The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.
Metabolic and cellular plasticity in white adipose tissue I: effects of β3-adrenergic receptor activation
Abstract
Selective agonists of β 3-adrenergic receptors (Adrb3) exhibit potent anti-diabetes properties in rodent models when given chronically, yet the mechanisms involved are poorly understood. A salient feature of chronic Adrb3 activation is pronounced remodeling of white adipose tissue (WAT), which includes mitochondrial biogenesis and elevation of metabolic rate. To gain insights into potential mechanisms underlying WAT remodeling, the time course of remodeling induced by the Adrb3 agonist CL-316,243 (CL) was analyzed using histological, physiological, and global gene profiling approaches. The results indicate that continuous CL treatment induced a transient proinflammatory response that was followed by cellular proliferation among stromal cells and multilocular adipoctyes. CL treatment strongly fragmented the central lipid storage droplet of mature adipocytes and induced mitochondrial biogenesis within these cells. Mitochondrial biogenesis was correlated with the upregulation of genes involved in fatty acid oxidation and mitochondrial electron transport activity. The elevated catabolic activity of WAT was temporally correlated with upregulation of peroxisome proliferator-activated receptor-α and its target genes, suggesting involvement of this transcription factor in coordinating the gene program that elevates WAT catabolic activity.
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“Recently, Kosteli and colleagues demonstrated that acute weight loss is unexpectedly associated with a rapid -albeit transient -lipolytic-driven recruitment of macrophages into AT (39), thereby confirming similar reports by Granneman and colleagues (44).”
From Adipose tissue remodeling and obesity (2011) · cites this paper as [44]
In the citing paper
“Mitochondrial levels in white adipocytes are also increased in response to adrenergic stimulation, -3 agonists, and CB1 blockade in mice (195,199,200), again in parallel with enhanced insulin sensitivity.”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [199]
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Metadata
- Authors
- Granneman, J. G., Li, P., Zhu, Z., & Lu, Y.
- Affiliations
- Wayne State University (US)
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2005-10
- Volume
- 289
- Issue
- 4
- Pages
- E608-E616
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W1981281539
- Cited by
- 298
- References
- 46
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 9 · 2023: 11 · 2022: 6 · 2021: 14 · 2020: 11 · 2019: 17 · 2018: 12 · 2017: 15 · 2016: 23 · 2015: 22 · 2014: 28 · 2013: 26 · 2012: 21
- FWCI
- 5.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r21dk066505-02)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 062292, DK 066505)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- beta3-adrenergic receptor, white adipose tissue remodeling, CL316,243, mitochondrial biogenesis, adipocyte lipolysis, fatty acid oxidation, PPARα, adipocyte inflammation, adipocyte proliferation, metabolic rate, anti-diabetic effects, adipocyte gene expression
- MeSH terms
- Adaptation, Physiological, Adipose Tissue, Animals, Dioxoles, Energy Metabolism, Male, Mice, Inbred C57BL, Mitochondria, Gene Expression Profiling, Receptors, Adrenergic, beta-3, Cell Size, Cell Proliferation, Mice, Adrenergic beta-3 Receptor Agonists
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