hypothalamus Brain Drug Effects Immunology Complications Prevention & Control Cytokines Secretion Fatty Acids, Omega-3 Therapeutic Use Feeding Behavior Liver Receptor, Insulin Risk Factors
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Pharmacology

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