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Your search keyword '"Kobayashi, Masatoshi"' showing total 4 results
Start Over Author "Kobayashi, Masatoshi" Topic macrophages
4 results on '"Kobayashi, Masatoshi"'

1. Adiponectin enhances insulin sensitivity by increasing hepatic IRS-2 expression via a macrophage-derived IL-6-dependent pathway.

Author

Awazawa M, Ueki K, Inabe K, Yamauchi T, Kubota N, Kaneko K, Kobayashi M, Iwane A, Sasako T, Okazaki Y, Ohsugi M, Takamoto I, Yamashita S, Asahara H, Akira S, Kasuga M, and Kadowaki T

Subjects
Adiponectin deficiency, Adiponectin genetics, Animals, Disease Models, Animal, Insulin Receptor Substrate Proteins genetics, Insulin Resistance, Interleukin-6 deficiency, Interleukin-6 genetics, Mice, Mice, Obese, NF-kappa B metabolism, Promoter Regions, Genetic, Receptors, Adiponectin metabolism, STAT3 Transcription Factor genetics, STAT3 Transcription Factor metabolism, Signal Transduction, Adiponectin metabolism, Insulin Receptor Substrate Proteins metabolism, Interleukin-6 metabolism, Liver metabolism, Macrophages metabolism
Abstract

Insulin resistance is often associated with impeded insulin signaling due either to decreased concentrations or functional modifications of crucial signaling molecules including insulin receptor substrates (IRS) in the liver. Many actions of adiponectin, a well-recognized antidiabetic adipokine, are currently attributed to the activation of two critical molecules downstream of AdipoR1 and R2: AMP-activated kinase (AMPK) and peroxisome proliferator-activated receptor α (PPARα). However, the direct effects of adiponectin on insulin signaling molecules remain poorly understood. We show here that adiponectin upregulates IRS-2 through activation of signal transducer and activator of transcription-3 (STAT3). Surprisingly, this activation is associated with IL-6 production from macrophages induced by adiponectin through NFκB activation independent of its authentic receptors, AdipoR1 and AdipoR2. These data have unraveled an insulin-sensitizing action initiated by adiponectin leading to upregulation of hepatic IRS-2 via an IL-6 dependent pathway through a still unidentified adiponectin receptor., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Published
2011
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2. Overexpression of monocyte chemoattractant protein-1 in adipose tissues causes macrophage recruitment and insulin resistance.

Author

Kamei N, Tobe K, Suzuki R, Ohsugi M, Watanabe T, Kubota N, Ohtsuka-Kowatari N, Kumagai K, Sakamoto K, Kobayashi M, Yamauchi T, Ueki K, Oishi Y, Nishimura S, Manabe I, Hashimoto H, Ohnishi Y, Ogata H, Tokuyama K, Tsunoda M, Ide T, Murakami K, Nagai R, and Kadowaki T

Subjects
Adipose Tissue cytology, Animals, Antimetabolites metabolism, Body Weight, Cells, Cultured, Chemokine CCL2 genetics, Deoxyglucose metabolism, Diet, Dietary Fats, Fatty Acid-Binding Proteins genetics, Fatty Acid-Binding Proteins metabolism, Fatty Acids, Nonesterified metabolism, Glucose metabolism, Glucose Clamp Technique, Insulin metabolism, Interleukin-6 genetics, Interleukin-6 metabolism, Mice, Mice, Inbred C57BL, Mice, Obese, Mice, Transgenic, Myoblasts, Skeletal cytology, Myoblasts, Skeletal metabolism, Promoter Regions, Genetic, Signal Transduction physiology, Tumor Necrosis Factor-alpha genetics, Tumor Necrosis Factor-alpha metabolism, Adipose Tissue metabolism, Chemokine CCL2 metabolism, Insulin Resistance immunology, Macrophages metabolism
Abstract

Adipose tissue expression and circulating concentrations of monocyte chemoattractant protein-1 (MCP-1) correlate positively with adiposity. To ascertain the roles of MCP-1 overexpression in adipose, we generated transgenic mice by utilizing the adipocyte P2 (aP2) promoter (aP2-MCP-1 mice). These mice had higher plasma MCP-1 concentrations and increased macrophage accumulation in adipose tissues, as confirmed by immunochemical, flow cytometric, and gene expression analyses. Tumor necrosis factor-alpha and interleukin-6 mRNA levels in white adipose tissue and plasma non-esterified fatty acid levels were increased in transgenic mice. aP2-MCP-1 mice showed insulin resistance, suggesting that inflammatory changes in adipose tissues may be involved in the development of insulin resistance. Insulin resistance in aP2-MCP-1 mice was confirmed by hyperinsulinemic euglycemic clamp studies showing that transgenic mice had lower rates of glucose disappearance and higher endogenous glucose production than wild-type mice. Consistent with this, insulin-induced phosphorylations of Akt were significantly decreased in both skeletal muscles and livers of aP2-MCP-1 mice. MCP-1 pretreatment of isolated skeletal muscle blunted insulin-stimulated glucose uptake, which was partially restored by treatment with the MEK inhibitor U0126, suggesting that circulating MCP-1 may contribute to insulin resistance in aP2-MCP-1 mice. We concluded that both paracrine and endocrine effects of MCP-1 may contribute to the development of insulin resistance in aP2-MCP-1 mice.

Published
2006
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4. Blockade of class IB phosphoinositide-3 kinase ameliorates obesity-induced inflammation and insulin resistance

Author

Kobayashi, Naoki, Ueki, Kohjiro, Okazaki, Yukiko, Iwane, Aya, Kubota, Naoto, Ohsugi, Mitsuru, Awazawa, Motoharu, Kobayashi, Masatoshi, Sasako, Takayoshi, Kaneko, Kazuma, Suzuki, Miho, Nishikawa, Yoshitaka, Hara, Kazuo, Yoshimura, Kotaro, Koshima, Isao, Goyama, Susumu, Murakami, Koji, Sasaki, Junko, Nagai, Ryozo, Kurokawa, Mineo, Sasaki, Takehiko, Kadowaki, Takashi, and Cantley, Lewis Clayton

Published
2011

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