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Results: 1 to 2 of 2

Publication Record


Rosiglitazone promotes development of a novel adipocyte population from bone marrow-derived circulating progenitor cells.
Crossno JT, Majka SM, Grazia T, Gill RG, Klemm DJ
(2006) J Clin Invest 116: 3220-8
MeSH Terms: Adipocytes, Adiponectin, Animals, Blotting, Western, Bone Marrow Cells, Bone Marrow Transplantation, CD11 Antigens, Carrier Proteins, Cell Differentiation, Collagenases, Dietary Fats, Female, Flow Cytometry, Green Fluorescent Proteins, Hypoglycemic Agents, Leptin, Leukocyte Common Antigens, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Phase-Contrast, PPAR gamma, Perilipin-1, Phosphoproteins, Reverse Transcriptase Polymerase Chain Reaction, Rosiglitazone, Stem Cells, Thiazolidinediones
Show Abstract · Added August 4, 2015
Obesity and weight gain are characterized by increased adipose tissue mass due to an increase in the size of individual adipocytes and the generation of new adipocytes. New adipocytes are believed to arise from resident adipose tissue preadipocytes and mesenchymal progenitor cells. However, it is possible that progenitor cells from other tissues, in particular BM, could also contribute to development of new adipocytes in adipose tissue. We tested this hypothesis by transplanting whole BM cells from GFP-expressing transgenic mice into wild-type C57BL/6 mice and subjecting them to a high-fat diet or treatment with the thiazolidinedione (TZD) rosiglitazone (ROSI) for several weeks. Histological examination of adipose tissue or FACS of adipocytes revealed the presence of GFP(+) multilocular (ML) adipocytes, whose number was significantly increased by ROSI treatment or high-fat feeding. These ML adipocytes expressed adiponectin, perilipin, fatty acid-binding protein (FABP), leptin, C/EBPalpha, and PPARgamma but not uncoupling protein-1 (UCP-1), the CD45 hematopoietic lineage marker, or the CDllb monocyte marker. They also exhibited increased mitochondrial content. Appearance of GFP(+) ML adipocytes was contemporaneous with an increase in circulating levels of mesenchymal and hematopoietic progenitor cells in ROSI-treated animals. We conclude that TZDs and high-fat feeding promote the trafficking of BM-derived circulating progenitor cells to adipose tissue and their differentiation into ML adipocytes.
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28 MeSH Terms
Chronic ethanol feeding suppresses beta-adrenergic receptor-stimulated lipolysis in adipocytes isolated from epididymal fat.
Kang L, Nagy LE
(2006) Endocrinology 147: 4330-8
MeSH Terms: 3',5'-Cyclic-AMP Phosphodiesterases, 4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone, Adipocytes, Adrenergic beta-Agonists, Animals, Carrier Proteins, Cyclic AMP, Cyclic AMP-Dependent Protein Kinases, Cyclic Nucleotide Phosphodiesterases, Type 4, Diet, Epididymis, Ethanol, Glycerol, Isoproterenol, Lipolysis, Male, Perilipin-1, Phosphodiesterase Inhibitors, Phosphoproteins, Phosphorylation, Rats, Rats, Wistar, Receptors, Adrenergic, beta, Sterol Esterase
Show Abstract · Added March 5, 2013
Chronic ethanol consumption disrupts G protein-dependent signaling pathways in rat adipocytes. Because lipolysis in adipocytes is regulated by G protein-mediated cAMP signal transduction, we hypothesized that cAMP-regulated lipolysis may be vulnerable to long-term ethanol exposure. Male Wistar rats were fed a liquid diet containing ethanol as 35% of total calories or pair-fed a control diet that isocalorically substituted maltose dextrins for ethanol for 4 wk. Lipolysis was measured by glycerol release over 1 h with or without agonists in adipocytes isolated from epididymal fat. Chronic ethanol feeding decreased beta-adrenergic receptor-stimulated lipolysis, but had no effect on basal lipolysis. In response to beta-adrenergic activation, the early peak of cAMP accumulation was suppressed after ethanol feeding, although the basal cAMP concentration in adipocytes did not differ between pair- and ethanol-fed rats. The suppression in cAMP accumulation caused by ethanol feeding was associated with increased activity of phosphodiesterase 4. Chronic ethanol feeding also decreased beta-adrenergic receptor-stimulated protein kinase A activation and phosphorylation of its downstream proteins, perilipin A and hormone-sensitive lipase, the primary lipase-mediating lipolysis. In conclusion, these data suggest that chronic ethanol feeding increased phosphodiesterase 4 activity in adipocytes, resulting in decreased accumulation of cAMP in response to beta-adrenergic activation and a suppression of beta-adrenergic stimulation of lipolysis.
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24 MeSH Terms