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      The Inhibitory Effects of Juglanin on Adipogenesis in 3T3-L1 Adipocytes

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          Deregulation of adipogenesis plays an important role in obesity and other metabolism disorders. PPAR, C/EBP and SREBP1c are key transcriptional factors involved in adipogenesis and lipogenesis. Juglanin is a natural compound belonging to flavonoids, and it has been reported that juglanin has a potent inhibitory effect on inflammation and certain type of cancers. However, the effects of juglanin in adipogenesis have not been reported before.

          Materials and Methods

          3T3-L1 preadipocytes were incubated with differentiation induction medium in the presence or absence of 0.5, 2.5, or 5 µM juglanin for an 8-day differentiation period. The lipid droplets accumulated in the cytoplasm were monitored by Oil Red O staining on days 0, 2, 5, and 8. The regulatory effects of juglanin on adipogenesis-related genes and proteins were investigated by real-time polymerase chain reaction and Western blot analysis.


          Juglanin significantly decreased lipid accumulation in differentiated adipocytes. Our findings show that juglanin reduced the expression of C/EBPα, C/EBPβ, and SREBP-1c without affecting PPARα or PPARγ expression. Additionally, juglanin increased the activation of the SIRT1/AMPK signaling pathway through the phosphorylation of AMPKα. Finally, we performed an AMPK inhibitor experiment, which revealed that the inhibitory effects of juglanin on adipogenesis are mediated through AMPK.


          Juglanin can prevent adipogenesis by suppressing lipid accumulation and the differentiation of preadipocytes. The mechanism of juglanin regulating adipogenesis requires further investigation. Future clinical study in vivo could shed more light on its implication in modulating obesity and metabolic disorders.

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          Most cited references 46

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          Adipose-selective targeting of the GLUT4 gene impairs insulin action in muscle and liver.

           Y. Kim,  Kwang Kim,  E Hadro (2001)
          The earliest defect in developing type 2 diabetes is insulin resistance, characterized by decreased glucose transport and metabolism in muscle and adipocytes. The glucose transporter GLUT4 mediates insulin-stimulated glucose uptake in adipocytes and muscle by rapidly moving from intracellular storage sites to the plasma membrane. In insulin-resistant states such as obesity and type 2 diabetes, GLUT4 expression is decreased in adipose tissue but preserved in muscle. Because skeletal muscle is the main site of insulin-stimulated glucose uptake, the role of adipose tissue GLUT4 downregulation in the pathogenesis of insulin resistance and diabetes is unclear. To determine the role of adipose GLUT4 in glucose homeostasis, we used Cre/loxP DNA recombination to generate mice with adipose-selective reduction of GLUT4 (G4A-/-). Here we show that these mice have normal growth and adipose mass despite markedly impaired insulin-stimulated glucose uptake in adipocytes. Although GLUT4 expression is preserved in muscle, these mice develop insulin resistance in muscle and liver, manifested by decreased biological responses and impaired activation of phosphoinositide-3-OH kinase. G4A-/- mice develop glucose intolerance and hyperinsulinaemia. Thus, downregulation of GLUT4 and glucose transport selectively in adipose tissue can cause insulin resistance and thereby increase the risk of developing diabetes.
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            Interaction between obesity and the gut microbiota: relevance in nutrition.

            This review examines mechanisms by which the bacteria present in the gut interact with nutrients and host biology to affect the risk of obesity and associated disorders, including diabetes, inflammation, and liver diseases. The bacterial metabolism of nutrients in the gut is able to drive the release of bioactive compounds (including short-chain fatty acids or lipid metabolites), which interact with host cellular targets to control energy metabolism and immunity. Animal and human data demonstrate that phylogenic changes occur in the microbiota composition in obese versus lean individuals; they suggest that the count of specific bacteria is inversely related to fat mass development, diabetes, and/or the low levels of inflammation associated with obesity. The prebiotic and probiotic approaches are presented as interesting research tools to counteract the drop in target bacteria and thereby to estimate their relevance in the improvement of host metabolism.
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              The forkhead transcription factor Foxo1 regulates adipocyte differentiation.

              An outstanding question in adipocyte biology is how hormonal cues are relayed to the nucleus to activate the transcriptional program that promotes adipogenesis. The forkhead transcription factor Foxo1 is regulated by insulin via Akt-dependent phosphorylation and nuclear exclusion. We show that Foxo1 is induced in the early stages of adipocyte differentiation but that its activation is delayed until the end of the clonal expansion phase. Constitutively active Foxo1 prevents the differentiation of preadipocytes, while dominant-negative Foxo1 restores adipocyte differentiation of fibroblasts from insulin receptor-deficient mice. Further, Foxo1 haploinsufficiency protects from diet-induced diabetes in mice. We propose that Foxo1 plays an important role in the integration of hormone-activated signaling pathways with the complex transcriptional cascade that promotes adipocyte differentiation.

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                02 December 2020
                : 14
                : 5349-5357
                [1 ]Department of Intensive Care Unit, The First Hospital of Jilin University , Changchun, Jilin 130033, People’s Republic of China
                [2 ]Department of Neurosurgery, China-Japan Union Hospital of Jilin University , Changchun, Jilin 130033, People’s Republic of China
                [3 ]Department of Periodontology, School and Hospital of Stomatology, Jilin University , Changchun, Jilin 130033, People’s Republic of China
                [4 ]Department of Urology, China-Japan Union Hospital of Jilin University, Jilin Key Laboratory of Urologic Oncology , Changchun, Jilin 130033, People’s Republic of China
                [5 ]Department of Obstetrics and Gynecology, China-Japan Union Hospital of Jilin University , Changchun, Jilin 130033, People’s Republic of China
                [6 ]Department of Endocrinology and Metabolism, The First Hospital of Jilin University , Changchun, Jilin 130033, People’s Republic of China
                Author notes
                Correspondence: Heyuan Wang Department of Endocrinology and Metabolism, The First Hospital of Jilin University , Changchun, Jilin130033, People’s Republic of China Tel/Fax +86-431-88782222 Email wangheyuan220@163.com

                These authors contributed equally to this work

                © 2020 Wang et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 8, References: 46, Pages: 9
                Original Research

                Pharmacology & Pharmaceutical medicine

                ampk, juglanin, lipid metabolism, obesity, adipogenesis


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