Publications by authors named "Atsuyuki Tsutsumi"

Tumor necrosis factor α (TNFα) is a pro-inflammatory cytokine and one of the major mediators of obesity-induced insulin resistance. TNFα is generated through TNFα converting enzyme (TACE)-mediated cleavage of the transmembrane precursor pro-TNFα. Inhibition of TACE resulted in the improvement in glucose and insulin levels in diabetic animals, suggesting a crucial role of TACE activity in glucose metabolism.

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Endoplasmic reticulum (ER) stress plays a crucial role in the development of insulin resistance and diabetes. Although caloric restriction (CR) improves obesity-related disorders, the effects of CR on ER stress in obesity remain unknown. To investigate how CR affects ER stress in obesity, ob/ob mice were assigned to either ad libitum (AL) (ob-AL) or CR (ob-CR) feeding (2 g food/day) for 1-4 weeks.

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Objective: Nifedipine, an L-type calcium channel blocker, protects against the progression of atherosclerosis. We investigated the molecular basis of the antiatherosclerotic effect of nifedipine in macrophages and apolipoprotein E-deficient mice.

Methods And Results: In macrophages, nifedipine increased peroxisome proliferator-activated receptor-gamma (PPARgamma) activity without increasing PPARgamma-binding activity.

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Macrophage-derived foam cells play important roles in the progression of atherosclerosis. We reported previously that ERK1/2-dependent granulocyte/macrophage colony-stimulating factor (GM-CSF) expression, leading to p38 MAPK/ Akt signaling, is important for oxidized low density lipoprotein (Ox-LDL)-induced macrophage proliferation. Here, we investigated whether activation of AMP-activated protein kinase (AMPK) could suppress macrophage proliferation.

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Article Synopsis
  • AMP-activated protein kinase (AMPK) plays a key role as a cellular energy sensor and is a potential therapeutic target for vascular diseases.
  • The study investigated the impact of rottlerin, a known inhibitor of protein kinase Cdelta, on AMPK activation in vascular smooth muscle cells and isolated rabbit aorta, finding that rottlerin reduces ATP levels and activates AMPK.
  • Results indicate that the presence of LKB1 is crucial, as overexpressing a dominant-negative form of LKB1 reduced AMPK activation, suggesting LKB1 mediates the effects of rottlerin on AMPK in vascular tissues.
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ACTH-independent macronodular adrenal hyperplasia (AIMAH) is a rare cause of Cushing's syndrome. Recently, aberrant expression of adrenal receptors for various hormones and/or cytokines has been identified in several cases with AIMAH, which may act as a pathogenetic factor for the disorder. We report here an AIMAH patient with a Rathke's cleft cyst.

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