Dietary marine-derived long-chain monounsaturated fatty acids and cardiovascular disease risk: a mini review

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Abstract

Regular fish/fish oil consumption is widely recommended for protection against cardiovascular diseases (CVD). Fish and other marine life are rich sources of the cardioprotective long-chain n-3 polyunsaturated fatty acids (n-3 PUFA) eicosapentaenoic acid (C20:5 n-3; EPA) and docosahexaenoic acid (C22:6 n-3; DHA). The lipid content and fatty acid profile of fish, however, vary greatly among different fish species. In addition to n-3 PUFA, certain fish, such as saury, pollock, and herring, also contain high levels of long-chain monounsaturated fatty acids (LCMUFA), with aliphatic tails longer than 18 C atoms (i.e., C20:1 and C22:1 isomers). Compared with well-studied n-3 PUFA, limited information, however, is available on the health benefits of marine-derived LCMUFA, particularly in regard to CVD. Our objective in this review is to summarize the current knowledge and provide perspective on the potential therapeutic value of dietary LCMUFA-rich marine oil for improving CVD risk factors. We will also review the possible mechanisms of LCMUFA action on target tissues. Finally, we describe the epidemiologic data and small-scaled clinical studies that have been done on marine oils enriched in LCMUFA. Although there are still many unanswered questions about LCMUFA, this appears to be promising new area of research that may lead to new insights into the health benefits of a different component of fish oils besides n-3 PUFA.

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Resolution of Inflammation: What Controls Its Onset?

Michelle A. Sugimoto, Lirlândia Sousa, Vanessa Pinho … (2016)

An effective resolution program may be able to prevent the progression from non-resolving acute inflammation to persistent chronic inflammation. It has now become evident that coordinated resolution programs initiate shortly after inflammatory responses begin. In this context, several mechanisms provide the fine-tuning of inflammation and create a favorable environment for the resolution phase to take place and for homeostasis to return. In this review, we focus on the events required for an effective transition from the proinflammatory phase to the onset and establishment of resolution. We suggest that several mediators that promote the inflammatory phase of inflammation can simultaneously initiate a program for active resolution. Indeed, several events enact a decrease in the local chemokine concentration, a reduction which is essential to inhibit further infiltration of neutrophils into the tissue. Interestingly, although neutrophils are cells that characteristically participate in the active phase of inflammation, they also contribute to the onset of resolution. Further understanding of the molecular mechanisms that initiate resolution may be instrumental to develop pro-resolution strategies to treat complex chronic inflammatory diseases, in humans. The efforts to develop strategies based on resolution of inflammation have shaped a new area of pharmacology referred to as “resolution pharmacology.”

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The distinction of metabolically 'healthy' from 'unhealthy' obese individuals.

Matthias Blüher (2010)

The prevalence and severity of obesity are dramatically increasing throughout the world. Obesity causes a decline in life expectancy due to its associated metabolic and cardiovascular comorbid disorders. Therefore, it will become more important to distinguish obese individuals at high risk for obesity-related metabolic diseases from those who are metabolically 'healthy'. This review focuses on recent evidence suggesting that normal adipose tissue function contributes to the healthy obese phenotype. The majority of individuals with obesity develop insulin resistance, type 2 diabetes, dyslipidemia, gout, hypertension and cardiovascular disease. However, approximately 10-25% of obese individuals are metabolically healthy most likely due to preserved insulin sensitivity. Recent studies suggest that inflammation of visceral adipose tissue, ectopic fat deposition and adipose tissue dysfunction mediate insulin resistance in human obesity independently of total body fat mass. This suggests that mechanisms beyond a positive caloric balance such as inflammation and adipokine release determine the pathological metabolic consequences in patients with obesity. Recommendations for obesity treatment should distinguish the metabolically 'healthy' from 'unhealthy' obese phenotype to identify early the obese person who will benefit the most from losing weight. In addition, novel antiobesity treatment strategies targeting adipose tissue dysfunction are needed.

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The metabolically healthy but obese individual presents a favorable inflammation profile.

Antony Karelis, May Faraj, Jean-Philippe Bastard … (2005)

The purpose of this study was to investigate the inflammatory state in obese women displaying the "metabolically healthy but obese" (MHO) phenotype. We examined the metabolic characteristics of 88 obese, sedentary postmenopausal women. Subjects were classified as MHO or as "at risk" based on the upper and lower quartiles of insulin sensitivity as measured by the hyperinsulinemic-euglycemic clamp technique. Thereafter, we determined 1) body composition, 2) body fat distribution, 3) plasma lipid and lipoprotein levels, 4) glucose homeostasis, 5) resting blood pressure, 6) peak oxygen consumption, and 7) inflammation markers as potential modulators of differences in the coronary risk profile. Twenty-two MHO women displayed high insulin sensitivity (15.35 +/- 2.3 mg/min.kg fat-free mass), and 22 at risk subjects with low insulin sensitivity (7.98 +/- 1.4 mg/min.kg fat-free mass) were identified. Despite comparable total body fatness between groups (47.7 +/- 4.8 vs. 45.5 +/- 4.4%; not significant), MHO individuals had significantly lower levels of visceral fat, fasting insulin, plasma triglycerides, high-sensitivity C-reactive protein (CRP), and alpha-1 antitrypsin levels and higher levels of high-density lipoprotein cholesterol than at risk individuals (P < 0.05). Stepwise regression analysis showed that CRP, fasting triglycerides, and the lean body mass index explained 19.5, 8.5, and 4.0%, respectively, of the variance observed in glucose disposal (total r(2) = 0.320; P < 0.001). Results of the present study indicate that postmenopausal women displaying the MHO phenotype also have a favorable inflammation profile as shown by lower CRP and alpha-1 antitrypsin levels compared with insulin-resistant women. This suggests that a lower inflammation state, as attested by low CRP levels, could play a role in the protective profile of the MHO individual, and this may be associated metabolically to a lower risk for cardiovascular disease.

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Author and article information

Contributors

Zhi-Hong Yang:

ORCID: http://orcid.org/0000-0002-1885-3162

zhihong.yang@nih.gov

Beatrice Emma-Okon: boemmaokon@outlook.com

Alan T. Remaley: aremaley1@nhlbi.nih.gov

Journal

Journal ID (nlm-ta): Lipids Health Dis

Journal ID (iso-abbrev): Lipids Health Dis

Title: Lipids in Health and Disease

Publisher: BioMed Central (London )

ISSN (Electronic): 1476-511X

Publication date (Electronic): 22 November 2016

Publication date PMC-release: 22 November 2016

Publication date Collection: 2016

Volume: 15

Electronic Location Identifier: 201

Affiliations

[1 ]Lipoprotein Metabolism Section, Cardio-Pulmonary Branch, National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD 20892-1666 USA

[2 ]Central Research Laboratory, Tokyo Innovation Center, Nippon Suisan Kaisha, 32-3 Nanakuni 1 Chome Hachioji, Tokyo, 192-0991 Japan

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Zhi-Hong Yang http://orcid.org/0000-0002-1885-3162

Article

Publisher ID: 366

DOI: 10.1186/s12944-016-0366-5

PMC ID: 5120510

PubMed ID: 27876051

SO-VID: 2c6b616e-d7b8-4fdc-817d-4c6520613cda

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 18 September 2016

Date accepted : 9 November 2016

Funding

Funded by: FundRef http://dx.doi.org/10.13039/100000050, National Heart, Lung, and Blood Institute;

Funded by: FundRef http://dx.doi.org/10.13039/100000063, Office of Dietary Supplements;

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ScienceOpen disciplines: Biochemistry

Keywords: long-chain monounsaturated fatty acids,cardiovascular disease,atherosclerosis,peroxisome proliferator-activated receptor signaling pathway,inflammation

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ScienceOpen disciplines: Biochemistry

Keywords: long-chain monounsaturated fatty acids, cardiovascular disease, atherosclerosis, peroxisome proliferator-activated receptor signaling pathway, inflammation

Dietary marine-derived long-chain monounsaturated fatty acids and cardiovascular disease risk: a mini review

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Most cited references 65

Resolution of Inflammation: What Controls Its Onset?

The distinction of metabolically 'healthy' from 'unhealthy' obese individuals.

The metabolically healthy but obese individual presents a favorable inflammation profile.

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