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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).
Bioenergetics
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
In adipocytes, there are two enzymes that are involved in degrading triglycerides: hormone-sensitive lipase and adipose triglyceride lipase. Adipose triglyceride lipase has a greater affinity for triglycerides compared to hormone sensitive lipase, and acts as the primary enzyme for triglyceride hydrolysis in adipocytes. Hormone sensitive lipase is found in small concentrations in muscle and can provide an intramuscular source of FFA and glycerol. In the sarcoplasm of muscle fibers, FFA are bound to CoA. Using a carnitine carrier, the FFA -acyl CoA molecule enters the mitochondria (35, 51, 129, 143). The triglyceride “backbone” glycerol can be converted to glycerol 3 phosphate and enter glycolysis for energy production.
Women’s Heath
Published in James M. Rippe, Manual of Lifestyle Medicine, 2021
It used to be thought that adipocytes were largely a reservoir for excess fat; however, it is now clear that they are metabolically very active. In particular, obesity has been demonstrated to increase inflammation, insulin resistance, and elevations of thrombotic markers such as fibrinogen and plasminogen activator inhibitor-1. Among inflammatory markers increased with excess adipose tissue are interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and c-reactive protein.
Eunos 2022: Birmingham, United Kingdom, 20th – 23rd June 2022
Published in Neuro-Ophthalmology, 2022
Sophie L. P. Mollan, Susan P. Mollan
A whole session was dedicated to idiopathic intracranial hypertension (IIH). Both the incidence and prevalence of IIH in the preceding decades has increased, linked to the worldwide obesity epidemic. Whilst the pathophysiology of IIH is unknown, recent work in Birmingham, UK has provided evidence to suggest that IIH is a systemic metabolic disease with patients noted to have truncal adiposity correlating closely with raised intracranial pressure. Our patients have also been found to have associated insulin resistance, a differential adipocyte function and increased cardiovascular disease risk. One of the most memorable talks was from Associate Professor Sally Abbott (Coventry, UK) who tackled how to engage your patients to lose weight. Obesity which is a relapsing and recurring chronic illness has social stigma and professional management should be offered for those with IIH. Dr Clare Fraser joined us from Australia where she presented on the importance of screening and onwards management of obstructive sleep apnoea in people with IIH.
Toxic effects and molecular mechanism of doxorubicin on different organs – an update
Published in Toxin Reviews, 2022
Kaviyarasi Renu, Lakshmi Prasanna Pureti, Balachandar Vellingiri, Abilash Valsala Gopalakrishnan
Doxorubicin administration impairs glucose and lipid metabolism due to which the body homeostasis is disrupted (Biondo et al.2016, de Lima Junior et al.2016, Heart et al.2016). Adipose tissue is of two types. One is white adipose tissue, which is considered to be an energy reservoir, and brown adipose tissue acts as a thermal insulator and generates heat during cold conditions (Saely et al.2012). Adipose tissue is the main organ involved in the process of glucose uptake upon insulin stimuli. Doxorubicin exhibits dual nature, which means it shows differential gene expression at different concentrations (Arunachalam et al.2012). Doxorubicin administration is found to impair lipid metabolism in adipose tissue. Doxorubicin at a lower dosage has down-regulated the process of lipogenesis via 5’AMPK signaling (Biondo et al.2016). The process of glucose transport across the adipocytes was dysregulated, which may be due to insulin resistance (Renu et al.2019). The mechanism of doxorubicin-induced adipotoxicity upon different animal models is elucidated in Figure 5 and Table 1.
Lipopolysaccharides derived from gram-negative bacterial pool of human gut microbiota promote inflammation and obesity development
Published in International Reviews of Immunology, 2022
Liyu Du, Xi Lei, Jie Wang, Li Wang, Qingping Zhong, Xiang Fang, Pan Li, Bing Du, Yutao Wang, Zhenlin Liao
Obesity is characterized by the increased number and volume of adipocytes, accompanied by metabolic and inflammatory complications. Inflammation of adipose tissue in obese people has been the focus of recent studies on obesity and its related metabolic diseases. Adipose tissue was the first site where inflammation was found to be associated with obesity. Hotamisligil et al. [34]first found in vivo in animal models an abnormal increase in TNF-α expression by adipocytes in obese rats and mice. The main reason for this is the presence of LPS, which attracts macrophages to infiltrate into adipose tissue, causing an inflammatory immune response and the release of inflammatory factors (TNF-α, etc.). In some models, it was also found that high-fat diet-induced obesity and lipid accumulation cause high expression of inflammatory factors such as IL-1β, TNF-α, IL-6, intercellular adhesion molecule 1 (ICAM 1), and monocyte chemotactic protein-1 (MCP-1) [35–40].