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Adiposity, Humans, Inflammation etiology, Insulin Resistance physiology, Risk Factors, Anti-Inflammatory Agents therapeutic use, Inflammation therapy, and Metabolic Syndrome complications

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.
(Copyright © 2016 Elsevier Inc. All rights reserved.)

Boston epidemiology, Cardiovascular Diseases epidemiology, Cardiovascular Diseases etiology, Cardiovascular Diseases prevention control, Cross-Over Studies, Down-Regulation, Equol metabolism, Female, Humans, Hyperlipidemias etiology, Hypertension etiology, Inflammation Mediators blood, Intercellular Adhesion Molecule-1 blood, Intercellular Adhesion Molecule-1 chemistry, Metabolic Syndrome immunology, Metabolic Syndrome metabolism, Metabolic Syndrome physiopathology, Middle Aged, Postmenopause, Risk Factors, Solubility, Equol blood, Functional Food, Hyperlipidemias prevention control, Hypertension prevention control, Metabolic Syndrome diet therapy, Seeds, and Soybeans

Objective: Soy has been associated with lower risk of cardiovascular disease in Asian countries which consume daily soy. Our study examined whether production of equol, an estrogen metabolite, affected the ability of soy nuts to improve cardiovascular risk factors.
Materials/methods: Sixty postmenopausal women participated in a randomized, controlled, crossover trial of a Therapeutic Lifestyle Changes (TLC) diet alone and a TLC diet in which 0.5 cup of soy nuts (25 g of soy protein and 101 mg of aglycone isoflavones) replaced 25 g of nonsoy protein daily. Each diet was followed for 8 weeks at the end of which blood pressure (BP), lipid levels, adhesion molecules and inflammatory markers were measured.
Results: Women with MetS had significantly higher baseline body mass index (BMI), BP, triglycerides (TG), and soluble intercellular adhesion molecule (sICAM) than women without MetS. In women with MetS on the soy diet, significant reductions in diastolic BP (7.7%; P=0.02), TG (22.9%; P=0.02), C-reactive protein (CRP) (21.4%; P=0.01) and sICAM (7.3%; P=0.03) were noted among equol producers compared to levels on the TLC diet. No significant changes were noted in equol nonproducers. Similarly, in women without MetS, only equol producers had significant reductions in diastolic BP (3.3%, P=0.02) and CRP (30%, P=0.04). In contrast to women with MetS, TG and sICAM levels were not affected in women without MetS, a finding possibly related to lower baseline levels.
Conclusions: Cardiovascular risk reduction with soy nuts is not uniform and may be greater among producers of equol.
(Copyright © 2015 Elsevier Inc. All rights reserved.)

Aged, Apolipoprotein B-100, Apolipoprotein B-48, Cholesterol blood, Cholesterol, HDL blood, Cholesterol, LDL blood, Chronic Disease, Glomerular Filtration Rate physiology, Humans, Hyperlipidemias etiology, Kidney Diseases complications, Lipids blood, Lipoproteins blood, Male, Metabolic Syndrome complications, Middle Aged, Models, Biological, Obesity complications, Apolipoprotein A-I metabolism, Apolipoproteins B metabolism, Kidney Diseases metabolism, Metabolic Syndrome metabolism, and Obesity metabolism

The metabolism of apolipoproteins (apo)B-48, B-100, and A-I was studied with a primed constant infusion of deuterium-labeled leucine in the fed state in 3 male individuals with chronic kidney disease (CKD), a glomerular filtration rate (GFR) of 28 to 57 mL/min/1.73 m2, obesity (body mass index [BMI] 33.1), and the metabolic syndrome. Compared to 5 obese controls (BMI 30.1) and 13 non-obese controls (BMI 25.2), these CKD subjects had high plasma levels of triglycerides (TG) (343 +/- 27.5 mg/dL v 144 +/- 34.4 in the obese controls, P < .001) and low apoA-I (86.7 +/- 3.9 mg/dL). An abnormal high-density lipoprotein (HDL) particle subpopulation pattern was found, with low levels of pre beta-1 and alpha1. Compared to the obese controls, very-low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL) apoB-100 levels were elevated 2- to 3-fold, while LDL apoB-100 levels were slightly lower (-7 %) and apoB-48 levels were comparable. The high TG levels were not associated with statistically significant changes in VLDL apoB-100 kinetics, although the production rate (PR) was higher and the fractional catabolic rate (FCR) was lower. The slightly lower LDL apoB-100 levels were accompanied by a significant 3-fold increase in the FCR and a 2.7-fold increase in the PR. The lower apoA-I levels were accompanied by a 1.6-fold increase in the FCR. Compared to the non-obese controls, the PR of apoA-I was increased by 61% and 38%, respectively (P < .001) in CKD and in obese control subjects. In the control subjects, the PR of apoA-I was significantly correlated with the BMI (r = 0.81, P < .0001). The kinetic results are consistent with these hypotheses: (1) CKD is associated with decreased clearance of the TG-rich lipoproteins (TRLs) and increased catabolism of LDL; (2) obesity increases apoB-100 and apoA-I production; and (3) in CKD, TG transfer to HDL, making HDL more susceptible to catabolism, accounts for the low apoA-I levels.