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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
More adiposity, as a consequence of excessive food intake coupled with absence of energy expenditure, leads to an imbalance in energy homeostasis (Aydin, 2014). Therefore, an efficient weight management demands the building of a negative energy balance by means of increasing energy expenditures. It can be possible by three ways viz., obligatory energy expenditure, physical activity and adaptive thermogenesis. Most anti-obesity products characteristically control body weight through raising mandatory energy expenditure. In the human body, brown adipose tissue is mainly responsible for transferring energy from food into heat. It plays a pivotal role in thermogenic effect through UCP-1 (also known as thermogenin). Thus, increasing energy expenditure to upregulate UCP-1 gene expression could be a prospective approach for achieving an anti-obesity effect (Kajimura and Saito, 2014).
Fuel Metabolism in the Fetus
Published in Emilio Herrera, Robert H. Knopp, Perinatal Biochemistry, 2020
Since the fetus is maintained at a controlled temperature, the newborn has to respond to an abrupt decrease in environmental temperature. Thermogenesis is then necessary to maintain body temperature. The anatomical site of this thermogenesis, so-called “nonshivering thermogenesis”, has been recognized as Brown Adipose Tissue.22
Investigating links between diet and health outcomes
Published in Geoffrey P. Webb, Nutrition, 2019
This is more than just an interesting observation because it was a factor in misleading researchers about the cause of obesity. Genetically obese, ob/ob. mice have long been known to have a lower body temperature than their lean siblings. They are susceptible to the cold and may die if suddenly exposed to fridge temperatures (<4°C). In the late 1970s and the 1980s, this was widely interpreted as a failure of their brown fat to generate sufficient heat because of genetically defective brown fat i.e. a failure of their heat-generating system. This led many obesity researchers, like Jean Himms-Hagen in the following quote, to suggest that defective heat generation in brown fat was a major cause of obesity.“Recent studies on brown adipose tissue have shown that a defect in this tissue is one probable cause of obesity” J. Himms-Hagen (1979).
Myostain is involved in ginsenoside Rb1-mediated anti-obesity
Published in Pharmaceutical Biology, 2022
Hong-Shi Li, Jiang-Ying Kuang, Gui-Jun Liu, Wei-Jie Wu, Xian-Lun Yin, Hao-Dong Li, Lei Wang, Tao Qin, Wen-Cheng Zhang, Yuan-Yuan Sun
Under the influence of environmental and genetic factors, obesity is associated with energy-balance dysregulation (Kopelman 2000). The biological characteristics of obesity are adipocyte hypertrophy and excessive adipose accumulation. The maintenance of lipid homeostasis depends on lipolysis and lipogenesis in adipocytes. Adipose tissue, as an important energy storage organ, has become a therapeutic target for obesity. BAT plays an important role in promoting total energy consumption in regulating the body's energy metabolism by producing heat (Algire et al. 2013). It is more interesting that brown adipose tissue has the ability to protect against obesity by releasing batokines, clearing triglycerides, and reducing insulin resistance (Jeremic et al. 2017). Browning of white fat helps to restrict obesity and obesity-related disorders. Although the most common factor for fat browning has been exercise, there may be other factors, such as Rb1, that are involved. In our study, we found a smaller adipocyte diameter and increased basic metabolic activity in Rb1 treated mice.
Arsenic: an emerging role in adipose tissue dysfunction and muscle toxicity
Published in Toxin Reviews, 2022
Kaviyarasi Renu, Aditi Panda, Balachandar Vellingiri, Alex George, Abilash Valsala Gopalakrishnan
The studies show that arsenic affects brown adipose tissue. This arsenic can mediate oxidative stress, which is connected to disorders in adipose tissue metabolism, such as diabetes and obesity. The brown adipose tissue plays an important role in thermogenesis via producing heat. The brown adipocyte pathophysiology acts as an effective mechanism for connecting arsenic and metabolic disorders. Exposure to arsenic reduces brown adipose tissue differentiation, thermogenesis, mitochondrial biogenesis, and lipogenesis. Exposure to arsenic impairs the level of Sestrin2 and Unc-51 like autophagy activating kinase (ULK1). This impaired Sestrin2 via AMP-activated protein kinase (AMPK) mediates the ULK1 [autophagy-related 1 (Atg1)] via autophagosome. This alters the level of p62 and leads to the condition of autophagy. On the other hand, arsenic impairs Atg5/7, activates LC3B (Atg8), and activates autophagy. The impaired Sestrin2 hinders the activity of mTORC1 activates S6K and leads to autophagy. Mammalian target of rapamycin complex 1 (mTORC1) inhibits ULK1 (Atg1), p62, and autophagy. This inhibited autophagy leads to decreased brown adipocyte, mitochondrial biogenesis, mitochondrial respiration. This further causes decreased thermogenesis via decreased PGC1α, UCP, and PPAR-γ (Bae et al.2019) (represented in Figure 2).
Understanding mitochondrial biogenesis through energy sensing pathways and its translation in cardio-metabolic health
Published in Archives of Physiology and Biochemistry, 2018
Abhijit Nirwane, Anuradha Majumdar
Mitochondria play inimitable role in adipose tissue metabolism orchestrating metabolic homeostasis and thermogenesis (Boudina and Graham 2014). Adipose tissue exists in two major types, white adipose tissue (WAT) and brown adipose tissue (BAT) having contradictory functions to each other. The WAT primarily serves as storage site for triglycerides. The BAT is predominantly responsible for thermogenesis (Gil et al.2011). Decrease in WAT mitochondrial content and function were primary outcomes in rodent diabetic studies as well as in overweight or obese humans with IR (Sutherland et al.20082009, Montgomery and Turner 2015). Transcriptional coactivators PGC-1α and PGC-1β are implicated in coordinated expression of nuclear and mitochondrial genes in adipose tissues (Puigserver et al. 1998, Pardo et al.2011). Seemingly, downregulation of PGC-1α mRNA levels were observed in morbidly obese individuals (Tiraby et al.2003). In connection, ablation of PGC-1α in WAT presented the downregulation of mitochondrial and thermogenic genes in mice, which further developed glucose intolerance and IR upon high-fat diet challenge (Kleiner et al. 2012).