A transgenic mutant mouse line accompanied by the complete deletion of interleukin-33 showed insulin and leptin resistances

Research output: Working paperResearch

Standard

A transgenic mutant mouse line accompanied by the complete deletion of interleukin-33 showed insulin and leptin resistances. / Watanabe, Taku; Takeuchi, Tomonori; Kubota, Naoto; Wainai, Tasuku; Kataoka, Keisuke; Nakaya, Toshitaka; Sugimoto, Ayako; Sato, Takahiro; Ohira, Hiroshi; Tsujino, Ichizo; Kumagai, Katsuyoshi; Kubota, Tetsuya; Hasegawa, Chiaki; Tokuyama, Kumpei; Ueki, Kohjiro; Yamauchi, Toshimasa; Mishina, Masayoshi; Kadowaki, Takashi.

bioRxiv, 2018.

Research output: Working paperResearch

Harvard

Watanabe, T, Takeuchi, T, Kubota, N, Wainai, T, Kataoka, K, Nakaya, T, Sugimoto, A, Sato, T, Ohira, H, Tsujino, I, Kumagai, K, Kubota, T, Hasegawa, C, Tokuyama, K, Ueki, K, Yamauchi, T, Mishina, M & Kadowaki, T 2018 'A transgenic mutant mouse line accompanied by the complete deletion of interleukin-33 showed insulin and leptin resistances' bioRxiv. <http://biorxiv.org/content/early/2018/09/13/416529.abstract>

APA

Watanabe, T., Takeuchi, T., Kubota, N., Wainai, T., Kataoka, K., Nakaya, T., Sugimoto, A., Sato, T., Ohira, H., Tsujino, I., Kumagai, K., Kubota, T., Hasegawa, C., Tokuyama, K., Ueki, K., Yamauchi, T., Mishina, M., & Kadowaki, T. (2018). A transgenic mutant mouse line accompanied by the complete deletion of interleukin-33 showed insulin and leptin resistances. bioRxiv. http://biorxiv.org/content/early/2018/09/13/416529.abstract

CBE

Watanabe T, Takeuchi T, Kubota N, Wainai T, Kataoka K, Nakaya T, Sugimoto A, Sato T, Ohira H, Tsujino I, Kumagai K, Kubota T, Hasegawa C, Tokuyama K, Ueki K, Yamauchi T, Mishina M, Kadowaki T. 2018. A transgenic mutant mouse line accompanied by the complete deletion of interleukin-33 showed insulin and leptin resistances. bioRxiv.

MLA

Vancouver

Author

Watanabe, Taku ; Takeuchi, Tomonori ; Kubota, Naoto ; Wainai, Tasuku ; Kataoka, Keisuke ; Nakaya, Toshitaka ; Sugimoto, Ayako ; Sato, Takahiro ; Ohira, Hiroshi ; Tsujino, Ichizo ; Kumagai, Katsuyoshi ; Kubota, Tetsuya ; Hasegawa, Chiaki ; Tokuyama, Kumpei ; Ueki, Kohjiro ; Yamauchi, Toshimasa ; Mishina, Masayoshi ; Kadowaki, Takashi. / A transgenic mutant mouse line accompanied by the complete deletion of interleukin-33 showed insulin and leptin resistances. bioRxiv, 2018.

Bibtex

@techreport{4926a7f831364ea1a1c9f11b28815fef,
title = "A transgenic mutant mouse line accompanied by the complete deletion of interleukin-33 showed insulin and leptin resistances",
abstract = "Interleukin (IL) -33 has been identified as a member of the IL-1 family. Members of the IL-1 family have been reported to be involved in the regulation of energy homeostasis and glucose metabolism. Homozygous transgenic mutant mice of FLP14 line, that we previously generated, unexpectedly developed mature-onset obesity and diabetes. Through genetic investigations, we found that insertion of the transgenes had resulted in complete deletion of the Il33 gene. These obese male homozygous mutant mice exhibited hyperphagia with hyperleptinemia and insulin resistance caused by increased hepatic gluconeogenesis and decreased glucose uptake in skeletal muscle. As a result of examining preobese male homozygous mutant mice to investigate with the exclusion of the effect of obesity, hyperphagia with hyperleptinemina and insulin resistance caused by decreased glucose uptake in skeletal muscle were already observed, but the increased hepatic glucose production was not. To investigate whether the insulin resistance was caused by deletion of the Il33 gene, we treated these preobese homozygous mutant mice with recombinant IL-33 protein and noted a significant improvement in insulin resistance. Thus, insulin resistance in these homozygous mutant mice was caused, at least in part, by IL-33 deficiency, suggesting a favorable role of IL-33 for glucose metabolism in the skeletal muscle.",
author = "Taku Watanabe and Tomonori Takeuchi and Naoto Kubota and Tasuku Wainai and Keisuke Kataoka and Toshitaka Nakaya and Ayako Sugimoto and Takahiro Sato and Hiroshi Ohira and Ichizo Tsujino and Katsuyoshi Kumagai and Tetsuya Kubota and Chiaki Hasegawa and Kumpei Tokuyama and Kohjiro Ueki and Toshimasa Yamauchi and Masayoshi Mishina and Takashi Kadowaki",
year = "2018",
language = "English",
publisher = "bioRxiv",
type = "WorkingPaper",
institution = "bioRxiv",

}

RIS

TY - UNPB

T1 - A transgenic mutant mouse line accompanied by the complete deletion of interleukin-33 showed insulin and leptin resistances

AU - Watanabe, Taku

AU - Takeuchi, Tomonori

AU - Kubota, Naoto

AU - Wainai, Tasuku

AU - Kataoka, Keisuke

AU - Nakaya, Toshitaka

AU - Sugimoto, Ayako

AU - Sato, Takahiro

AU - Ohira, Hiroshi

AU - Tsujino, Ichizo

AU - Kumagai, Katsuyoshi

AU - Kubota, Tetsuya

AU - Hasegawa, Chiaki

AU - Tokuyama, Kumpei

AU - Ueki, Kohjiro

AU - Yamauchi, Toshimasa

AU - Mishina, Masayoshi

AU - Kadowaki, Takashi

PY - 2018

Y1 - 2018

N2 - Interleukin (IL) -33 has been identified as a member of the IL-1 family. Members of the IL-1 family have been reported to be involved in the regulation of energy homeostasis and glucose metabolism. Homozygous transgenic mutant mice of FLP14 line, that we previously generated, unexpectedly developed mature-onset obesity and diabetes. Through genetic investigations, we found that insertion of the transgenes had resulted in complete deletion of the Il33 gene. These obese male homozygous mutant mice exhibited hyperphagia with hyperleptinemia and insulin resistance caused by increased hepatic gluconeogenesis and decreased glucose uptake in skeletal muscle. As a result of examining preobese male homozygous mutant mice to investigate with the exclusion of the effect of obesity, hyperphagia with hyperleptinemina and insulin resistance caused by decreased glucose uptake in skeletal muscle were already observed, but the increased hepatic glucose production was not. To investigate whether the insulin resistance was caused by deletion of the Il33 gene, we treated these preobese homozygous mutant mice with recombinant IL-33 protein and noted a significant improvement in insulin resistance. Thus, insulin resistance in these homozygous mutant mice was caused, at least in part, by IL-33 deficiency, suggesting a favorable role of IL-33 for glucose metabolism in the skeletal muscle.

AB - Interleukin (IL) -33 has been identified as a member of the IL-1 family. Members of the IL-1 family have been reported to be involved in the regulation of energy homeostasis and glucose metabolism. Homozygous transgenic mutant mice of FLP14 line, that we previously generated, unexpectedly developed mature-onset obesity and diabetes. Through genetic investigations, we found that insertion of the transgenes had resulted in complete deletion of the Il33 gene. These obese male homozygous mutant mice exhibited hyperphagia with hyperleptinemia and insulin resistance caused by increased hepatic gluconeogenesis and decreased glucose uptake in skeletal muscle. As a result of examining preobese male homozygous mutant mice to investigate with the exclusion of the effect of obesity, hyperphagia with hyperleptinemina and insulin resistance caused by decreased glucose uptake in skeletal muscle were already observed, but the increased hepatic glucose production was not. To investigate whether the insulin resistance was caused by deletion of the Il33 gene, we treated these preobese homozygous mutant mice with recombinant IL-33 protein and noted a significant improvement in insulin resistance. Thus, insulin resistance in these homozygous mutant mice was caused, at least in part, by IL-33 deficiency, suggesting a favorable role of IL-33 for glucose metabolism in the skeletal muscle.

M3 - Working paper

BT - A transgenic mutant mouse line accompanied by the complete deletion of interleukin-33 showed insulin and leptin resistances

PB - bioRxiv

ER -