Pre(peri)-natal ω-3 PUFA deficiency-induced hypertension and its broader implications

Das, Undurti N.

doi:10.1038/hr.2011.225

Cited by 9 publications

(7 citation statements)

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“…Dietary saturated fat can adversely influence BP levels by increasing oxidative stress and decreasing nitric oxide (NO) production within the endothelium [ 30 ]. Alterations in the metabolism of PUFAs might be a predisposing factor to the development of essential hypertension [ 31 – 33 ]. A case-control study of plasma phospholipids FA profile analysis revealed that higher 16:0, 18:0, 18:3n-6 and lower 18:2n-6 were found in hypertensive patients compared to normal controls [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Exploratory serum fatty acid patterns associated with blood pressure in community-dwelling middle-aged and elderly Chinese

et al. 2016

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BackgroundEpidemiological studies have assessed relationships between circulating levels of fatty acid (FA) and blood pressure (BP), and their results remain controversial. Nevertheless, data are sparse on serum FA as biomarker and BP in China. The aim of the study was to investigate the association between serum FA and BP in Chinese populations.MethodsWe conducted a cross-sectional study nested within a community-based cohort of 2447 Chinese participants aged 35–79 years who completed a baseline assessment between October 2012 and April 2013. Baseline assessment included the collection of fasting blood samples, anthropometric measurements and a personal interview using a validated questionnaire. Serum FA was determined by gas-liquid chromatography. Exploratory factor analyses were employed to identify FA-factor as a reflection of serum FA pattern. A multiple regression model was conducted to estimate adjusted mean of BP with 95 % confidence interval (CI) by tertile groups of the generated FA-factor scores.ResultsHypertensive patients have significantly higher serum 14:0, 16:0, 16:1n-7, 18:3n-6, 20:3n-6 and Δ6-desaturase index (18:3n-6/18:2n-6) as well as lower 18:2n-6, 22:6n-3 and Δ5-desaturase index (20:4n-6/20:3n-6) compared with normotensive participants. Factor 1 (low linoleic acid/high saturated FA pattern: 14:0, 16:0, 16:1n-7, 18:2n-6, 18:3n-6, 20:3n-6) and Factor 2 (n-3 PUFA pattern: 20:5n-3, 22:5n-3, 22:6n-3, 18:1n-9) were identified as indicators of the serum FA pattern. After adjustment for age, gender, body mass index, hypertension treatment, smoking, alcohol intake, education, profession, exercise habit, salt intake, family history of hypertension, heart rate, blood lipids and fasting blood-glucose levels, per a standard deviation (SD) increment of Factor 1 scores was associated with an increment of 2.44 (95 % CI: 1.73, 3.15) mm Hg for systolic BP, whereas per a SD increment of Factor 2 scores was associated with a reduction of 1.40 (95 % CI: 0.80, 2.04) mm Hg for diastolic BP.ConclusionsThe serum FA pattern characterized by low proportions of 14:0, 16:0, 16:1n-7 and 18:3n-6 as well as high 18:2n-6 and 22:6n-3 was beneficially associated with BP levels in this Chinese population. This evidence well supports the current dietary recommendations in the communities to replace saturated fat with polyunsaturated fat.Electronic supplementary materialThe online version of this article (doi:10.1186/s12944-016-0226-3) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Exploratory serum fatty acid patterns associated with blood pressure in community-dwelling middle-aged and elderly Chinese

et al. 2016

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“…It is suggested that in conditions such as hypertension, schizophrenia, depression, Alzheimer's disease and Huntington's disease, PUFAs, LXs, Rvs, protectins and MaRs may act not only on peripheral tissues, but also on specific areas of the brain, such as the hypothalamus. For instance, hyper tension could be due to enhanced production of free radicals and lipid peroxides, and generation of NO and content of PUFAs in the vascular tissue (particularly endothelial cells), leukocytes, the kidney and the hypothalamus, and other areas of the brain, may be reduced [124,[144][145][146][147][148][149][150][151][152]. It is possible, but not yet proven, that the content of PUFAs in the cell membrane of the specific cells concerned with these diseases may be altered, such that the membrane fluidity that determines the number of receptors for various growth factors, neurotransmitters, insulin, angiotensin-II and other factors is abnormal, leading to the initiation and progression of the respective diseases.…”

Section: Pufas Lxs Rvs Mars and Nitrolipids In Other Diseasesmentioning

confidence: 99%

“…Similar to their beneficial action in STZ-induced Type 1 DM and diet-induced Type 2 DM, LXs, Rvs, protectins and nitrolipids are likely to be useful in the prevention and management of other inflammatory conditions, such as lupus, rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, diabetic retinopathy and age-related macular degeneration [37,124,135,[140][141][142][143][144][145][146][147][148][149][150][151][152]. It is likely that all diseases in which low-grade systemic inflammation play a significant role, such as obesity, nonalcoholic fatty liver disease, hypertension, atherosclerosis, hyperlipidemia, CHD, depression, schizophrenia, Alzheimer's disease, aging, osteoporosis, Huntington's disease, polycystic ovarian syndrome, dermatitis, psoriasis, glomerulonephritis of different etiologies, scleroderma and other collagen vascular diseases may be due to deficiency of cyto protective LXs, Rvs, protectins, MaRs and nitrolipids [37,124,136,[141][142][143][144][145][146][147][148][149][150][151][152].…”

Section: Pufas Lxs Rvs Mars and Nitrolipids In Other Diseasesmentioning

confidence: 99%

“…It is likely that all diseases in which low-grade systemic inflammation play a significant role, such as obesity, nonalcoholic fatty liver disease, hypertension, atherosclerosis, hyperlipidemia, CHD, depression, schizophrenia, Alzheimer's disease, aging, osteoporosis, Huntington's disease, polycystic ovarian syndrome, dermatitis, psoriasis, glomerulonephritis of different etiologies, scleroderma and other collagen vascular diseases may be due to deficiency of cyto protective LXs, Rvs, protectins, MaRs and nitrolipids [37,124,136,[141][142][143][144][145][146][147][148][149][150][151][152]. It is suggested that in conditions such as hypertension, schizophrenia, depression, Alzheimer's disease and Huntington's disease, PUFAs, LXs, Rvs, protectins and MaRs may act not only on peripheral tissues, but also on specific areas of the brain, such as the hypothalamus.…”

Section: Pufas Lxs Rvs Mars and Nitrolipids In Other Diseasesmentioning

confidence: 99%

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Lipoxins, resolvins, protectins, maresins and nitrolipids, and their clinical implications with specific reference to diabetes mellitus and other diseases: part II

Das¹

2013

Clinical Lipidology

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“…Previously, we showed that PUFAs and their metabolites play a critical role in the pathobiology of hypertension, pre-eclampsia, type 2 diabetes mellitus and metabolic syndrome [14,17,18,[22][23][24][25][26][27][28][29][30][31][32][33][34] . We, previously showed that AA prevents chemical-induced type 1 and type 2 diabetes, partly, due to its conversion to anti-inflammatory LXA4, [17,18] implying that the precursor PUFAs need to be converted to their specific anti-inflammatory metabolites to produce their beneficial actions.…”

Section: Interaction(s) Among Ang-ii Cytokines Ros and Pufas And Thmentioning

confidence: 99%

Is aortic aneurysm preventable?

Das¹

2017

Journal of Translational Internal Medicine

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Abdominal aortic aneurysm (AAA) is a chronic inflammatory condition, triggered by the local accumulation of macrophages, oxidative stress and damage to the aortic wall. Pro-inflammatory eicosanoids seem to play a significant role in AAA. The pro-inflammatory events seen in AAA could be due to a deficiency of anti-inflammatory eicosanoids such as lipoxin A4 (LXA4), resolvins, protectins and maresins as a result of reduced tissue concentrations of their precursors: arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Thus, an imbalance between pro- and anti-inflammatory eicosanoids may underlie AAA. Angiotensin-II (Ang-II), a pro-inflammatory molecule, seems to have a role in AAA. I propose that AAA is due to the local (abdominal aortic wall) deficiency of AA and other PUFAs and their anti-inflammatory metabolites especially LXA4. The beneficial action of EPA and DHA reported in the animal experimental models of AAA induced by Ang-II infusion can be attributed to their (EPA and DHA) ability to enhance the formation of not only resolvins, protectins and maresins but also LXA4. It is likely that abdominal aortic tissue (endothelial cells, smooth muscle cells and other cells) may be deficient in AA, EPA and DHA, and have defective activity of 5-, 12-, and 15-lipoxygenases and cyclooxygenase, especially COX-2 resulting in decreased formation of LXA4, resolvins, protectins and maresins. Thus, methods designed to enhance the formation of LXA4 and other anti-inflammatory eicosanoids may form a new approach to prevent and manage AAA.

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Pre(peri)-natal ω-3 PUFA deficiency-induced hypertension and its broader implications

Cited by 9 publications

References 41 publications

Exploratory serum fatty acid patterns associated with blood pressure in community-dwelling middle-aged and elderly Chinese

Exploratory serum fatty acid patterns associated with blood pressure in community-dwelling middle-aged and elderly Chinese

Lipoxins, resolvins, protectins, maresins and nitrolipids, and their clinical implications with specific reference to diabetes mellitus and other diseases: part II

Is aortic aneurysm preventable?

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