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[논문] High-Sucrose Diet Accelerates Arthritis Progression in a Collagen-Induced Rheumatoid Arthritis Model

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논문제목(Title)

[논문] High-Sucrose Diet Accelerates Arthritis Progression in a Collagen-Induced Rheumatoid Arthritis Model

학술지명(Journal)

MOLECULAR NUTRITION & FOOD RESEARCH

ImpactFactor

5.2

ISSN_ISBN

1613-4125

학술지볼륨권호(Volume)

Volume 67, Issue 20

SCI구분

SCIE

초록(Abstract)

Scope: High dietary sugar and sweeteners are suspected to cause the
development of rheumatoid arthritis (RA) symptoms through the induction of
proinflammatory cytokine release. However, the mechanisms by which
increased dietary sugar affects RA etiology are not yet fully understood. The
study uses a mouse model of collagen-induced RA (CIA) to investigate the
relationship between excessive sugar consumption and RA risk.
Methods and results: RA-associated pathological features are assessed in the
nonimmunized (NI) control group, the CIA-positive control group, and the
CIA + high-sucrose diet (CIA+HS, 63% calories from sucrose) group.
Compared with the CIA group, the CIA+HS group shows a greater increase in
paw thickness and clinical scores, as well as, a higher degree of pannus
formation and inflammation in the knee, ankle, and sole tissues. Moreover,
the infiltration of immune cells is increased in the CIA+HS group. Although
the expression of hepatic lipogenic genes, is not altered, that of toll-like
receptor (TLR4) and IL-1𝜷 is considerably elevated in the CIA+HS group.
Conclusions: These findings suggest that excessive sucrose consumption
causes hepatic fibrosis and inflammation, contributing to the pathophysiology
of RA.

주저자명(FirstAuthor)

Yunhui Min, Yunji Heo

공동저자명(Co-Author)

Dahye Kim, Mangeun Kim, Jiwon Yang, Hyo Jin Kim, Youngheun Jee, Mrinmoy Ghosh, Inhae Kang,* and Young-Ok Son*

학술지출판일자(PublicationDate)

2023-09-08

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2023-12-07

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컬렉션
[손영옥] 괭생이모자반 기반 유효활성 성분의 호흡기 손상 억제 기전구명 및 NGS 생물학적 통합분석을 통한 호흡기손상 바이오마커 개발 및 표적인자 발굴(2023)
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2023-12-07
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  • Version 1 2023-12-05
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허윤지 ( 2023-12-07 ) [논문] High-Sucrose Diet Accelerates Arthritis Progression in a Collagen-Induced Rheumatoid Arthritis Model

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