Biglycan reduces body weight by regulating food intake in mice and improves glucose metabolism through AMPK/AKT dual pathways in skeletal muscle

In Hyeok Chung; Shin Ae Kim; Seolsong Kim; Jung Ok Lee; Clara Yongjoo Park; Juhee Lee; Jun Kang; Jin Young Lee; Ilhyeok Seo; Hye Jeong Lee; Jeong Ah Han; Min Ju Kang; Eunice Lim; Su Jin Kim; Sang Woo Wu; Joo Yeon Oh; Ji Hyung Chung; Eun Kyoung Kim; Hyeon Soo Kim; Min Jeong Shin

doi:10.1096/fj.202002039RR

Biglycan reduces body weight by regulating food intake in mice and improves glucose metabolism through AMPK/AKT dual pathways in skeletal muscle

In Hyeok Chung, Shin Ae Kim, Seolsong Kim, Jung Ok Lee, Clara Yongjoo Park, Juhee Lee, Jun Kang, Jin Young Lee, Ilhyeok Seo, Hye Jeong Lee, Jeong Ah Han, Min Ju Kang, Eunice Lim, Su Jin Kim, Sang Woo Wu, Joo Yeon Oh, Ji Hyung Chung, Eun Kyoung Kim, Hyeon Soo Kim, Min Jeong Shin

Research output: Contribution to journal › Article › peer-review

3 Citations (Scopus)

Abstract

While biglycan (BGN) is suggested to direct diverse signaling cascades, the effects of soluble BGN as a ligand on metabolic traits have not been studied. Herein, we tested the effects of BGN on obesity in high-fat diet (HFD)-induced obese animals and glucose metabolism, with the underlying mechanism responsible for observed effects in vitro. Our results showed that BGN administration (1 mg/kg body weight, intraperitoneally) significantly prevented HFD-induced obesity, and this was mainly attributed to reduced food intake. Also, intracerebroventricular injection of BGN reduced food intake and body weight. The underlying mechanism includes modulation of neuropeptides gene expression involved in appetite in the hypothalamus in vitro and in vivo. In addition, BGN regulates glucose metabolism as shown by improved glucose tolerance in mice as well as AMPK/AKT dual pathway-driven enhanced glucose uptake and GLUT4 translocation in L6 myoblast cells. In conclusion, our results suggest BGN as a potential therapeutic target to treat risk factors for metabolic diseases.

Original language	English
Article number	e21794
Journal	FASEB Journal
Volume	35
Issue number	8
DOIs	https://doi.org/10.1096/fj.202002039RR
Publication status	Published - 2021 Aug

Bibliographical note

Funding Information:
This study was supported by the Basic Science Research Program through the NRF funded by the Ministry of Science and ICT (NRF-2020R1A2C2005580 & NRF-2020R1A2B5B02001468)

Funding Information:
This study was supported by the Basic Science Research Program through the NRF funded by the Ministry of Science and ICT (NRF‐2020R1A2C2005580 & NRF‐2020R1A2B5B02001468)

Publisher Copyright:
© 2021 Federation of American Societies for Experimental Biology

Keywords

AKT
AMPK
biglycan
food intake
glucose uptake
obesity

ASJC Scopus subject areas

Biotechnology
Biochemistry
Molecular Biology
Genetics

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1096/fj.202002039RR

Cite this

Chung, I. H., Kim, S. A., Kim, S., Lee, J. O., Park, C. Y., Lee, J., Kang, J., Lee, J. Y., Seo, I., Lee, H. J., Han, J. A., Kang, M. J., Lim, E., Kim, S. J., Wu, S. W., Oh, J. Y., Chung, J. H., Kim, E. K., Kim, H. S., & Shin, M. J. (2021). Biglycan reduces body weight by regulating food intake in mice and improves glucose metabolism through AMPK/AKT dual pathways in skeletal muscle. FASEB Journal, 35(8), Article e21794. https://doi.org/10.1096/fj.202002039RR

Chung, IH, Kim, SA, Kim, S, Lee, JO, Park, CY, Lee, J, Kang, J, Lee, JY, Seo, I, Lee, HJ, Han, JA, Kang, MJ, Lim, E, Kim, SJ, Wu, SW, Oh, JY, Chung, JH, Kim, EK, Kim, HS & Shin, MJ 2021, 'Biglycan reduces body weight by regulating food intake in mice and improves glucose metabolism through AMPK/AKT dual pathways in skeletal muscle', FASEB Journal, vol. 35, no. 8, e21794. https://doi.org/10.1096/fj.202002039RR

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title = "Biglycan reduces body weight by regulating food intake in mice and improves glucose metabolism through AMPK/AKT dual pathways in skeletal muscle",

abstract = "While biglycan (BGN) is suggested to direct diverse signaling cascades, the effects of soluble BGN as a ligand on metabolic traits have not been studied. Herein, we tested the effects of BGN on obesity in high-fat diet (HFD)-induced obese animals and glucose metabolism, with the underlying mechanism responsible for observed effects in vitro. Our results showed that BGN administration (1 mg/kg body weight, intraperitoneally) significantly prevented HFD-induced obesity, and this was mainly attributed to reduced food intake. Also, intracerebroventricular injection of BGN reduced food intake and body weight. The underlying mechanism includes modulation of neuropeptides gene expression involved in appetite in the hypothalamus in vitro and in vivo. In addition, BGN regulates glucose metabolism as shown by improved glucose tolerance in mice as well as AMPK/AKT dual pathway-driven enhanced glucose uptake and GLUT4 translocation in L6 myoblast cells. In conclusion, our results suggest BGN as a potential therapeutic target to treat risk factors for metabolic diseases.",

keywords = "AKT, AMPK, biglycan, food intake, glucose uptake, obesity",

author = "Chung, {In Hyeok} and Kim, {Shin Ae} and Seolsong Kim and Lee, {Jung Ok} and Park, {Clara Yongjoo} and Juhee Lee and Jun Kang and Lee, {Jin Young} and Ilhyeok Seo and Lee, {Hye Jeong} and Han, {Jeong Ah} and Kang, {Min Ju} and Eunice Lim and Kim, {Su Jin} and Wu, {Sang Woo} and Oh, {Joo Yeon} and Chung, {Ji Hyung} and Kim, {Eun Kyoung} and Kim, {Hyeon Soo} and Shin, {Min Jeong}",

note = "Funding Information: This study was supported by the Basic Science Research Program through the NRF funded by the Ministry of Science and ICT (NRF-2020R1A2C2005580 & NRF-2020R1A2B5B02001468) Funding Information: This study was supported by the Basic Science Research Program through the NRF funded by the Ministry of Science and ICT (NRF‐2020R1A2C2005580 & NRF‐2020R1A2B5B02001468) Publisher Copyright: {\textcopyright} 2021 Federation of American Societies for Experimental Biology",

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AU - Chung, In Hyeok

AU - Kim, Shin Ae

AU - Kim, Seolsong

AU - Lee, Jung Ok

AU - Park, Clara Yongjoo

AU - Lee, Juhee

AU - Kang, Jun

AU - Lee, Jin Young

AU - Seo, Ilhyeok

AU - Lee, Hye Jeong

AU - Han, Jeong Ah

AU - Kang, Min Ju

AU - Lim, Eunice

AU - Kim, Su Jin

AU - Wu, Sang Woo

AU - Oh, Joo Yeon

AU - Chung, Ji Hyung

AU - Kim, Eun Kyoung

AU - Kim, Hyeon Soo

AU - Shin, Min Jeong

N1 - Funding Information: This study was supported by the Basic Science Research Program through the NRF funded by the Ministry of Science and ICT (NRF-2020R1A2C2005580 & NRF-2020R1A2B5B02001468) Funding Information: This study was supported by the Basic Science Research Program through the NRF funded by the Ministry of Science and ICT (NRF‐2020R1A2C2005580 & NRF‐2020R1A2B5B02001468) Publisher Copyright: © 2021 Federation of American Societies for Experimental Biology

PY - 2021/8

Y1 - 2021/8

N2 - While biglycan (BGN) is suggested to direct diverse signaling cascades, the effects of soluble BGN as a ligand on metabolic traits have not been studied. Herein, we tested the effects of BGN on obesity in high-fat diet (HFD)-induced obese animals and glucose metabolism, with the underlying mechanism responsible for observed effects in vitro. Our results showed that BGN administration (1 mg/kg body weight, intraperitoneally) significantly prevented HFD-induced obesity, and this was mainly attributed to reduced food intake. Also, intracerebroventricular injection of BGN reduced food intake and body weight. The underlying mechanism includes modulation of neuropeptides gene expression involved in appetite in the hypothalamus in vitro and in vivo. In addition, BGN regulates glucose metabolism as shown by improved glucose tolerance in mice as well as AMPK/AKT dual pathway-driven enhanced glucose uptake and GLUT4 translocation in L6 myoblast cells. In conclusion, our results suggest BGN as a potential therapeutic target to treat risk factors for metabolic diseases.

AB - While biglycan (BGN) is suggested to direct diverse signaling cascades, the effects of soluble BGN as a ligand on metabolic traits have not been studied. Herein, we tested the effects of BGN on obesity in high-fat diet (HFD)-induced obese animals and glucose metabolism, with the underlying mechanism responsible for observed effects in vitro. Our results showed that BGN administration (1 mg/kg body weight, intraperitoneally) significantly prevented HFD-induced obesity, and this was mainly attributed to reduced food intake. Also, intracerebroventricular injection of BGN reduced food intake and body weight. The underlying mechanism includes modulation of neuropeptides gene expression involved in appetite in the hypothalamus in vitro and in vivo. In addition, BGN regulates glucose metabolism as shown by improved glucose tolerance in mice as well as AMPK/AKT dual pathway-driven enhanced glucose uptake and GLUT4 translocation in L6 myoblast cells. In conclusion, our results suggest BGN as a potential therapeutic target to treat risk factors for metabolic diseases.

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KW - AMPK

KW - biglycan

KW - food intake

KW - glucose uptake

KW - obesity

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DO - 10.1096/fj.202002039RR

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JO - FASEB Journal

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ER -

Biglycan reduces body weight by regulating food intake in mice and improves glucose metabolism through AMPK/AKT dual pathways in skeletal muscle

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

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