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Journal articles on the topic 'Obligatory thermogenesis'
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1
Himms-Hagen, Jean. "Role of thermogenesis in the regulation of energy balance in relation to obesity." Canadian Journal of Physiology and Pharmacology 67, no. 4 (April 1, 1989): 394–401. http://dx.doi.org/10.1139/y89-063.
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Obligatory thermogenesis is a necessary accompaniment of all metabolic processes involved in maintenance of the body in the living state, and occurs in ail organs. It includes energy expenditure involved in ingesting, digesting, and processing food (thermic effect of food (TEF)). At certain life stages extra energy expenditure for growth, pregnancy, or lactation would also be obligatory. Facultative thermogenesis is superimposed on obligatory thermogenesis and can be rapidly switched on and rapidly suppressed by the nervous system. Facultative thermogenesis is important in both thermal balance, in which control of thermoregulatory thermogenesis (shivering in muscle, nonshivering in brown adipose tissue (BAT)) balances neural control of heat loss mechanisms, and in energy balance, in which control of facultative thermogenesis (exercise-induced in muscle, diet-induced thermogenesis (DIT) in BAT) balances control of energy intake. Thermal balance (i.e., body temperature) is much more stringently controlled than energy balance (i.e., body energy stores). Reduced energy expenditure for thermogenesis is important in two types of obesity in laboratory animals. In the first type, deficient DIT in BAT is a prominent feature of altered energy balance. It may or may not be associated with hyperphagia. In a second type, reduced cold-induced thermogenesis in BAT as well as in other organs is a prominent feature of altered thermal balance. This in turn results in altered energy balance and obesity, exacerbated in some examples by hyperphagia. In some of the hyperphagic obese animals it is likely that the exaggerated obligatory thermic effect of food so alters thermal balance that BAT thermogenesis is suppressed. In all obese animals, deficient hypothalamic control of facultative thermogenesis and (or) food intake is implicated.Key words: thermogenesis, brown adipose tissue, energy balance, obesity, cold, thermoregulation, diet.
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King, R. F. G. J., M. J. McMahon, and D. J. Almond. "Evidence for adaptive diet-induced thermogenesis in man during intravenous nutrition with hypertonic glucose." Clinical Science 71, no. 1 (July 1, 1986): 31–39. http://dx.doi.org/10.1042/cs0710031.
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1. This study was designed to investigate the thermogenic effect of intravenously administered nutrition with glucose (given with a fixed nitrogen intake of 12.5 g daily as amino acids) as the principal source of energy. The protocol was designed so that each patient received their energy intake in five consecutive periods of 3 days with intakes ranging from 6650 to 17100 kJ/day with increments or decrements of 2600 kJ. 2. Thermogenesis from administered glucose was evident between levels of energy supply of 6650 kJ/day and 17100 kJ/day. The progressive rise in oxygen consumption and carbon dioxide production accounted for a total of 31% of the additional glucose which was administered. The net rate of fat synthesis from glucose reached a maximum 147 g/day at an energy supply of 14 500 kJ/day. 3. This study suggests that both fat synthesis and the associated obligatory thermogenesis is the main component of diet-induced thermogenesis in response to glucose intakes in excess of 150 kJ day−1 kg−1. If the energy cost of fat synthesis (fat associated obligatory thermogenesis) is taken to be 22% of the total energy of the increase in glucose supplied, then only 9% (31–22%) of the glucose can be accounted for by adaptive thermogenesis.
3
Hohtola, Esa. "Facultative and obligatory thermogenesis in young birds: a cautionary note." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 131, no. 4 (April 2002): 733–39. http://dx.doi.org/10.1016/s1095-6433(02)00011-9.
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Yau, Winifred W., and Paul M. Yen. "Thermogenesis in Adipose Tissue Activated by Thyroid Hormone." International Journal of Molecular Sciences 21, no. 8 (April 24, 2020): 3020. http://dx.doi.org/10.3390/ijms21083020.
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Thermogenesis is the production of heat that occurs in all warm-blooded animals. During cold exposure, there is obligatory thermogenesis derived from body metabolism as well as adaptive thermogenesis through shivering and non-shivering mechanisms. The latter mainly occurs in brown adipose tissue (BAT) and muscle; however, white adipose tissue (WAT) also can undergo browning via adrenergic stimulation to acquire thermogenic potential. Thyroid hormone (TH) also exerts profound effects on thermoregulation, as decreased body temperature and increased body temperature occur during hypothyroidism and hyperthyroidism, respectively. We have termed the TH-mediated thermogenesis under thermoneutral conditions “activated” thermogenesis. TH acts on the brown and/or white adipose tissues to induce uncoupled respiration through the induction of the uncoupling protein (Ucp1) to generate heat. TH acts centrally to activate the BAT and browning through the sympathetic nervous system. However, recent studies also show that TH acts peripherally on the BAT to directly stimulate Ucp1 expression and thermogenesis through an autophagy-dependent mechanism. Additionally, THs can exert Ucp1-independent effects on thermogenesis, most likely through activation of exothermic metabolic pathways. This review summarizes thermogenic effects of THs on adipose tissues.
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Astrup, A., J. Bulow, N. J. Christensen, J. Madsen, and F. Quaade. "Facultative thermogenesis induced by carbohydrate: a skeletal muscle component mediated by epinephrine." American Journal of Physiology-Endocrinology and Metabolism 250, no. 2 (February 1, 1986): E226—E229. http://dx.doi.org/10.1152/ajpendo.1986.250.2.e226.
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In addition to the obligatory thermogenesis due to processing and storage, carbohydrate ingestion is accompanied by a facultative thermogenesis mediated by catecholamines via beta-adrenoceptors. The anatomical origin of facultative thermogenesis has hitherto not been determined. The possible involvement of skeletal muscle was examined in lean, healthy subjects by measuring the response in forearm oxygen consumption to an oral glucose load. The study demonstrates an early component of skeletal muscle thermogenesis coinciding with the local glucose uptake, followed by a late facultative thermogenesis. The arterial epinephrine concentration increased to a maximum of 200% above base-line values 4 h after glucose. This value greatly exceeds the physiological threshold for the thermogenic action of epinephrine. In forearm venous blood the corresponding increase in epinephrine was only approximately 50% due to enhanced peripheral extraction, which accompanies an increase in arterial epinephrine levels. Due to venous sampling previous studies have overlooked the magnitude of the late postglucose increase in arterial epinephrine, and its potential thermogenic effect has been disregarded. The facultative thermogenesis in skeletal muscle may be of importance for the regulation of body weight in humans.
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Iossa, S., L. Lionetti, M. P. Mollica, A. Barletta, and G. Liverini. "Thermic effect of food in hypothyroid rats." Journal of Endocrinology 148, no. 1 (January 1996): 167–74. http://dx.doi.org/10.1677/joe.0.1480167.
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Abstract The regulatory and obligatory components of cephalic and gastrointestinal phases of the thermic effect of food (TEF) were measured in control and hypothyroid rats. A significant decrease (P<0·05) in regulatory and obligatory components of cephalic and gastrointestinal TEF, after either a control or energy-dense meal, was found in hypothyroid rats compared with control rats. Our findings indicate that hypothyroidism is associated with a decreased thermogenic response to food which contributes to the reduced energy expenditure of hypothyroid rats. Our results also suggest that tri-iodothyronine is involved in the regulation of postprandial thermogenesis directly as well as through its influence on β-adrenergic response and insulin release. Journal of Endocrinology (1996) 148, 167–174
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Richard, D., P. Lachance, and Y. Deshaies. "Effects of exercise-rest cycles on energy balance in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 4 (April 1, 1989): R886—R891. http://dx.doi.org/10.1152/ajpregu.1989.256.4.r886.
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The present study investigated the nutritional energetics of rats exercised either intermittently or continually. Male rats were divided into three groups: a sedentary group, an intermittently trained group, and a continually trained group. Continually trained rats were exercised every day for a period of 8 wk. Over the same period, intermittently trained rats were exercised for 4 wk, each week being followed by a week of rest. Rats were trained on a rodent treadmill at a moderate intensity. Carcasses were analyzed for energy, fat, and protein contents. Brown adipose tissue (BAT) thermogenesis was assessed by measuring mitochondrial guanosine 5'-diphosphate binding. Energy intake was lower in both intermittently and continually trained rats than in sedentary animals. The weight, fat, and protein gains were, in continually trained rats, significantly lower than in sedentary animals. Similarly, intermittently trained rats had lower gains than sedentary animals, although the difference between the two groups was not as marked as the difference between sedentary and continually trained animals. Energy expenditure, which represents the difference between energy intake and energy gain, was less than sedentary controls in both intermittently and continually trained rats. The low expenditure in trained groups did not, however, relate to changes in facultative BAT thermogenesis.A low energy expenditure on components such as basal metabolic rate and obligatory diet-induced thermogenesis would most likely account for the difference in expenditure between sedentary and trained rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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Silva, J. Enrique. "Thermogenic Mechanisms and Their Hormonal Regulation." Physiological Reviews 86, no. 2 (April 2006): 435–64. http://dx.doi.org/10.1152/physrev.00009.2005.
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Increased heat generation from biological processes is inherent to homeothermy. Homeothermic species produce more heat from sustaining a more active metabolism as well as from reducing fuel efficiency. This article reviews the mechanisms used by homeothermic species to generate more heat and their regulation largely by thyroid hormone (TH) and the sympathetic nervous system (SNS). Thermogenic mechanisms antecede homeothermy, but in homeothermic species they are activated and regulated. Some of these mechanisms increase ATP utilization (same amount of heat per ATP), whereas others increase the heat resulting from aerobic ATP synthesis (more heat per ATP). Among the former, ATP utilization in the maintenance of ionic gradient through membranes seems quantitatively more important, particularly in birds. Regulated reduction of the proton-motive force to produce heat, originally believed specific to brown adipose tissue, is indeed an ancient thermogenic mechanism. A regulated proton leak has been described in the mitochondria of several tissues, but its precise mechanism remains undefined. This leak is more active in homeothermic species and is regulated by TH, explaining a significant fraction of its thermogenic effect. Homeothermic species generate additional heat, in a facultative manner, when obligatory thermogenesis and heat-saving mechanisms become limiting. Facultative thermogenesis is activated by the SNS but is modulated by TH. The type II iodothyronine deiodinase plays a critical role in modulating the amount of the active TH, T3, in BAT, thereby modulating the responses to SNS. Other hormones affect thermogenesis in an indirect or permissive manner, providing fuel and modulating thermogenesis depending on food availability, but they do not seem to have a primary role in temperature homeostasis. Thermogenesis has a very high energy cost. Cold adaptation and food availability may have been conflicting selection pressures accounting for the variability of thermogenesis in humans.
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Argyropoulos, George, and Mary-Ellen Harper. "Invited Review: Uncoupling proteins and thermoregulation." Journal of Applied Physiology 92, no. 5 (May 1, 2002): 2187–98. http://dx.doi.org/10.1152/japplphysiol.00994.2001.
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Energy balance in animals is a metabolic state that exists when total body energy expenditure equals dietary energy intake. Energy expenditure, or thermogenesis, can be subcategorized into groups of obligatory and facultative metabolic processes. Brown adipose tissue (BAT), through the activity of uncoupling protein 1 (UCP1), is responsible for nonshivering thermogenesis, a major component of facultative thermogenesis in newborn humans and in small mammals. UCP1, found in the mitochondrial inner membrane in BAT, uncouples energy substrate oxidation from mitochondrial ATP production and hence results in the loss of potential energy as heat. Mice that do not express UCP1 (UCP1 knockouts) are markedly cold sensitive. The recent identification of four new homologs to UCP1 expressed in BAT, muscle, white adipose tissue, brain, and other tissues has been met by tremendous scientific interest. The hypothesis that the novel UCPs may regulate thermogenesis and/or fatty acid metabolism guides investigations worldwide. Despite several hundred publications on the new UCPs, there are a number of significant controversies, and only a limited understanding of their physiological and biochemical properties has emerged. The discovery of UCP orthologs in fish, birds, insects, and even plants suggests the widespread importance of their metabolic functions. Answers to fundamental questions regarding the metabolic functions of the new UCPs are thus pending and more research is needed to elucidate their physiological functions. In this review, we discuss recent findings from mammalian studies in an effort to identify potential patterns of function for the UCPs.
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LeBlanc, Jacques, Diane Lupien, Pierre Diamond, Marcos Macari, and Denis Richard. "Thermogenesis in response to various intakes of palatable food." Canadian Journal of Physiology and Pharmacology 64, no. 7 (July 1, 1986): 976–82. http://dx.doi.org/10.1139/y86-167.
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Complete energy balance studies were made on groups of overfed (A) and underfed (B) Wistar rats. In experiment A one group was fed cafeteria diet ad libitum (the intake was 29% larger than the control), two other groups were fed the same diet but in restricted quantities (18 and 9% above control), and a fourth group, fed a stock diet, served as control. In experiment B, caloric intake was restricted by 12 and 31% in two groups fed cafeteria diet, and by 21 and 34% in two other groups fed stock diet. The experiments lasted 41 days and during that period the protein gain was comparable between the control and the cafeteria-29% group (643.4 ± 33.3 vs. 578.1 ± 25.0) but the fat gain was significantly different between the two groups (863.2 ± 81.6 vs. 1663.2 ± 99.8 kJ). When energy expenditure (EE) (metabolizable energy less storage added to the cost of storage) is expressed as a percentage of metabolizable energy (ME) intake no significant difference was found among the groups. The average value was [Formula: see text]. This finding would not support the presence of dietary-induced thermogenesis in animals overfed on the cafeteria diet. However, since the obligatory cost associated with storing energy would not explain the higher EE of the overfed groups, it is suggested that the level of ME intake exerts continuous proportional regulatory action on EE and, as a result, energy is spared by underfeeding and it is wasted by overfeeding. Rats fed the cafeteria diet, independent of whether they are overfed or restricted were shown to increase both brown adipose tissue (BAT) protein content and thermogenic capacity in response to norepinephrine. For that reason it is suggested that it is not the caloric content of the diet which affects BAT but instead other factors such as fat content or palatability of the food. The results also suggest that BAT is not directly implicated in the regulatory responses associated with various intakes of food. Indeed in the underfed experiment, although the capacity of the BAT was enhanced in the cafeteria groups, the EE was not different from that of the animals fed the stock diet.
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Bauwens, Jake D., Eric G. Schmuck, Christopher R. Lindholm, Rebecca L. Ertel, Jacob D. Mulligan, Ian Hovis, Benoit Viollet, and Kurt W. Saupe. "Cold tolerance, cold-induced hyperphagia, and nonshivering thermogenesis are normal in α1-AMPK−/− mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 2 (August 2011): R473—R483. http://dx.doi.org/10.1152/ajpregu.00444.2010.
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Recent studies indicate that a substantial amount of metabolically active brown adipose tissue (BAT) exists in adult humans. Given the unique ability of BAT to convert calories to heat, there is intense interest in understanding the regulation of BAT metabolism in hopes that its manipulation might be an effective way of expending excess calories. Because of the established role of AMP-activated protein kinase (AMPK) as a “metabolic master switch” and its extremely high levels of activity in BAT, it was hypothesized that AMPK might play a central role in regulating BAT metabolism. To test this hypothesis, whole body α1-AMPK−/− (knockout) and wild-type mice were studied 1) under control (room temperature) conditions, 2) during chronic cold exposure (14 days at 4°C), and 3) during acute nonshivering thermogenesis (injection of a β3-adrenergic agonist). Under control conditions, loss of α1-AMPK resulted in downregulation of two important prothermogenic genes in BAT, thyrotropin-releasing hormone (−9.2-fold) and ciliary neurotrophic factor (−8.7-fold). Additionally, it caused significant upregulation of α2-AMPK activity in BAT, white adipose tissue, and liver, but not cardiac or skeletal muscle. During acute nonshivering thermogenesis and chronic cold exposure, body temperature was indistinguishable in the α1-AMPK−/− and wild-type mice. Similarly, the degree of cold-induced hyperphagia was identical in the two groups. We conclude that α1-AMPK does not play an obligatory role in these processes and that adaptations to chronic loss of α1-AMPK are able to compensate for its loss via several mechanisms.
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Warwick, Penelope M., and Janis Baines. "Point of view: Energy factors for food labelling and other purposes should be derived in a consistent fashion for all food components." British Journal of Nutrition 84, no. 6 (December 2000): 897–902. http://dx.doi.org/10.1017/s000711450000252x.
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In Australia, the process by which food energy factors are derived for food labelling purposes is under review. One of the questions of international relevance is whether energy factors should be derived using a definition of metabolisable energy (ME) or a definition of net (metabolisable) energy (NME), or some mixture of the two. ME describes the food energy available for heat production and body gains. NME deducts obligatory thermogenesis from ME in an attempt to reflect the food energy that can be converted to ATP energy within the body. Some countries use NME to derive energy factors for novel food ingredients such as sugar alcohols and polydextrose, but continue to use ME for protein, fat, carbohydrate, and alcohol. The present paper puts a case for using a consistent system (ME at the present time) for all food components. Reasons for this include: consistent application to all food components allows valid comparisons between products; food energy values and estimates of energy expenditure (food energy requirements) should be directly comparable; NME does not account for all sources of thermogenesis; differences between ME and NME for sugar alcohols and polydextrose are small in the context of the whole diet; and the ME system does not preclude information about metabolic efficiency being provided as additional information. Any major change to the way in which energy values are expressed (e.g. global adoption of the NME system) merits wide discussion among the human nutrition community. One aim of this present paper is to stimulate this discussion.
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Schutz, Yves. "Role of substrate utilization and thermogenesis on body-weight control with particular reference to alcohol." Proceedings of the Nutrition Society 59, no. 4 (November 2000): 511–17. http://dx.doi.org/10.1017/s0029665100000744.
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Alcohol (ethanol; EtOH) provides fuel energy to the body (29·7 kJ (7·1 kcal)/g, 23·4 kJ (5·6 kcal)/ml), as do other macronutrients, but no associated essential nutrients. The thermogenic effect of EtOH (on average 15 % of its metabolizable value) is much greater than that of the main substrates utilized by the body, i.e. fat and carbohydrates (CHO), suggesting a lower net efficiency of energy utilization for EtOH than for fat and CHO. EtOH cannot be stored in the body and is toxic, so that there is an obligatory continuous oxidation of EtOH and it becomes the priority fuel to be metabolized. In contrast to CHO, its rate of oxidation does not depend on the dose ingested. As with CHO intake, it engenders a shift in postprandial substrate utilization (decrease in fat oxidation), but by a non-insulin-mediated mechanism. A limited amount of EtOH can be converted to fatty acids by hepatic de novo lipogenesis (as occurs with high levels of CHO feeding) from acetate production, which inhibits lipolysis in peripheral tissues. There is no evidence that EtOH consumed under normoenergetic conditions (i.e. isoenergetically replacing CHO or fat) leads to greater body fat storage than fat or CHO. However, there is still a lack of experimental studies on the influence of EtOH on the level of spontaneous physical activity in man. This effect may well depend on the dose of EtOH consumed as well as other intrinsic factors.
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Speakman, John R. "The physiological costs of reproduction in small mammals." Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1490 (August 8, 2007): 375–98. http://dx.doi.org/10.1098/rstb.2007.2145.
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Life-history trade-offs between components of fitness arise because reproduction entails both gains and costs. Costs of reproduction can be divided into ecological and physiological costs. The latter have been rarely studied yet are probably a dominant component of the effect. A deeper understanding of life-history evolution will only come about once these physiological costs are better understood. Physiological costs may be direct or indirect. Direct costs include the energy and nutrient demands of the reproductive event, and the morphological changes that are necessary to facilitate achieving these demands. Indirect costs may be optional ‘compensatory costs’ whereby the animal chooses to reduce investment in some other aspect of its physiology to maximize the input of resource to reproduction. Such costs may be distinguished from consequential costs that are an inescapable consequence of the reproductive event. In small mammals, the direct costs of reproduction involve increased energy, protein and calcium demands during pregnancy, but most particularly during lactation. Organ remodelling is necessary to achieve the high demands of lactation and involves growth of the alimentary tract and associated organs such as the liver and pancreas. Compensatory indirect costs include reductions in thermogenesis, immune function and physical activity. Obligatory consequential costs include hyperthermia, bone loss, disruption of sleep patterns and oxidative stress. This is unlikely to be a complete list. Our knowledge of these physiological costs is currently at best described as rudimentary. For some, we do not even know whether they are compensatory or obligatory. For almost all of them, we have no idea of exact mechanisms or how these costs translate into fitness trade-offs.
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Kopecky, J., L. Sigurdson, I. R. Park, and J. Himms-Hagen. "Thyroxine 5'-deiodinase in hamster and rat brown adipose tissue: effect of cold and diet." American Journal of Physiology-Endocrinology and Metabolism 251, no. 1 (July 1, 1986): E1—E7. http://dx.doi.org/10.1152/ajpendo.1986.251.1.e1.
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Thyroxine 5'-deiodinase (type II) is present in a microsomal fraction of brown adipose tissue (BAT) of Syrian hamsters. Cold exposure increased specific activity in homogenates after a lag period of approximately 2 h to reach a maximum by 1-3 days. Total activity increased 80 times in cold-acclimated hamsters. During deacclimation, a rapid decrease occurred again after a lag period of approximately 2 h. The increase did not parallel increases in protein or in thermogenic state of mitochondria (mitochondrial GDP binding), which occurred more slowly. Changes in serum 3,5,3'-triiodothyronine concentration paralleled changes in BAT 5'-deiodinase during both acclimation to cold and deacclimation. The cold-induced increase in BAT 5'-deiodinase activity occurred more slowly but was much larger in hamsters than in rats. Eating a palatable diet increased BAT protein content and thermogenic activity in both hamsters and rats but did not alter total 5'-deiodinase activity in either species. We conclude that the trophic response of brown adipose tissue to cold in both hamsters and rats is accompanied by an enhanced endogenous production of triiodothyronine that may play a role in control of tissue growth. The trophic response to a palatable diet differs in that enhanced endogenous production of triiodothyronine is not an obligatory accompaniment. Specific stimulation of 5'-deiodinase by cold might modify thermogenesis in tissues other than BAT by providing triiodothyronine and be of greater significance in hamsters than in rats.
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Manger, Paul R., Nina Patzke, Muhammad A. Spocter, Adhil Bhagwandin, Karl Æ. Karlsson, Mads F. Bertelsen, Abdulaziz N. Alagaili, et al. "Amplification of potential thermogenetic mechanisms in cetacean brains compared to artiodactyl brains." Scientific Reports 11, no. 1 (March 9, 2021). http://dx.doi.org/10.1038/s41598-021-84762-0.
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AbstractTo elucidate factors underlying the evolution of large brains in cetaceans, we examined 16 brains from 14 cetartiodactyl species, with immunohistochemical techniques, for evidence of non-shivering thermogenesis. We show that, in comparison to the 11 artiodactyl brains studied (from 11 species), the 5 cetacean brains (from 3 species), exhibit an expanded expression of uncoupling protein 1 (UCP1, UCPs being mitochondrial inner membrane proteins that dissipate the proton gradient to generate heat) in cortical neurons, immunolocalization of UCP4 within a substantial proportion of glia throughout the brain, and an increased density of noradrenergic axonal boutons (noradrenaline functioning to control concentrations of and activate UCPs). Thus, cetacean brains studied possess multiple characteristics indicative of intensified thermogenetic functionality that can be related to their current and historical obligatory aquatic niche. These findings necessitate reassessment of our concepts regarding the reasons for large brain evolution and associated functional capacities in cetaceans.
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Sonoda, Junichiro, Mark Z. Chen, and Amos Baruch. "FGF21-receptor agonists: an emerging therapeutic class for obesity-related diseases." Hormone Molecular Biology and Clinical Investigation 30, no. 2 (May 19, 2017). http://dx.doi.org/10.1515/hmbci-2017-0002.
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AbstractFibroblast growth factor 21 (FGF21) analogs and FGF21 receptor agonists (FGF21RAs) that mimic FGF21 ligand activity constitute the new “FGF21-class” of anti-obesity and anti-diabetic molecules that improve insulin sensitivity, ameliorate hepatosteatosis and promote weight loss. The metabolic actions of FGF21-class proteins in obese mice are attributed to stimulation of brown fat thermogenesis and increased secretion of adiponectin. The therapeutic utility of this class of molecules is being actively investigated in clinical trials for the treatment of type 2 diabetes and non-alcoholic steatohepatitis (NASH). This review is focused on various FGF21-class molecules, their molecular designs and the preclinical and clinical activities. These molecules include modified FGF21 as well as agonistic antibodies against the receptor for FGF21, namely the complex of FGF receptor 1 (FGFR1) and the obligatory coreceptor βKlotho (KLB). In addition, a novel approach to increase endogenous FGF21 activity by inhibiting the FGF21-degrading protease fibroblast activation protein (FAP) is discussed.
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Jackson, Travis C., Kiersten Gorse, Jeremy R. Herrmann, and Patrick M. Kochanek. "Hippocampal and Prefrontal Cortical Brain Tissue Levels of Irisin and GDF15 Receptor Subunits in Children." Molecular Neurobiology, January 7, 2021. http://dx.doi.org/10.1007/s12035-020-02250-4.
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AbstractCold-stress hormones (CSHs) stimulate thermogenesis and have direct neuroprotective effects on the brain. The obligatory receptor components of two new CSHs (irisin and growth differentiation factor-15 [GDF15]) were recently discovered. Irisin binds integrin-αV/β5 heterodimers while GDF-15 binds to the orphan receptor glial cell-derived neurotrophic factor (GDNF) family receptor α-like (GFRAL). In addition, integrin-αV/β5 was just identified as the key receptor mediating Zika virus infection in the CNS. We measured integrin-αV, integrin-β5, and GFRAL protein levels across 78 high-quality human male/female brain tissues in infants, toddlers, preschoolers, adolescent, and adults—providing the most robust analysis to date on their levels in the human cortex and hippocampus. We report that integrin-αV was detected at all ages in the prefrontal cortex with levels greatest in adults. Integrin-αV was also detected in the hippocampus in all age groups. In contrast, integrin-β5 was detected in cortex and hippocampus largely restricted to infants. Co-expression of integrin-αV/β5 in the human infant hippocampus and cortex suggests the possibility that irisin has a more robust effect on the developing vs. the adult brain and may have implications for Zika virus infection in infants and young children.
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Trayhurn, Paul, and Jonathan R. S. Arch. "Is energy expenditure reduced in obese mice with mutations in the leptin/leptin receptor genes?" Journal of Nutritional Science 9 (2020). http://dx.doi.org/10.1017/jns.2020.19.
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Abstract Rodents with mutations in the leptin, or leptin receptor, genes have been extensively used to investigate the regulation of energy balance and the factors that underlie the development of obesity. The excess energy gain of these mutants has long been considered as being due in part to increased metabolic efficiency, consequent to reduced energy expenditure, but this view has recently been challenged. We argue, particularly though not exclusively, from data on ob/ob mice, that three lines of evidence support the proposition that reduced expenditure is important in the aetiology of obesity in leptin pathway mutants (irrespective of the genetic background): (i) milk intake is similar in suckling ob/ob and +/? mice; (ii) ob/ob mice deposit excess energy when pair-fed to the ad libitum food intake of lean siblings; (iii) in several studies mutant mice have been shown to exhibit a lower RMR ‘per animal’ at temperatures below thermoneutrality. When metabolic rate is expressed ‘per unit body weight’ (inappropriately, because of body composition differences), then it is invariably lower in the obese than the lean. It is important to differentiate the causes from the consequences of obesity. Hyperphagic, mature obese animals weighing 2–3 times their lean siblings may well have higher expenditure ‘per animal’, reflecting the costs of being larger and of enhanced obligatory diet-induced thermogenesis resulting from the increased food intake. This cannot, however, be used to inform the aetiology of their obesity.