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Association of low serum Meteorin like (Metrnl) concentrations with worsening of glucose tolerance, impaired endothelial function and atherosclerosis. | LitMetric

Objective: Meteorin-like (Metrnl) is a novel secreted protein that has a beneficial effect on glucose homeostasis with anti-inflammatory properties. Our goal is to determine whether low serum Metrnl levels are associated with worsening of glucose tolerance, impaired endothelial function, and atherosclerosis.

Methods: This study included 260 adults, 89 of whom had normal oral glucose tolerance (nOGT), 77 with glucose tolerance impairment (GTI) and 94 with type 2 diabetes (T2DM). Insulin resistance was assessed by evaluating the homeostasis model assessment of insulin resistance (HOMA-IR). Serum Metrnl level, proinflammatory, biochemical, endothelial and atherosclerosis parameters were measured.

Results: Serum Metrnl levels decreased significantly in patients with T2DM versus subjects with nOGT (P < 0.001). Metrnl levels were negatively correlated with fasting blood glucose, 2-h postload glucose (2 h-PLG), fasting insulin, HOMA-IR, HbA1c, high-sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), Carotid intima media thickness (CIMT), brachial-ankle pulse wave velocity (baPWV), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin. High serum Metrnl level was significantly correlated with reduced risk of T2DM as revealed by multivariate logistic regression analysis after control of potential risk factors for diabetes. Furthermore, the association remains significant after further adjustment for IL-6, TNF-α, hs-CRP, CIMT, baPWV, ICAM-1, VCAM-1 and E-selectin.

Conclusions: Low Serum Metrnl may be associated with worsening of glucose tolerance, impaired endothelial function and atherosclerosis. It may also be considered a possible surrogate marker of endothelial dysfunction, and atherosclerosis and an independent risk factor of T2DM.

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http://dx.doi.org/10.1016/j.diabres.2019.02.026DOI Listing

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