Background-Macrophage and lymphocyte infiltration in adipose tissue may contribute to the pathogenesis of obesity-mediated metabolic disorders. Natural killer T (NKT) cells, which integrate proinflammatory cytokines, have been demonstrated in the atherosclerotic lesions and in visceral adipose tissue. Objective-To determine whether NKT cells are involved in glucose intolerance and adipose tissue inflammation in diet-induced obese mice. Methods and Results-To determine whether NKT cells are involved in the development of glucose intolerance, male ␤ 2 -microglobulin knockout (KO) mice lacking NKT cells and C57BL/6J (wild-type) mice were fed with a high-fat diet (HFD) for 13 weeks. Body weight and visceral obesity were comparable between wild-type and KO mice. However, macrophage infiltration was reduced in adipose tissue and glucose intolerance was significantly ameliorated in KO mice.To further confirm that NKT cells are involved in these abnormalities, ␣-galactosylceramide, 0.1 g/g body weight, which specifically activates NKT cells, was administered after 13 weeks of HFD feeding. ␣-Galactosylceramide significantly exacerbated glucose intolerance and macrophage infiltration as well as cytokine gene expression in adipose tissue. O besity, specifically visceral obesity, increases the risk for metabolic disorders, such as type 2 diabetes mellitus, dyslipidemia, and hypertension as well as atherosclerotic cardiovascular diseases. Previous studies have demonstrated that the accumulation of macrophages within adipose tissue is well documented in obese individuals and that adipose tissue inflammation plays an important role in the pathogenesis of these metabolic disorders. 1,2 Macrophages are attracted by chemokines, such as monocyte chemoattractant protein 1 (MCP-1), and contribute to local inflammation through the release of other inflammatory cytokines, such as tumor necrosis factor (TNF) ␣. In high-fat diet (HFD)-fed obese mice, it has been shown that infiltration of macrophages into adipose tissue coincides with the occurrence of obesitymediated metabolic disorders. 2 The important role of adipose tissue macrophages in the pathogenesis of metabolic disorders has further been supported by recent data in C-C motif chemokine receptor 2 (CCR2)-deficient mice. 3 The CCR2 Ϫ/Ϫ mice exhibited a reduction in adipose tissue macrophages in association with an improvement of glucose homeostasis and insulin sensitivity. However, the abolished monocyte and macrophage recruitment into peripheral tissue via interaction with MCP-1 could not completely inhibit HFD-mediated metabolic disorders, suggesting that other inflammatory cells may play a role in this context. Wu et al 4 and Rocha et al 5 demonstrated that CD3-positive T lymphocytes are present in human adipose tissue; and regulated upon activation, normal T cell expressed secreted (RANTES), a T-cell-specific chemokine, and its respective receptor CCR5 are expressed in adipose tissue from obese patients. However, the role of other types of lymphocytes in adipose tissue inflam...

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SummaryLeft ventricular (LV) diastolic dysfunction is considered the main cause of heart failure with preserved ejection fraction (HFpEF). There have been few reports on the correlation between LV diastolic dysfunction and arterial stiffness in patients with clinical cardiovascular disease.This cross-sectional study enrolled 100 patients (67 men, 33 women; mean age, 70 years). All participants were diagnosed with cardiovascular disease. A total of 89 (89%) patients had coronary artery disease or HF. Patients with reduced EF and valvular disease were excluded. Arterial stiffness was assessed by the cardio-ankle vascular index (CAVI), and LV diastolic dysfunction was estimated using echocardiography. The patients were divided into two groups based on the median value of CAVI. In all patients the ratio of early diastolic transmitral flow velocity to early diastolic mitral annular velocity (E/e') was significantly higher in the high CAVI group than in the low CAVI group (15.5 ± 6.4 versus 12.5 ± 2.9, P = 0.003). In the HF subgroup, E/e' was also significantly higher in the high CAVI group than in the low CAVI group (17.2 ± 5.9 versus 13.0 ± 3.1, P = 0.026). In univariate regression analysis, CAVI was significantly associated with E/e' in all patients (β = 0.28, P = 0.004) and in HF patients (β = 0.4, P = 0.028). Also in multivariate analysis, CAVI remained as an independent predictive factor of E/e' (β = 0.252, P = 0.037).A high CAVI was independently associated with LV diastolic dysfunction in patients with clinical cardiovascular disease. These results suggested that arterial stiffness contributed to the development of LV diastolic dysfunction. (Int Heart J 2016; 57: 729-735)

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