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Altitude, temperature, circadian rhythms and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Henning Wackerhage, Kenneth A. Dyar, Martin Schönfelder
So how do we maintain our core body temperature? Several processes either increase or decrease our body temperature. Body temperature is increased mainly by two processes (Figure 11.5 (36)): Non-shivering thermogenesis: While most of our adipose tissue is white adipose tissue, we have two types that can generate heat via the “short cut” protein UCP1. These are brown (37) and so-called beige (or brite) adipose tissue (38). Hormones such as catecholamines, secretin (39) as well as metabolites, myokines and miRNAs regulate the expression of the UCP1 gene or the activity of the heat-generating UCP1 protein which generates heat, raises energy expenditure and has beneficial metabolic effects (39, 40).Muscle contraction in the form of exercise or shivering: Skeletal muscle is an organ that converts the chemical energy of nutrients into work (i.e. muscle contraction and exercise) and heat. For example, during cycling only approximately 20% of the chemical energy is converted into work, whereas 80% of it is typically converted into heat. This is why we become warm when we exercise. Moreover, involuntary muscle contractions during shivering also generate heat via the same mechanism.
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
The β3-AR agonist treatment resulted in weight loss in obese mice without a reduction in food intake (Yoshida, Sakane et al. 1994) which has been attributed to increased thermogenesis in brown adipose tissue (Himms-Hagen, Cui et al. 1994). This effect could be related to stimulation of UCP1 (Inokuma, Okamatsu-Ogura et al. 2006). UCP-1 is a mitochondrial carrier protein in brown adipose tissue and has a role in energy consumption as heat. The lipolytic effects of β3-AR, on the other hand, involve mobilization of fat as free fatty acids from white adipose tissue deposits which are oxidized and used in thermogenesis in brown adipose tissue (Ursino, Vasina et al. 2009). Predisposition to abdominal obesity, it has been suggested, is associated with the presence of the Arg64 allele in the first intracellular loop of β3-ARs gene which could further lead to insulin resistance (Widen, Lehto et al. 1995). Moreover, a Trp64 Arg mutation of β3-AR has been found to be related to the early onset of type 2 diabetes in obese Pima North American Indians (Walston, Silver et al. 1995). This mutation is also associated with mild gestational diabetes (Festa, Krugluger et al. 1999).
Noninsulin-Dependent Animal Models of Diabetes Mellitus
Published in John H. McNeill, Experimental Models of Diabetes, 2018
Christopher H. S. McIntosh, Raymond A. Pederson
Several uncoupling proteins have now been identified. The original protein cloned (UCP1) was identified as a membrane proton transporter found in mitochondria, expressed specifically in brown adipose tissue. Activation of the protein results in dissipation of the proton gradient and heat production. DNA polymorphisms in human UCP1 were found to correlate with age-associated increases in body fat.406 Mutations in the protein could lead to reduced energy expenditure and, thus, weight gain. UCP1 knockout mice were shown to consume less oxygen in response to a β3-adrenergic receptor agonist and were more sensitive to cold.407 However, neither obesity nor hyperphagia was observed. Since animals in which BAT had been completely ablated developed marked obesity with increasing age, hyperglycemia, marked hyperinsulinemia, and glucose intolerance,408 the mild pathology of the UCP1 knockout was probably due to compensation by UCP2,409,410 therefore, double knockouts are needed to determine the effect of overall UCP ablation. It is of interest that UCP2 is also found in pancreatic islet β-cells, where it is likely to play a role in insulin secretion, and overexpression of leptin resulted in tenfold increases in UCP2 gene expression.411 This suggests that altered UCP2 expression, resulting from loss of leptin responsiveness, could contribute to the development of obesity/NIDDM.
The effect of nutrition and exercise training on irisin and semaphorin-3E levels in obese patients
Published in Archives of Physiology and Biochemistry, 2022
Gülay Sezgin, Fatih Kar, Sema Uslu
Boström et al. (2012) discovered a myokine called irisin. The irisin, which protects the person from metabolic diseases and is released from the skeletal muscle by the effect of exercise or cold, causes an increase in UCP1. UCP1 in mitochondria are referred to as increased white adipose tissue cells, beige adipose tissue. These cells work like brown fat tissue cells and provide thermogenesis. Increased expression of UCP1 increases heat production. This profitable event provides energy expenditure in terms of glucose/fat metabolism in insulin-resistant individuals and obese individuals (Aydin 2014). Irisin may play a possible role in glucose metabolism. Irisin protein has been shown to be associated with an increase in metabolic syndrome, insulin resistance and 10-year cardiovascular disease risk. Although there are studies showing that plasma irisin levels change with weight loss or exercise, contradictory results reveal that further studies are necessary (Hee Park et al.2013). Similarly, sema-3E and plexin-D1 have been shown to contribute significantly to inflammation of adipose tissue as a result of a high-calorie diet leading to various metabolic abnormalities (Schmidt and Moore 2013). However, there are no studies in the literature showing how it changed the expression of sema-3E and plexin-D1 as a result of nutrition and exercise training in obesity.
Pepper and cinnamon improve cold induced cognitive impairment via increasing non-shivering thermogenesis; a study
Published in International Journal of Hyperthermia, 2018
Chaitanya Pandit, S. Sai Latha, T. Usha Rani, K. R. Anilakumar
The present results are in agreement with those demonstrating cognitive impairments following cold exposure [4–7]. Treatment with green tea and both the spices significantly improved performance, but only in the cold exposed group. We reasoned that it may be due to the following factors. Firstly, the enhanced heat generation and hence a lowered fall in CBT helps restore temperature homeostasis to a large extent. This implies that the major problem of central cooling or hypothermia is primarily addressed which in turn prevents the slowing down of physiological processes that are required to maintain cognition. The spices increase physiological heat generation by activating or potentiating NST in BAT. The sympathetic nervous system responds by releasing NOR which in turn result in an enhanced expression of UCP1 in BAT. UCP1 is the protein responsible for uncoupling oxidative phosphorylation resulting in an increased heat generation. Although the cue from SNS activating BAT is the primary reaction, an orchestral response from other organs which release factors that activate BAT directly or indirectly are now known [24–26]. It is of interest to note that animals with decreased fall in CBT were more mobile and active. Hence the chances of them making any choice between the novel and old object were high when compared to the control animals which were mostly immobile or seemed to forget the task itself.
Polyunsaturated fatty acids and endocannabinoids in health and disease
Published in Nutritional Neuroscience, 2018
Hércules Rezende Freitas, Alinny Rosendo Isaac, Renato Malcher-Lopes, Bruno Lourenço Diaz, Isis Hara Trevenzoli, Ricardo Augusto De Melo Reis
The effect of the ECS on brown adipose tissue can be direct or indirect through sympathetic activation. Brown adipocyte function is highly dependent on the sympathetic nervous system (SNS) with activation of beta 3-adrenoceptor signaling (β3AR). Adrenergic signaling results in the activation of thermogenic program and heat production, which is dependent on the activity of uncoupling protein 1 (UCP1), a protein located in the inner membrane of mitochondria. UCP1 is responsible for proton leak from the intermembrane space to the mitochondrial matrix with production of energy in the form of heat instead of ATP. Recent studies have been conducted to better understand the physiology and the pathophysiological aspects of the BAT in metabolic disorders such as obesity, especially because it was demonstrated that brown adipocytes are active in adult humans (reviewed at Labbe et al.215).