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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
As a general rule, except in Brown Adipose Tissue, coupling between substrate oxidation and ADP phosphorylation in the mitochondria is due to an electrochemical gradient of protons, on either side of the mitochondrial membrane. During the transfer of electrons to oxygen, protons are extruded from the mitochondrial matrix. These protons cannot be readily reintroduced into the matrix, except in the part of the membrane where ATP-synthase is located. This results in ATP production (Figure 3a left side). Thus electron transfer from substrates to oxygen leads to stochiometric amounts of ATP (coupled oxidative phosphorylation). By contrast, in brown adipocyte mitochondria, the permeability of the inner membrane to protons is abnormally high and protons can readily cross the mitochondrial membrane. The free energy of substrates will therefore be released without ATP synthesis (uncoupled oxidative phosphorylation) and this will result in heat production22 (Figure 3a right side). The high permeability of the inner membrane to protons is related to a specific protein called the uncoupling protein or thermogenin. Interestingly, recent data indicate that thermogenin is present in late gestation in brown adipose tissue of fetuses from many species.25,26
Structure, Function and Evolutionary Aspects of Mitochondria
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Puja Agarwal, Mehali Mitra, Sujit Roy
Under certain conditions protons are diffused into the matrix without contributing two ATP synthesis, in which potential energy of the proton electro chemical gradient is unutilized, releasing heat energy. Thermogenin (33 kDa protein) carry out this process and is commonly found in brown fat or brown adipose tissue responsible for non-shivering thermogenesis (Yun and Finkel, 2014).
Dasatinib-related pleural effusion and lymphocytosis rates are different between adult and pediatric patients with Philadelphia chromosome-positive leukemias: are age and comorbidities only to blame?
Published in Expert Review of Respiratory Medicine, 2022
Necati Alp Kılıçaslan, Şermin Börekçi, Gül Nihal Özdemir, Müge Sayitoğlu, Ahmet Emre Eşkazan
In addition to these mechanisms, some preventive substances on the pediatric pleura may exist against PE as in the regulation of thermogenesis and homeostasis through thermogenin protein in the brown adipose tissue [36]. Structures like thermogenin may be found in pediatric pleura to prevent the formation of PE and these structures may vanish overtime, causing pleura vulnerable to PE generation under dasatinib.