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Mitigation of Obesity: A Phytotherapeutic Approach
Published in Amit Baran Sharangi, K. V. Peter, Medicinal Plants, 2023
A.B. Sharangi, Suddhasuchi Das
Adipocytes release fatty acid, which are used as fuel by organs in times of limited glucose. These fatty acids are the outcomes from triacylglycerol breakdown, which contain more energy per unit mass compared to carbohydrates. Lipid homeostasis and energy balance is centrally regulated by adipocytes. According to changing energy demands they release free fatty acids from stored triglycerides. The hyperplasia and hypertrophy of adipocytes both are involved with adipocyte tissue growth, which led to the development of natural products which helps in anti-obesity therapy that exclusively target adipogenesis inhibition. Some research has also proposed that through blockade of several transcription factors like C/EBP_ (CCAAT/enhancer-binding protein beta) and PPAR (peroxisome proliferator-activated receptor-gamma) adipocyte differentiation could be inhibited (Kang et al., 2013).
Roles of Daily Diet and Beta-Adrenergic System in the Treatment of Obesity and Diabetes
Published in Nilanjana Maulik, Personalized Nutrition as Medical Therapy for High-Risk Diseases, 2020
Ebru Arioglu Inan, Belma Turan
In differentiated OP9 cells, quercetin has been demonstrated to decrease adipogenesis (Seo, Kang et al. 2015). It also resulted in downregulation of expression of transcription factors which have a role in adipogenesis, such as PPARγ, C/EBPα and SREBP-1c. In this study, quercetin increased lipolytic activity in adipocytes and was associated with expression of lipolytic enzymes such as ATGL, HSL and LPL. Another form of quercetin, quercetin 3-O glucoside (Q3G), has also been reported to inhibit lipogenesis (Lee, Seo et al. 2017). It decreased body weight and adipocyte size in epididymal adipose tissue in high fat-fed mice. It suppressed expression levels of some proteins related to lipid metabolism, such as peroxisome proliferator-activated receptor γ (PPARγ), sterol regulatory element-binding transcription factor 1 (SREBP-1c) and fatty acid synthase (FAS). Lee et al. showed the browning effect of quercetin which was attributed to activation of AMPK (Lee, Seo et al. 2017; Lee, Parks et al. 2017). Furthermore, Arias et al. demonstrated that quercetin combined with resveratrol caused a browning effect in rats fed with an obesogenic diet (Arias, Pico et al. 2017).
Digestive and Metabolic Actions of Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Obesity is defined as >20% increase over the ideal weight of an individual and is associated with higher risks of morbidity and mortality. Obesity results from enlargement of the adipocytes via enhanced lipid accumulation (hypertrophy) and/or from increased cell number (hyperplasia). The latter begins with the recruitment of stem cells to the adipocyte lineage [96], followed by adipogenesis of committed preadipocytes, which takes 7–10 days and culminates in their transformation into lipid-filled large mature adipocytes [83]. About 10% of fat cells are renewed annually, irrespective of body mass index, without an increase in their overall number in adults.
Current and emerging drug treatment strategies for polycystic ovary syndrome
Published in Expert Opinion on Pharmacotherapy, 2023
Nafiye Helvaci, Bulent Okan Yildiz
Thiazolidinediones (TZDs) are selective ligands of the nuclear transcription factor peroxisome proliferator activated receptor γ (PPAR-γ). PPAR-γ regulates the transcription of several genes involved in adipogenesis and glucose and lipid metabolism. TZD-induced PPAR-γ activation promotes adipocyte differentiation and increases fatty acid uptake and storage in the adipose tissue, thereby reducing excessive accumulation of these fatty acids in peripheral tissues (skeletal muscle, liver, pancreas). Moreover, PPAR-γ activation in adipose tissue decreases secretion of proinflammatory cytokines and increases secretion of adiponectin. These primary effects of TZDs alleviate IR, reduce circulating insulin levels, and improve β-cell function. TZDs can also act on androgen excess either directly by inhibiting the steroidogenic enzymes or indirectly by reducing hyperinsulinemia [35].
Anti-inflammatory effects of troxerutin are mediated through elastase inhibition
Published in Immunopharmacology and Immunotoxicology, 2020
Ramachandran Vidhya, Carani Venkatraman Anuradha
Lipid accumulation in TNFα-treated cells could be related to changes in adipokines. In vitro and in vivo rodent studies have clearly indicated a direct role for inflammation-related adipokines like TNFα, IL-6, MCP-1, leptin, RETN and CHEM on lipid metabolism [43]. TNFα promotes lipolytic events like disintegration of lipid droplets (LDs) thereby increasing the accessibility of TG to hormone sensitive lipase (HSL) and also cause reduction in gene expression leading to adipogenesis [44]. IL-6 increases adipocyte lipolysis and suppresses lipoprotein lipase activity [45,46]. Leptin stimulates lipolysis of TG [47] and reduces gene expression of acetyl CoA carboxylase (ACC) [48] in adipocytes and sterol regulatory element binding protein (SREBP-1c) inhibiting lipogenesis. RETN could be involved in storage and release of energy by adipose tissue and in the metabolism of free fatty acid (FFA) and TG [49]. CHEM induces adipocyte lipolysis [50]. Adiponectin has favorable effects like stimulation of adipogenesis, reduction in ceramide accumulation in liver, hepatic steatosis and maintenance of lipid metabolism [51].
Automated lipid droplet quantification system for phenotypic analysis of adipocytes using CellProfiler
Published in Toxicology Mechanisms and Methods, 2020
Victoria Adomshick, Yong Pu, Almudena Veiga-Lopez
Adipogenesis is the process by which mesenchymal stromal cells or committed preadipocytes differentiate into mature adipocytes. This is a tightly controlled process that may be altered by several factors, including nutrition, stress, as well as environmental factors (Ghaben and Scherer 2019). Understanding how these factors can alter adipogenesis can help provide insights into strategies to prevent adipose tissue accumulation resulting in metabolic disorders and/or obesity (Ghaben and Scherer 2019). Studies to understand adipogenesis often use the preadipocyte mouse cell line 3T3-L1. Preadipocytes are induced to differentiate in vitro for 8–12 days during which cells are exposed to a differentiation cocktail that may contain insulin, peroxisome proliferator-activated receptor gamma (PPARγ) agonists, and/or 3-isobutyl-1-methylxanthine (IMBX), among others (Zhao et al. 2019). During the differentiation process, cells begin to accumulate lipid droplets leading to the formation of mature adipocytes with a specific transcriptomic profile, including increased PPARγ, FABP4, and adiponectin expression (Lee et al. 2019).