Orally administrated acetate inhibits atherosclerosis progression through AMPK activation via GPR43 in plaque macrophages.

Background And Aims: Oral administration of acetic acid, a short-chain fatty acid, has been shown to efficiently reduce obesity and insulin resistance in both experimental animals and humans. The anti-atherosclerotic effect of acetate is expected owing to its anti-inflammatory and anti-oxidative stress characteristics; however, this remains to be fully understood.

Methods: For 12 weeks, apolipoprotein E-deficient mice were administered 0.

Protein-protein interaction-mediated regulation of lysine biosynthesis of Thermus thermophilus through the function-unknown protein LysV.

Thermus thermophilus biosynthesizes lysine via α-aminoadipate as an intermediate using the amino-group carrier protein, LysW, to transfer the attached α-aminoadipate and its derivatives to biosynthetic enzymes. A gene named lysV, which encodes a hypothetical protein similar to LysW, is present in the lysine biosynthetic gene cluster. Although the knockout of lysV did not affect lysine auxotrophy, lysV homologs are conserved in the lysine biosynthetic gene clusters of microorganisms belonging to the phylum Deinococcus-Thermus, suggesting a functional role for LysV in lysine biosynthesis.

Impact of tissue macrophage proliferation on peripheral and systemic insulin resistance in obese mice with diabetes.

Introduction: Obesity-related insulin resistance is a widely accepted pathophysiological feature in type 2 diabetes. Systemic metabolism and immunity are closely related, and obesity represents impaired immune function that predisposes individuals to systemic chronic inflammation. Increased macrophage infiltration and activation in peripheral insulin target tissues in obese subjects are strongly related to insulin resistance.

Inhibition of inflammation-mediated DPP-4 expression by linagliptin increases M2 macrophages in atherosclerotic lesions.

Background And Aims: Dipeptidyl peptidase-4 (DPP-4) inhibitors have been reported to suppress atherosclerosis progression in atherosclerotic mouse models through unclear mechanisms. In this study, we investigated the effect of the DPP-4 inhibitor, linagliptin, on macrophage polarization in vitro and in vivo.

Methods: Mouse bone marrow macrophages (BMMs) were used in in vitro assays.

Pioglitazone suppresses macrophage proliferation in apolipoprotein-E deficient mice by activating PPARγ.

Background And Aims: Local macrophage proliferation is linked to enhanced atherosclerosis progression. Our previous study found that troglitazone, a thiazolidinedione (TZD), suppressed oxidized low-density lipoprotein (Ox-LDL)-induced macrophage proliferation. However, its effects and mechanisms are unclear.

Inhibition of Local Macrophage Growth Ameliorates Focal Inflammation and Suppresses Atherosclerosis.

Objective: Macrophages play a central role in various stages of atherosclerotic plaque formation and progression. The local macrophages reportedly proliferate during atherosclerosis, but the pathophysiological significance of macrophage proliferation in this context remains unclear. Here, we investigated the involvement of local macrophage proliferation during atherosclerosis formation and progression using transgenic mice, in which macrophage proliferation was specifically suppressed.