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The metabolic syndrome has received increased attention in the past few years. This statement from the American Heart Association (AHA) and the National Heart, Lung, and Blood Institute (NHLBI) is intended to provide up-to-date guidance for professionals on the diagnosis and management of the metabolic syndrome in adults.

The metabolic syndrome is a constellation of interrelated risk factors of metabolic origin— metabolic risk factors —that appear to directly promote the development of atherosclerotic cardiovascular disease (ASCVD).1 Patients with the metabolic syndrome also are at increased risk for developing type 2 diabetes mellitus. Another set of conditions, the underlying risk factors , give rise to the metabolic risk factors. In the past few years, several expert groups have attempted to set forth simple diagnostic criteria to be used in clinical practice to identify patients who manifest the multiple components of the metabolic syndrome. These criteria have varied somewhat in specific elements, but in general they include a combination of both underlying and metabolic risk factors.

The most widely recognized of the metabolic risk factors are atherogenic dyslipidemia, elevated blood pressure, and elevated plasma glucose. Individuals with these characteristics commonly manifest a prothrombotic state and a pro-inflammatory state as well. Atherogenic dyslipidemia consists of an aggregation of lipoprotein abnormalities including elevated serum triglyceride and apolipoprotein B (apoB), increased small LDL particles, and a reduced level of HDL cholesterol (HDL-C). The metabolic syndrome is often referred to as if it were a discrete entity with a single cause. Available data suggest that it truly is a syndrome, ie, a grouping of ASCVD risk factors, but one that probably has more than one cause. Regardless of cause, the syndrome identifies individuals at an elevated risk for ASCVD. The magnitude of the increased risk can vary according to which components of the syndrome are …

https://www.lipidcenter.com/pdf/metabolic.pdf

Diagnosis and Management of the Metabolic Syndrome An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement

Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights into inflammation in atherosclerosis not only increase our understanding of this disease, but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance.

/pdf/inflammation-and-atherosclerosis-1q9qkglell.pdf

Inflammation and Atherosclerosis

Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute scientific statement.

The metabolic syndrome

Corrigendum to "Knockout of toll-like receptor-4 attenuates the pro-inflammatory state of diabetes" [Cytokine 55 (2011) 441-445]

Validation of the newly FDA-approved Buhlmann fCal Turbo assay for measurement of fecal calprotectin in a pediatric population.

Mo1216 Salivary microRNAs in Eosinophilic Esophagitis: Pathobiologic Implications and Potential As Noninvasive Biomarker

Fecal Microbiome Signatures are Different in Food Allergic Children Compared to Siblings and Healthy Children

Obesity is a world-wide epidemic and is associated with increased diabetes and cardiovascular complications. Several prospective studies and meta-analyses have shown the beneficial effects of the significant and pronounced weight reduction after bariatric surgery on cardiometabolic risk. Bariatric surgery has resulted in a reduction in visceral fat, resolution of type 2 diabetes, hypertension, improved lipid profile, improvement in nonalcoholic fatty liver disease, obstructive sleep apnea, insulin resistance, inflammation, and endothelial function. Most importantly, bariatric surgery results in reduction in cardiovascular as well as all-cause mortality. Emerging evidence supports the role of gut microbiota in regulation of inflammation and obesity and insulin resistance in obesity, metabolic syndrome, and diabetes. Previously, we have reported on the role of endotoxemia because of increased gut permeability, contributing to inflammation and insulin resistance through activation of TLR4. Bariatric surgery alters the composition of microbiota. Trimethylamine-N-oxide (TMAO) is formed in the liver from trimethylamine (TMA), mainly through flavin monooxygenase 3 (FMO3). TMA is produced by the action of gut microbiota on dietary choline, phosphatidylcholine, and carnitine, products that are abundant in red meat, dairy products, eggs, and seafood. TMAO is not a widely recognized metabolite in mammals, although its role as a marine bacterial metabolite is emerging. It is a tertiary amine, very volatile at ambient temperatures, and is believed to be important in osmoregulation. Recent studies have demonstrated that TMAO may have direct biological activity that promotes atherosclerosis such as stimulating foam cell formation and impairment of reverse cholesterol transport. Direct dietary exposure to TMAO or its precursors, choline or l-carnitine (in presence of gut microbiota), elicited significant reductions in reverse cholesterol transport in vivo in mouse models, as well as alterations in cholesterol and sterol metabolic pathways in the artery wall, the liver, and the intestines. TMAO also induces changes in bile acid pool and composition. TMAO levels are influenced by hepatic FMO3, which is under complex control, including regulation by the farnesoid X receptor, a bile acid-activated nuclear receptor. Studies have also shown that TMAO promotes foam cell formation and atherosclerosis. TMAO has previously been shown to be increased in obesity, and increased TMAO levels predict myocardial infarction and stroke and augur a worse prognosis in patients with heart failure. There is a paucity of data examining the effect of bariatric surgery on TMAO levels. In this issue of the journal, Troseid et al. investigated, in a longitudinal study, the effect of bariatric surgery on plasma TMAO levels in 34 patients (19 females, 15 males), 1 year after surgery. Bariatric surgery decreases cardiovascular risk and events as reviewed earlier; however, in this study, the authors demonstrate a paradoxical doubling (139% increase) of circulating TMAO levels 1 year postsurgery. This pattern was seen regardless of surgical method, Roux-en-Y gastric bypass for body mass index (BMI) <50 kg/m, or duodenal switch for BMI >50 kg/m. In a previous article, they examined C-reactive protein (CRP) as a marker of inflammation and cardiovascular risk, 1 year postbariatric surgery and reported a significant decrease. They did not find a significant correlation in the increase in TMAO with the decrease in CRP in this cohort, but showed an inverse correlation with HbA1C. Since insulin inhibits FMO3, they also hypothesize that the improved insulin sensitivity evidenced by a decrease in HBA1C and possible decreased insulin levels could reduce the repression on FMO3, resulting in increased activity and increase in TMAO. However, insulin levels or any measure of insulin sensitivity was not reported. Also alterations in bile acid metabolism and a decrease in hepatic steatosis could be advanced as potential mechanisms, resulting in increase in TMAO levels because of an increase in FMO3 activity. Furthermore, they rule out renal impairment as a cause for the increase in TMAO levels because there was a decrease in creatinine levels in their patients. Although the strength of the study is that it is longitudinal and robust, they surmise that this is an effect dependent on the gut microbiota composition switching after bariatric surgery. The limitation of this study is that there is no information provided on gut microbiota composition or changes in dietary composition. The strongest support for their conclusions of bariatric surgery increasing TMAO is from previous studies on rat models as well as the study by Tremaroli et al. who also

Sridevi Devaraj

Papers

Corrigendum to "Knockout of toll-like receptor-4 attenuates the pro-inflammatory state of diabetes" [Cytokine 55 (2011) 441-445]

Validation of the newly FDA-approved Buhlmann fCal Turbo assay for measurement of fecal calprotectin in a pediatric population.

Mo1216 Salivary microRNAs in Eosinophilic Esophagitis: Pathobiologic Implications and Potential As Noninvasive Biomarker

Fecal Microbiome Signatures are Different in Food Allergic Children Compared to Siblings and Healthy Children

The Paradox of Increased Trimethylamine-N-Oxide Levels Following Bariatric Surgery.