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The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Overexpression of Monocyte Chemoattractant Protein-1 in Adipose Tissues Causes Macrophage Recruitment and Insulin Resistance

Open access
Kamei, Nozomu, Tobe, Kazuyuki, Suzuki, Ryo, Ohsugi, Mitsuru, Watanabe, Taku, Kubota, Naoto, Ohtsuka-Kowatari, Norie, Kumagai, Katsuyoshi, Sakamoto, Kentaro, Kobayashi, Masatoshi, Yamauchi, Toshimasa, Ueki, Kohjiro, Oishi, Yumiko, Nishimura, Satoshi, Manabe, Ichiro, Hashimoto, Haruo, Ohnishi, Yasuyuki, Ogata, Hitomi, Tokuyama, Kumpei, Tsunoda, Masaki, Ide, Tomohiro, Murakami, Koji, Nagai, Ryozo, Kadowaki, Takashi·2006·Journal of Biological Chemistry

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.

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Metadata

Authors
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., & Kadowaki, T.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2006-09
Volume
281
Issue
36
Pages
26602-26614
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2144032315
Cited by
917
References
9
FWCI
36.08
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Overexpression of Monocyte Chemoattractant Protein-1 in Adipose Tissues Causes Macrophage Recruitment and Insulin Resistance. https://app.cochat.ai/papers/10.1074/jbc.m601284200
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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., . . . Kadowaki, T. (2006). Overexpression of Monocyte Chemoattractant Protein-1 in Adipose Tissues Causes Macrophage Recruitment and Insulin Resistance. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m601284200

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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