Luteolin Enhances Insulin Sensitivity via Activation of PPARγ Transcriptional Activity in Adipocytes

Ding, Li; Jin, Daozhong; Chen, Xiaoli

doi:10.1016/j.jnutbio.2009.07.009

Cited by 159Flavonoids in Medical ResearchAdipokines, Inflammation, and Metabolic DiseasesNatural Antidiabetic Agents Studies

Luteolin Enhances Insulin Sensitivity via Activation of PPARγ Transcriptional Activity in Adipocytes

Ding, Li, Jin, Daozhong, Chen, Xiaoli·2010·The Journal of Nutritional Biochemistry

DOI 10.1016/j.jnutbio.2009.07.009

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Abstract

Obesity and insulin resistance have been linked to a low-grade chronic inflammatory response characterized by increased macrophage infiltration, altered cytokine production and activation of inflammatory signaling pathway in adipose tissue. Pharmacological agents and natural products that are capable of reducing inflammatory activity possess anti-diabetic properties. Luteolin, a naturally occurring flavonoid, has been demonstrated to inhibit lipopolysaccharide-induced tumor necrosis factor-α (TNFα) release and activation of NF-κB pathway in macrophages. However, little is known about the mechanism and effect of luteolin on inflammation-related insulin resistance in adipocytes. In this study, we investigated the effect of luteolin on insulin action in 3T3-L1 adipocytes and primary adipose cells. Here we showed that luteolin treatment for 24 h increased the response of glucose uptake to insulin stimulation in 3T3-L1 adipocytes. Our results also demonstrated that luteolin enhanced Akt2 phosphorylation in an insulin-stimulated state. Furthermore, luteolin treatment decreased mRNA levels of TNFα, interleukin-6 and MCP-1, while it increased the gene expression of adiponectin and leptin in 3T3-L1 adipocytes and primary mouse adipose cells. Most interestingly, we found that treatment of luteolin markedly enhanced peroxisome proliferator-activated receptor γ (PPARγ) transcriptional activity in 3T3-L1 adipocytes, and luteolin-increased expression of adiponectin and leptin was blocked by GW9662, a PPARγ antagonist. Thus, our data suggest that luteolin influences insulin action and production of adipokines/cytokines in adipocytes by activating the PPARγ pathway.

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Luteolin improves insulin sensitivity in many cell types, including adipocytes and endothelial cells.
“luteolin has been shown to improve insulin sensitivity in many cell types, including adipocytes and endothelial cells (Ding et al., 2010; Deqiu et al., 2011)”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Ding et al., 2010

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Luteolin is a bioflavonoid that attenuates adipocyte-derived inflammatory responses via suppression of nuclear factor-κB/mitogen-activated protein kinases pathway
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Authors: Ding, L., Jin, D., & Chen, X.
Affiliations: University of Minnesota (US)
Corresponding author: Chen, Xiaoli
ORCID: Ding, Li
Jin, Daozhong
Chen, Xiaoli
Venue: The Journal of Nutritional Biochemistry
Publisher: Elsevier BV
Published: 2010-10
Volume: 21
Issue: 10
Pages: 941-947
ISSN: 0955-2863 (ISSN-L)
DOI: 10.1016/j.jnutbio.2009.07.009
OpenAlex: W2133654191
Cited by: 159
References: 43
Citations by year: 2026: 4 · 2025: 9 · 2024: 15 · 2023: 16 · 2022: 12 · 2021: 12 · 2020: 17 · 2019: 12 · 2018: 8 · 2017: 4 · 2016: 8 · 2015: 9 · 2014: 9 · 2013: 10 · 2012: 9
FWCI: 3.37
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: The Journal of Nutritional Biochemistry (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (P30DK050456)
Topics: Health Sciences › Medicine › Pharmacology › Flavonoids in Medical Research
Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
Keywords: luteolin, insulin sensitivity, PPARγ, adipocytes, insulin resistance, adipose tissue inflammation, adipokines, adiponectin, leptin, TNF-α, interleukin-6, MCP-1, Akt2 phosphorylation, glucose uptake, flavonoids, obesity
MeSH terms: Animals, Base Sequence, Insulin Resistance, Phosphorylation, RNA, Messenger, Transcription, Genetic, Signal Transduction, Cytokines, Adipocytes, DNA Primers, Inflammation Mediators, Electrophoretic Mobility Shift Assay, 3T3-L1 Cells, Luteolin, PPAR gamma, Mice

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Luteolin Enhances Insulin Sensitivity via Activation of PPARγ Transcriptional Activity in Adipocytes

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Integrity signals

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