Artemisia scoparia Enhances Adipocyte Development and Endocrine Function In Vitro and Enhances Insulin Action In Vivo
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BACKGROUND: Failure of adipocytes to expand during periods of energy excess can result in undesirable metabolic consequences such as ectopic fat accumulation and insulin resistance. Blinded screening studies have indicated that Artemisia scoparia (SCO) extracts can enhance adipocyte differentiation and lipid accumulation in cultured adipocytes. The present study tested the hypothesis that SCO treatment modulates fat cell development and function in vitro and insulin sensitivity in adipose tissue in vivo. METHODS: In vitro experiments utilized a Gal4-PPARγ ligand binding domain (LBD) fusion protein-luciferase reporter assay to examine PPARγ activation. To investigate the ability of SCO to modulate adipogenesis and mature fat cell function in 3T3-L1 cells, neutral lipid accumulation, gene expression, and protein secretion were measured by Oil Red O staining, qRT-PCR, and immunoblotting, respectively. For the in vivo experiments, diet-induced obese (DIO) C57BL/6J mice were fed a high-fat diet (HFD) or HFD containing 1% w/w SCO for four weeks. Body weight and composition, food intake, and fasting glucose and insulin levels were measured. Phospho-activation and expression of insulin-sensitizing proteins in epididymal adipose tissue (eWAT) were measured by immunoblotting. RESULTS: Ethanolic extracts of A. scoparia significantly activated the PPARγ LBD and enhanced lipid accumulation in differentiating 3T3-L1 cells. SCO increased the transcription of several PPARγ target genes in differentiating 3T3-L1 cells and rescued the negative effects of tumor necrosis factor α on production and secretion of adiponectin and monocyte chemoattractant protein-1 in fully differentiated fat cells. DIO mice treated with SCO had elevated adiponectin levels and increased phosphorylation of AMPKα in eWAT when compared to control mice. In SCO-treated mice, these changes were also associated with decreased fasting insulin and glucose levels. CONCLUSION: SCO has metabolically beneficial effects on adipocytes in vitro and adipose tissue in vivo, highlighting its potential as a metabolically favorable botanical supplement.
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Disruption of adipocyte differentiation and expansion could lead to ectopic fat accumulation and metabolic alterations such as insulin resistance and type 2 diabetes mellitus.
“Although the inhibition of adipogenesis may be considered an interesting strategy for obesity prevention, some evidence highlights that the disruption of adipocyte differentiation and expansion could lead to ectopic fat accumulation and metabolic alterations, such as insulin resistance and type 2 diabetes mellitus [30].”
From The Role of Resveratrol Administration in Human Obesity (2021) · cites this paper as [30]
An ethanolic extract of Artemisia scoparia (SCO), a PPARγ agonist, showed both in-vitro and in-vivo beneficial effects on insulin sensitivity and adipocyte function.
“Interestingly, an agonist of PPARγ, an ethanolic extract of Artemisia scoparia (SCO), showed both in-vitro and in-vivo beneficial effects on insulin sensitivity and adipocyte function [30].”
From The Role of Resveratrol Administration in Human Obesity (2021) · cites this paper as [30]
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References 47 · Cited by 30
- Authors
- Richard, A. J., Fuller, S., Fedorcenco, V., Beyl, R., Burris, T. P., Mynatt, R., Ribnicky, D. M., & Stephens, J. M.
- Affiliations
- Pennington Biomedical Research Center (US)
- Saint Louis University (US)
- Rutgers, The State University of New Jersey (US)
- Corresponding author
- Stephens, Jacqueline M.
- ORCID
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2014-06-10
- Volume
- 9
- Issue
- 6
- Pages
- e98897
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4051605
- OpenAlex
- W1987525929
- Cited by
- 30
- References
- 47
- Citations by year
- 2026: 4 · 2023: 1 · 2022: 3 · 2021: 6 · 2020: 4 · 2019: 3 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 2
- FWCI
- 0.96
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Civil War Book Review (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Louisiana Clinical and Translational Science Center (U54GM104940, 1 U54 GM104940, GM104940)
- National Institutes of Health (NIH 2P30DK072476, GM104940)
- Nutrition Obesity Research Center, University of North Carolina (NIH 2P30‐DK072476, U54 GM104940)
- National Institute of General Medical Sciences (NIH-8-P20-GM103528, P20GM103528, GM104940, GM103528, U54GM104940)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK072476)
- National Center for Complementary and Integrative Health (P50AT002776, T32AT004094)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- Artemisia scoparia, adipogenesis, PPARγ activation, insulin sensitivity, diet-induced obesity, high-fat diet, adiponectin, MCP-1, TNF-α, AMPK phosphorylation, 3T3-L1 cells, lipid accumulation, herbal supplements, insulin resistance
- MeSH terms
- Adipose Tissue, Animals, Blood Glucose, Body Composition, Cell Line, Dose-Response Relationship, Drug, Endocrine System, Gene Expression Regulation, Humans, Insulin, Male, Plant Extracts, Tumor Necrosis Factor-alpha, Adipocytes, Artemisia, 3T3-L1 Cells, PPAR gamma, Adipogenesis, Mice, Adiponectin, Adipokines, AMP-Activated Protein Kinases
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