China
Africa
Explore chapters and articles related to this topic
Marine Algal Secondary Metabolites Are a Potential Pharmaceutical Resource for Human Society Developments
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Somasundaram Ambiga, Raja Suja Pandian, Lazarus Vijune Lawrence, Arjun Pandian, Ramu Arun Kumar, Bakrudeen Ali Ahmed Abdul
Obesity is defined as the unwanted accumulation of body fat and white adipose tissue (WAT), which inhibits the secretion of cytokines in adipose tissue and leads to a variety of other disorders such as diabetes, high cholesterol and stroke (Namvar et al., 2012). Thermogenesis plays an important role in the regulation of the mechanisms of obesity. Similarly, administration of algae to rats reduced plasma leptin and epididymal adipose tissue levels (Grasa-López et al., 2016). In addition, algae significantly reduced adipocyte size, fasting blood sugar and insulin levels in obese rats (Gammone and D’Orazio, 2015). Algae with fucoxanthin inhibited fat absorption and serum triglyceride levels in an in vivo model and have also been shown to have anti-obesity effects in mice (Kang et al., 2012).
Organic Chemicals
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Even within the context of obesity-induced metabolic disease, leukocyte activation can be adaptive. For example, WAT infiltration by inflammatory (M1) macrophages is a well-known, necessary component of metabolic disease; however, augmentation of this leukocyte population might be necessary for certain adaptive roles as well. Infiltration of Ly6cHi monocytes/M1-biased macrophages in early obesity seems to be driven by the necrosis/apoptosis of hypertrophic adipocytes.418 Although surrounding parenchymal cells can clear apoptotic debris in most organs, adipocyte death yields large lipid droplets whose uncontrolled lipolysis can be toxic to neighboring cells. This toxicity may be due to the liberation of toxic fat and also stored chemicals. Thus, in obese WAT, newly recruited M1 macrophages would encapsulate and sequester the lipid droplet and eventually eliminate it.418 Without professional phagocyte intervention, these adipocyte corpses would presumably persist, releasing necrotic cellular debris and free lipids as well as toxic chemicals to the detriment of surrounding tissue.
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
Adipose tissue is an endocrine organ that comprises a significant proportion of the breast volume (Wang et al. 2014) and secretes hormones and factors that significantly influence epithelial cell behavior and the mammary environment (Fonseca-Alaniz et al. 2007; Iyengar et al. 2003; Wang et al. 2009; Zangani et al. 1999). The white adipose tissue found within the mammary glands is a highly specialized connective tissue, which functions as an energy storage source within the body (Fonseca-Alaniz et al. 2007). White adipose tissue is primarily a collection of lipid-filled cells or adipocytes held together by collagen fibers. Adipose tissue also includes preadipocytes, which account for one-to two-thirds of adipose tissue composition. Dense blood vessels constituted of endothelial, smooth muscle, and red and white blood cells and fibroblasts are also an integral part of adipose tissue (Ailhaud et al. 1992; Albright and Stern 1998; Lanza et al. 2013; Sorisky 1999; Stillaert et al. 2006).
The obesogen tributyltin induces features of polycystic ovary syndrome (PCOS): a review
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Eduardo Merlo, Ian V. Silva, Rodolfo C. Cardoso, Jones B. Graceli
Obesity is an abnormal metabolic condition that is usually accompanied by WAT expansion, low-grade inflammation, insulin resistance, and abnormal secretion of adipokines (Bassaganya-Riera et al. 2009; Carlsen et al. 2009; Fantuzzi 2005; Frigolet, Torres, and Tovar 2013; Heilbronn and Campbell 2008; Leal and Mafra 2013; Mirzaei et al. 2013). The adipokines leptin and adiponectin are adipocyte-derived hormones exerting different roles in control of metabolic functions (Elias 2012; Frederich et al. 1995; Kadowaki 2006; Pan and Myers 2018). Leptin is produced in approximate proportion to the triglyceride stores; leptin thus represents a hormonal signal that circulates in proportion to body fat reserves (Pan and Myers 2018). Hyperleptinemia is associated with obesity and insulin resistance (Kraakman et al. 2014; Loffreda et al. 1998). Shi et al. (2009) found high visceral fat and leptin levels in the female JCR:LA-cp rat. Leptin resistance or hyperleptinemia was also detected in obese women with PCOS (Mantzoros, Dunaif, and Flier 1997). Newborns from PCOS mothers presented elevated leptin levels that might be associated with increased fetal adiposity and/or abnormal maternal metabolic conditions (Maliqueo et al. 2009). Adiponectin promotes peripheral insulin sensitivity (Kadowaki 2006; Ye and Scherer 2013), elevates mitochondrial density in adipocytes, and enhances pancreatic beta-cell survival and functionality (Brown et al. 2010; Holland et al. 2011; Rao et al. 2012). Reduced adiponectin levels may be one possible mechanism responsible for diminished insulin sensitivity in women with PCOS (Mannerås-Holm et al. 2011). Studies demonstrated that low adiponectin levels (Mannerås-Holm et al. 2011; Toulis et al. 2009), together with increased waist circumference and enlarged adipocyte size (Mannerås-Holm et al. 2011; Rebuffé-Scrive et al. 1989), may explain insulin resistance in women with PCOS. Benrick et al. (2017), using the adiponectin knockout and overexpressing transgenic mice, reported that elevated levels of adiponectin might prevent the prepubertal metabolic dysfunction seen in DHT-exposed mice (Benrick et al. 2017). Yuan et al. (2016) reported that transplantation of brown adipose tissue (BAT) reversed anovulation, hyperandrogenism, improved reproductive cyclicity and systemic insulin sensitivity, and reversed polycystic ovarian morphology in DHEA-treated rats. Despite no significant changes in food intake and body weight, improvements in glucose tolerance and insulin sensitivity, serum insulin levels, thermogenesis control and high BAT UPC-1 expression were observed in DHEA-treated rats that received BAT transplants. It is likely that BAT transplantation activated endogenous BAT and thereby produced a rise in circulating level of adiponectin, which plays a prominent role in whole-body energy metabolism, thus contributing to improvements in ovarian physiology in these animals.