Myokines are peptides produced and secreted by the skeletal muscle, with autocrine, paracrine, and endocrine actions. Many of them are overexpressed during physical exercise and appear to contribute to the benefits of exercise to metabolic homeostasis. Irisin, resulting from the cleavage of the membrane protein FNDC5, was shown to induce adipocyte browning, with increased lipid oxidation and thermogenesis. Myonectin was only recently discovered and initial studies revealed a role in fatty acid uptake and oxidation in adipose tissue and liver. However, the mechanisms of their regulation by exercise are not entirely established. Impaired secretion and action of myokines, such as irisin and myonectin, may have a role in the establishment of insulin resistance. On the other hand, several studies have shown that insulin resistance in the skeletal muscle may change myokines expression and secretion. This may have consequences on lipid and glucose metabolism in adipose tissue and lead to a vicious cycle between impaired myokines production and insulin resistance. This review summarizes the current knowledge about the influence of skeletal muscle insulin resistance on the secretion of irisin and myonectin, as well as its impact on adipose tissue metabolism.

Microvascular dysfunction has been suggested to trigger adipose tissue dysfunction in obesity. This study investigates the hypothesis that glycation impairs microvascular architecture and expandability with an impact on insulin signalling. Animal models supplemented with methylglyoxal (MG), maintained with a high-fat diet (HFD) or both (HFDMG) were studied for periepididymal adipose (pEAT) tissue hypoxia and local and systemic insulin resistance. Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) was used to quantify blood flow in vivo, showing MG-induced reduction of pEAT blood flow. Increased adipocyte size and leptin secretion were observed only in rats feeding the high-fat diet, without the development of hypoxia. In turn, hypoxia was only observed when MG was combined (HFDMG group), being associated with impaired activation of the insulin receptor (Tyr1163), glucose intolerance and systemic and muscle insulin resistance. Accordingly, the adipose tissue angiogenic assay has shown decreased capillarization after dose-dependent MG exposure and glyoxalase-1 inhibition. Thus, glycation impairs adipose tissue capillarization and blood flow, hampering its expandability during a high-fat diet challenge and leading to hypoxia and insulin resistance. Such events have systemic repercussions in glucose metabolism and may lead to the onset of unhealthy obesity and progression to type 2 diabetes.

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<b><i>Objective:</i></b> Patients submitted to carotid artery endarterectomy (CEA) have a long-term risk of major adverse cardiovascular events (MACE) of 6–9% at 2 years. Hematological parameters have been shown to have a predictive function in atherosclerotic diseases, namely the red blood cell distribution width-coefficient of variation (RDW-CV). This parameter has been associated with worse outcomes such as myocardial infarction (MI), stroke, and all-cause mortality. This study aims to evaluate the potential role of preoperative hematologic parameters such as RDW-CV in predicting perioperative and long-term cardiovascular adverse events and mortality in patients submitted to CEA. <b><i>Methods:</i></b> From January 2012 to January 2019, 180 patients who underwent CEA with regional anesthesia in a tertiary care and referral center were selected from a prospective cohort database. Blood samples were collected preoperatively 2 weeks before admission, including a full blood count. The primary outcome included long-term MACE. Secondary outcomes included all-cause mortality, stroke, MI, acute heart failure, and major adverse limb events (MALE). <b><i>Results:</i></b> At baseline, 27.2% of patients had increased RDW-CV. Increased RDW-CV was independently associated with baseline hemoglobin (adjusted odds ratio [aOR] 0.715, 95% CI 0.588–0.869, <i>p</i> = 0.001) and atrial fibrillation (aOR 4.028, 95% CI 1.037–15.639, <i>p</i> = 0.001). After a median follow-up of 50 months, log-rank univariate analysis of RDW-CV demonstrated a significant association between increased RDW-CV and long-term all-cause mortality (log-rank &#x3c;0.001), MACE (log-rank &#x3c;0.001), and MI (log-rank = 0.017). After multivariate Cox regression analysis, increased RDW-CV was associated with increased long-term mortality (adjusted hazard ratio [aHR] 2.455, 95% CI 1.231–4.894, <i>p</i> = 0.011) and MACE (aHR 2.047, 95% CI 1.202–3.487, <i>p</i> = 0.008). A decreased hemoglobin to platelet ratio (aHR 2.650e–8, 95% CI 9.049e–15 to 0.078, <i>p</i> = 0.019) was also associated with all-cause mortality. <b><i>Conclusion:</i></b> RDW is a widely available and low-cost marker that independently predicts long-term mortality, MACE, and MI after CEA. This biomarker could prove useful in assessing which patients would likely benefit from CEA in the long term.

Objective Stenting of the iliac veins is increasingly considered in the presence of symptomatic obstructive chronic lesions in the iliac vein segment. However, it is often necessary to extend the stented zone into the inferior vena cava, increasing the risk of contralateral iliac vein thrombosis. This study aims to review the current literature concerning the incidence of contralateral deep vein thrombosis after stenting across the iliocaval confluence. Methods A systematic review from potentially relevant published articles reporting contralateral deep vein thrombosis after iliac venous stenting between January 2007 and February 2019 was performed. Results A total of 764 references were retrieved initially. Twelve studies reporting events of contralateral deep vein thrombosis were selected for review, with a total of 1864 patients. Contralateral deep vein thrombosis incidence varied between 0% and 15.6%. The post-interventional and follow-up anticoagulation regimens were heterogeneous between studies. The decision to maintain patients on anticoagulation and the duration of treatment was based on the presence of comorbidities, hypercoagulable states, post-thrombotic syndrome and history of recurrent deep vein thrombosis. Patients with non-thrombotic iliac vein lesions were either anticoagulated for three or six months after stenting or received no anticoagulation. Patients with post-thrombotic syndrome were anticoagulated for longer periods. Most studies (eight studies) used an oral vitamin K antagonist agent. The data on compliance with anticoagulation treatment is scarce and few references present data on whether contralateral deep vein thrombosis occurred during anticoagulation treatment. The use of antiplatelet agents in addition to the anticoagulant treatment in the follow-up period was also variable. Conclusion The incidence of contralateral deep vein thrombosis due to iliac vein jailing is not negligible and reported being as high as 15.6%. Large-scale studies on the ideal antithrombotic treatment and its impact are necessary. It is possible that patients with stent crossing the iliocaval confluence might benefit from long-term antithrombotic treatment.

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