Catalpol Ameliorates High-Fat Diet-Induced Insulin Resistance and Adipose Tissue Inflammation by Suppressing the JNK and NF-Κb Pathways
Abstract
Catalpol, a bioactive component from the root of Rehmannia glutinosa, has been shown to possess hypoglycemic effects in type 2 diabetic animal models, however, the underlying mechanisms remain poorly understood. Here we investigated the effect of catalpol on high-fat diet (HFD)-induced insulin resistance and adipose tissue inflammation in mice. Oral administration of catalpol at 100 mg/kg for 4 weeks had no effect on body weight of HFD-induced obese mice, but it significantly improved fasting glucose and insulin levels, glucose tolerance and insulin tolerance. Moreover, macrophage infiltration into adipose tissue was markedly reduced by catalpol. Intriguingly, catalpol also significantly reduced mRNA expressions of M1 pro-inflammatory cytokines, but increased M2 anti-inflammatory gene expressions in adipose tissue. Concurrently, catalpol significantly suppressed the c-Jun NH2-terminal kinase (JNK) and nuclear factor-kappa B (NF-κB) signaling pathways in adipose tissue. Collectively, these results suggest that catalpol may ameliorate HFD-induced insulin resistance in mice by attenuating adipose tissue inflammation and suppressing the JNK and NF-κB pathways, and thus provide important new insights into the underlying mechanisms of the antidiabetic effect of catalpol.
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Catalpol ameliorates insulin resistance induced by HFD by suppressing the NF-κB pathway.
“Indeed, catalpol exerts an anti-hyperglicemic effect in STZ-induced diabetic rats (Huang et al., 2010) and ameliorates insulin resistance induced by HFD by suppressing the NF-κB pathway (Zhou et al., 2015).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Zhou et al., 2015
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- Authors
- Zhou, J., Xu, G., Ma, S., Li, F., Yuan, M., Xu, H., & Huang, K.
- Affiliations
- Huazhong University of Science and Technology (CN)
- Corresponding author
- Zhou, Jun
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 467
- Issue
- 4
- Pages
- 853-858
- ISSN
- 0006-291X (ISSN-L)
- OpenAlex
- W2160019821
- Cited by
- 97
- References
- 31
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 6 · 2023: 6 · 2022: 9 · 2021: 5 · 2020: 15 · 2019: 16 · 2018: 13 · 2017: 10 · 2016: 5
- FWCI
- 7.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochemical and Biophysical Research Communications (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31270870, 21001045)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- catalpol, Rehmannia glutinosa, insulin resistance, high-fat diet, adipose tissue inflammation, JNK signaling, NF-κB signaling, macrophage infiltration, macrophage polarization, inflammatory cytokines, type 2 diabetes, glucose tolerance, antidiabetic effect
- MeSH terms
- Adipose Tissue, Animals, Anti-Inflammatory Agents, Gene Expression Regulation, Insulin Resistance, Macrophages, Male, Mice, Inbred C57BL, Obesity, Panniculitis, NF-kappa B, MAP Kinase Signaling System, Iridoid Glucosides, Diet, High-Fat
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