Values are means ± SD. Statistical analyses were performed using two-sided paired Student’s t test. Asterisks denote significant differences compared with the value buy Torin 2 before switching to miglitol (*p < 0.05 and **p < 0.01). CVD cardiovascular disease, SD standard deviation, MCP monocyte chemoattractant protein, VCAM vascular cell adhesion molecule, ICAM intercellular adhesion molecule, tPAI total plasminogen activator inhibitor, FABP4 fatty acid binding protein, s soluble 4 Discussion In large-scale cohort studies, such as DECODE and FUNAGATA, it has been reported that postprandial hyperglycemia, rather than HbA1c, is closely associated with subsequent incidence of CVD [1–3]. Additionally,

the STOP-NIDDM and MeRIA7 trials have demonstrated that inhibition of postprandial hyperglycemia by the α-GI acarbose greatly reduces CVD events in subjects with IGT and type 2 diabetes [4, 5]. Thus, reduction of glucose fluctuations by miglitol may reduce CVD incidence in type 2 diabetic patients. In addition, we previously reported in 43 type 2 diabetic patients from the same sample that mRNA levels of inflammatory cytokines, such

as IL-1β and TNF-α, in peripheral leukocytes and circulating TNF-α proteins were reduced by the Pifithrin-�� datasheet switch to miglitol [19]. In this study we reanalyzed serum samples of 35 patients from the same sample and found that serum protein concentrations of MCP-1 and sE-selectin were reduced by the switch. MCP-1 induces migration of leukocytes to blood vessels

Eltanexor manufacturer and E-selectin facilitates leukocytes rolling onto the endothelium, resulting in the induction of the adhesion of leukocytes to blood vessels [21, 22]. Together, the results of this study and our previous study indicate that the switching from an α-GI (acarbose or voglibose) to miglitol suppresses glucose fluctuations, inflammatory cytokine expression in peripheral leukocytes, and circulating protein concentrations of MCP-1, sE-selectin, and TNF-α in type 2 diabetic patients in a clinical setting in Japan. Serum protein concentrations of sICAM-1, tPAI-1, and FABP4 were not altered and sVCAM-1 was slightly increased by the switch to miglitol. Ergoloid sICAM-1 and sVCAM-1 participate in inducing leukocyte attachment to blood vessels after leukocyte migration and rolling of leukocytes around blood vessels [23]. PAI-1 expressed from adipose tissues promotes atherogenesis by forming blocked blood vessels by inducing blood coagulation [24], and FABP4 expressed from adipose tissues and macrophages enhances atherogenesis by tracking cholesterol in atheromatosis [25]. These steps are later steps in the attachment of leukocytes to blood vessels. Thus, α-GIs, including miglitol, may inhibit CVD development by repressing the initial step of atheromatosis, i.e. inhibition of circulating MCP-1 and sE-selectin proteins via inhibition of postprandial hyperglycemia and glucose fluctuations.