Targeting inflammation in metabolic syndrome
Open accessAbstract
The metabolic syndrome (MetS) is comprised of a cluster of closely related risk factors, including visceral adiposity, insulin resistance, hypertension, high triglyceride, and low high-density lipoprotein cholesterol; all of which increase the risk for the development of type 2 diabetes and cardiovascular disease. A chronic state of inflammation appears to be a central mechanism underlying the pathophysiology of insulin resistance and MetS. In this review, we summarize recent research which has provided insight into the mechanisms by which inflammation underlies the pathophysiology of the individual components of MetS including visceral adiposity, hyperglycemia and insulin resistance, dyslipidemia, and hypertension. On the basis of these mechanisms, we summarize therapeutic modalities to target inflammation in the MetS and its individual components. Current therapeutic modalities can modulate the individual components of MetS and have a direct anti-inflammatory effect. Lifestyle modifications including exercise, weight loss, and diets high in fruits, vegetables, fiber, whole grains, and low-fat dairy and low in saturated fat and glucose are recommended as a first line therapy. The Mediterranean and dietary approaches to stop hypertension diets are especially beneficial and have been shown to prevent development of MetS. Moreover, the Mediterranean diet has been associated with reductions in total and cardiovascular mortality. Omega-3 fatty acids and peroxisome proliferator-activated receptor α agonists lower high levels of triglyceride; their role in targeting inflammation is reviewed. Angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone blockers comprise pharmacologic therapies for hypertension but also target other aspects of MetS including inflammation. Statin drugs target many of the underlying inflammatory pathways involved in MetS.
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ACE-I/ARBs are capable of reducing neuroinflammation.
“However, these agents are also capable of reducing neuroinflammation (Benicky et al, 2011;Welty et al, 2015)”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Welty et al, 2015
The Hypertension section on ACE inhibitors and ARBs says these agents inhibit inflammatory cytokine formation and describes anti-inflammatory effects involving T cells and monocytes (page not provided). It does not establish that they reduce neuroinflammation specifically. (LLM, conf=0.85)
Experimental — accuracy not yet measuredOmega-3 fatty acids decrease proinflammatory cytokines such as interleukin-6 and tumor necrosis factor-alpha and inhibit activation of IKK and NF-kB.
“Additionally, Ω3FAs' are precursors to the synthesis of specialized mediators capable of combating inflammation and have been demonstrated to decrease proinflammatory cytokines such as interleukine-6 and tumor necrosis factor-α and inhibit the activation of the ikappaB kinase and nuclear factor-κB, as well as several other transcription factors that inhibit reactive oxygen species [32,33].”
From Update on Omega-3 Polyunsaturated Fatty Acids on Cardiovascular Health (2022) · cites this paper as [33]
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Kelley, D. S., Siegel, D., Fedor, D. M., Adkins, Y. C., & Mackey, B. E. (2009) · Journal of Nutrition · doi:10.3945/jn.108.100354 · Cited by 139 · see citing works
n-3 Fatty Acids in the Treatment of Diabetic Patients
Caterina, R. D., Madonna, R., Bertolotto, A., & Schmidt, E. B. (2007) · Diabetes Care · doi:10.2337/dc06-1332 · Cited by 135 · see citing works
Dandona, P., Mohanty, P., Hamouda, W., Ghanim, H., Aljada, A., Garg, R., & Kumar, V. (2001) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.86.6.7745 · Cited by 135 · see citing works
Gyurko, R., Siqueira, C. C., Caldon, N., Gao, L., Kantarcı, A., & Dyke, T. E. V. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.177.10.7250 · Cited by 132 · see citing works
Robinson, E., & Grieve, D. (2009) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2009.03.003 · Cited by 130 · see citing works
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HDL Stimulation of Endothelial Nitric Oxide Synthase A Novel Mechanism of HDL Action
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Certain dietary patterns are beneficial for the metabolic syndrome: reviewing the evidence
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Apolipoprotein A-I and Its Role in Lymphocyte Cholesterol Homeostasis and Autoimmunity
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G-Protein-Coupled Receptor Kinase 2 and Hypertension
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The Arachidonic Acid Metabolome Serves as a Conserved Regulator of Cholesterol Metabolism
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A deficiency in the in vivo clearance of apoptotic cells is a feature of the NOD mouse
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Flagged first, then by citations
Research works printed but not linked: 1
- [149]FKW The Contribution of Triglycerides and Triglyceride-Rich Lipoproteins to Atherosclerosis Braunwald Textbook of Preventive Cardiology 1 Elsevier 2011
Cited by
Sorted by citations
Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond
Michopoulos, V., Powers, A., Gillespie, C. F., Ressler, K. J., & Jovanovic, T. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2016.146 · Cited by 786 · see citing works
Inflammation and cardiovascular disease: From mechanisms to therapeutics
Alfaddagh, A., Martin, S. S., Leucker, T. M., Michos, E. D., Blaha, M. J., Lowenstein, C. J., Jones, S. R., & Toth, P. P. (2020) · American Journal of Preventive Cardiology · doi:10.1016/j.ajpc.2020.100130 · Cited by 473 · see citing works
Self-citationControversies in the Use of Omega-3 Fatty Acids to Prevent Atherosclerosis
Quispe, R., Alfaddagh, A., Kazzi, B., Zghyer, F., Marvel, F. A., Blumenthal, R. S., Sharma, G., & Martin, S. S. (2022) · Current Atherosclerosis Reports · doi:10.1007/s11883-022-01031-9 · Cited by 17 · see citing works
Self-citation
- Authors
- Welty, F. K., Alfaddagh, A., & Elajami, T. K.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Welty, Francine K.
- Venue
- Translational Research
- Publisher
- Elsevier BV
- Published
- 2016-01
- Volume
- 167
- Issue
- 1
- Pages
- 257-280
- ISSN
- 1878-1810 (ISSN-L)
- 1931-5244
- PMC
- PMC6800061
- OpenAlex
- W748217515
- Cited by
- 287
- References
- 262
- Citations by year
- 2026: 8 · 2025: 30 · 2024: 25 · 2023: 27 · 2022: 30 · 2021: 29 · 2020: 36 · 2019: 15 · 2018: 23 · 2017: 32 · 2016: 27 · 2015: 4
- FWCI
- 3.73
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Translational research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (DE018184)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- metabolic syndrome, inflammation, insulin resistance, visceral fat, hypertension, dyslipidemia, hypertriglyceridemia, type 2 diabetes, cardiovascular disease, anti-inflammatory therapy, Mediterranean diet, DASH diet, omega-3 fatty acids, PPARα agonist, ACE inhibitors, angiotensin receptor blockers, statins, lifestyle modification
- MeSH terms
- Anti-Inflammatory Agents, Humans, Inflammation, Insulin Resistance, Risk Factors, Metabolic Syndrome, Adiposity
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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