Butein is a plant flavonoid chalcone, with presumed anti-adipogenic properties. It was reported to impair preadipocyte differentiation, limit adipose tissue (AT) development and enhance white AT browning in rodents. In this study, we investigated the hypothesis that these effects of butein may occur via reduction of ADAMTS5 (A Disintegrin And Metalloproteinase with ThromboSpondin motifs 5) expression. Murine 3T3-L1 or 3T3-F442A preadipocytes were differentiated into mature adipocytes in the presence of butein or vehicle. At regular time intervals RNA was collected for gene expression studies. Male hemizygous mice for Tg(Ucp1-luc2,-tdTomato)1Kajim (ThermoMouse) were exposed to butein or vehicle, after which ATs were analyzed for Adamts5 and uncoupling protein-1 (Ucp-1) mRNA level changes. During preadipocyte differentiation, butein (25 - 50 mM) did not affect Adamts5 or Ucp-1 expression. Oil Red O analysis and monitoring of differentiation markers failed to demonstrate effects of butein on the differentiation extent. Furthermore, butein administration to the ThermoMouse (10 or 20 mg/kg, 4 days) or to the C57BL6/Rj mice (20 mg/kg, 4 weeks) did not enhance Adamts5 or Ucp-1 expression. Thus, we could not demonstrate marked effects of butein on the preadipocyte differentiation extent or AT development and browning, nor on Adamts5 or Ucp-1 gene expression during these processes.
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http://dx.doi.org/10.1080/21623945.2019.1617619 | DOI Listing |
Int J Mol Sci
December 2024
Laboratorio Universitario de Análisis Clínicos e Investigación, Universidad de Sonora (LUACI) Departamento de Ciencias Químico-Biológicas y Agropecuarias, Campus Navojoa. Lázaro Cárdenas del Río #100, CP 85880 Navojoa, Sonora, Mexico.
Sucralose, a commonly nonnutritive sweetener used in daily products of habitual diet, is related to impairing the gut microbiome by disrupting inflammatory response, promoting weight gain by increasing adipose tissue and promoting chronic inflammatory processes. Considering the impact of sucralose in the development of metabolic diseases, in this work, we focused on the impact of sucralose on the adipocyte differentiation process to determine if sucralose can promote adipogenesis and increase adipose tissue depots in PCS 210 010 human preadipocytes cell line. Sucralose at 25 (S25) and 100 ng/µL (S100) concentrations were tested against control with no edulcorant (NS) during the adipocyte differentiation process at 48 h and 96 h.
View Article and Find Full Text PDFAntioxidants (Basel)
December 2024
Institute of Biomedical Sciences, Federal University of Rio de Janeiro (UFRJ), Avenida Carlos Chagas Filho 373, bloco F, 3° floor, room 301, Cidade Universitária, Rio de Janeiro CEP 21941-902, RJ, Brazil.
Obesity is characterized by an imbalance between energy intake and expenditure that triggers abnormal growth of adipose tissues. Dimethyl fumarate (DMF) and its primary active metabolite, monomethyl fumarate (MMF), are Nrf2 activators and have been recognized as strategic antioxidants. This study aimed to evaluate the potential of MMF and DMF to interfere with adipogenesis and obesity, and identify the molecular mechanisms involved.
View Article and Find Full Text PDFAnimals (Basel)
December 2024
College of Life Science and Engineering, Northwest Minzu University, Lanzhou 730030, China.
Tail fat is essential for sheep survival in extreme environments, yet its significance is often overlooked, leading to the decline of fat-tailed breeds. This study identified a novel lncRNA, (), through transcriptome sequencing, showing differential expression in the tail adipose tissues of Lanzhou Fat-Tailed (LFT) sheep and Tibetan (TS) sheep. Highly expressed in adipose tissues, inhibits preadipocyte proliferation and promotes 3T3-L1 differentiation, suggesting its role in regulating fat deposition.
View Article and Find Full Text PDFEMBO J
January 2025
Department of Immunology and Regenerative Biology, Weizmann Institute of Science, 76100, Rehovot, Israel.
Mitochondrial carrier homolog 2 (MTCH2) is a regulator of apoptosis, mitochondrial dynamics, and metabolism. Loss of MTCH2 results in mitochondrial fragmentation, an increase in whole-body energy utilization, and protection against diet-induced obesity. In this study, we used temporal metabolomics on HeLa cells to show that MTCH2 deletion results in a high ATP demand, an oxidized cellular environment, and elevated utilization of lipids, amino acids, and carbohydrates, accompanied by a decrease in several metabolites.
View Article and Find Full Text PDFPLoS One
December 2024
Metabolic Research Laboratories, Wellcome Trust-Medical Research Council Institute of Metabolic Science, University of Cambridge, Cambridge, United Kingdom.
Objective: A biallelic missense mutation in mitofusin 2 (MFN2) causes multiple symmetric lipomatosis and partial lipodystrophy, implicating disruption of mitochondrial fusion or interaction with other organelles in adipocyte differentiation, growth and/or survival. In this study, we aimed to document the impact of loss of mitofusin 1 (Mfn1) or 2 (Mfn2) on adipogenesis in cultured cells.
Methods: We characterised adipocyte differentiation of wildtype (WT), Mfn1-/- and Mfn2-/- mouse embryonic fibroblasts (MEFs) and 3T3-L1 preadipocytes in which Mfn1 or 2 levels were reduced using siRNA.
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