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Engineered Composites for 3D Mammary Tissue Systems
Published in Karen J.L. Burg, Didier Dréau, Timothy Burg, Engineering 3D Tissue Test Systems, 2017
Cheryl T. Gomillion, Chih-Chao Yang, Didier Dréau, Karen J. L. Burg
In addition to its energy storage metabolic role, adipocyte cells also secrete multiple proteins and cytokines, or adipokines, which influence other cells within the breast and other tissues of the body (Halberg et al. 2008; Hauner 2005; Karnoub and Weinberg 2006; Masaki and Yoshimatsu 2008; Miner 2004). Adipocyte factors influence numerous processes including ECM development, cell metabolism, and immunological functions (Halberg et al. 2008). The evaluation of the mammary extracellular and intracellular components of mammary adipose tissue yielded an extensive list of factors with potential influence on mammary epithelial cells (Celis et al. 2005). For example, stromal cells have been shown to modulate hormones that regulate ductal morphogenesis and branching, and adipose cells have been shown to promote functional differentiation of mammary epithelial cells synthesizing milk proteins (Levine and Stockdale 1985; Trujillo and Scherer 2006). Many sources have listed factors secreted by adipose cells in general (Halberg et al. 2008). Adipocyte-secreted factors that have been shown to influence epithelial cell behaviors are summarized in Table 9.1. Furthermore, adipocyte-secreted factors including matrix metalloproteinases (MMPs) also have key roles in breast tumor progression (Bouloumie et al. 2001; Chavey et al. 2003). These factors and their influence on epithelial cells must be taken into account when developing engineered model systems.
Anti-Arthritic Potential of Gold Nanoparticle
Published in Klaus D. Sattler, st Century Nanoscience – A Handbook, 2020
Jayeeta Sengupta, Sourav Ghosh, Antony Gomes
Obesity leads to increased adipokine and leptin expression in the human body, promoting proteases, pro-inflammatory cytokines, reactive oxygen species, and NO. Adipokine and leptin receptors are found in the cell membrane of chondrocytes, subchondral osteoblasts, and synoviocytes, activation of which leads to the secretion of proteases (especially matrix metalloproteinases), exerting the destruction of joint tissue. Increased body mass index is directly correlated with the pathogenesis of osteoarthritis.
Active ageing sportswear
Published in Gianni Montagna, Cristina Carvalho, Textiles, Identity and Innovation: In Touch, 2020
L. Piccinini, C. Carvalho, G. Montagna
Body fat increases with age and shifts from its peripheral location to a more central predominance, whether abdominal or visceral. Adipose tissue acts as an active endocrine organ capable of producing various cytokines and adipokines. Studies suggest that visceral fat in both obese and nonobese elderly contributes specifically to inflammation.
Hydroxychloroquine improves high-fat-diet-induced obesity and organ dysfunction via modulation of lipid level, oxidative stress, and inflammation
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Mohamed A Hasan, Omar A. Ammar, Maher A Amer, Azza I Othman, Fawzia Zigheber, Mohamed A El-Missiry
Obesity is associated with inflammation, and it is characterized by disturbance in the level of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) [5]. Moreover, adipokines such as leptin, adiponectin, resistin, and visfatin, which are secreted from adipose tissue, show disrupted levels in obesity [6]. Leptin synthesized and secreted by white adipose tissue regulates the appetite through leptin receptors primarily in the hypothalamic nuclei, and it is expressed in several organs and immune cells [7]. Adiponectin is a cytokine that is released from adipose tissues; thus, it can be grouped in adipokines. It plays a number of molecular and cellular roles in physiological processes, primarily lipid metabolism, immune response, inflammation, and insulin sensitivity [8]. Deregulation of these cytokines is implicated in obesity and diabetes-related inflammatory response [9]. Leptin and adiponectin secretions are regulated in relation to the degree of adiposity. Plasma leptin concentration is elevated in individuals with obesity in proportion to the body mass index, whereas adiponectin secretion decreases in relation to the amount of adipose tissue [10].
Lipogenesis inhibition and adipogenesis regulation via PPARγ pathway in 3T3-L1 cells by Zingiber cassumunar Roxb. rhizome extracts
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Natthawut Wong-a-nan, Kewalin Inthanon, Aroonchai Saiai, Angkhana Inta, Wutigri Nimlamool, Siriwadee Chomdej, Prasat Kittakoop, Weerah Wongkham
Regarding the glucose-uptake genes (IRS-1, GLUT4 and Adiponectin), differences in the level of IRS-1 gene expression in DA/ZCE and DA/ZCW were not significant, compared with the MA/nt group (Fig. 3B). The extracts, therefore, did not interfere with insulin signal transduction. Our observation that GLUT4 was reduced, after the exposure to the extracts, strongly suggests that adipogenic suppression at least performed through down regulation of the insulin-regulated glucose transporter. Reduction in GLUT4 on the membrane led to a decrease in glucose transport from the extracellular environment into the cells. This may explain the smaller sizes of lipid droplets in DA/ZCE and DA/ZCW indicating lower lipid content (Fig. 2A). The mRNA expression level of Adiponectin was significantly decreased in DA/ZCE and DA/ZCW (Fig. 3B). Adiponectin is an adipokine, secreted predominantly by adipose cells, which regulates both metabolic and vascular homeostasis in vivo. Adiponectin also increases insulin’s ability to maximally stimulate glucose uptake through increasing expression of the GLUT4 gene and increasing the recruitment of GLUT4 protein to the plasma membrane [41]. Suppression of Adiponectin by the extracts supports the idea that glucose transport through GLUT4 is reduced. This may also be a major target pathway of the extracts for their mechanisms of action to prevent the accumulation of lipid content in the cells.
Reallocating sitting time to standing or stepping through isotemporal analysis: associations with markers of chronic low-grade inflammation
Published in Journal of Sports Sciences, 2018
Joseph Henson, Charlotte L. Edwardson, Danielle H. Bodicoat, Kishan Bakrania, Melanie J. Davies, Kamlesh Khunti, Duncan C. S. Talbot, Thomas Yates
Low-grade inflammation has been proposed to be involved in the underlying pathogenesis of type 2 diabetes mellitus (T2DM) (Wang et al., 2013). This manifestation is thought to be a result of an ongoing acute-phase response, primarily characterised by alterations in acute-phase proteins, such as C-reactive protein (CRP) (Pradhan, Manson, Rifai, Buring, & Ridker, 2001). More specifically, mediators of inflammation which include the interleukin 6 (IL-6) family of cytokines have been proposed to affect glucose homeostasis and metabolism directly and indirectly by action on skeletal muscle cells (Kristiansen & Mandrup-Poulsen, 2005). Previous studies have established an inverse relationship between the amount of physical activity and proinflammatory cytokines in obesity, T2DM, and the metabolic syndrome (Hamer et al., 2012; Kasapis & Thompson, 2005). Therefore, the beneficial effects of physical activity may be partly mediated by changes in the adipokines profile.