Academic literature on the topic 'Obligatory thermogenesis'

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Journal articles on the topic "Obligatory thermogenesis"

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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.
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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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6

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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10

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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Dissertations / Theses on the topic "Obligatory thermogenesis"

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Laurila, M. (Mirja). "Thermoregulatory consequences of starvation and digestion in birds." Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514277147.

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Abstract In homeothermic birds and mammals, several thermoregulatory adaptations have evolved for surviving in unstable, food-restricted conditions. This study focuses on two adaptive mechanisms in pigeons (Columba livia) and quails (Coturnix coturnix japonica): hypothermia and the adaptive use obligatory heat production connected with feeding and digestion. The plasticity of the hypothermic response in fed and fasted birds and birds with restricted feeding was studied in laboratory and outdoor winter conditions. The other objective was to study adaptive timing of digestion, and substitution of facultative thermogenesis by obligatory heat production in cold and at thermoneutrality. The results showed that fasting has a strong influence on the level of nocturnal hypothermia in laboratory conditions: hypothermia becomes progressively deeper when fasting continues. In outdoor conditions, ambient temperature and predation risk modulated the daily body temperature (Tb) pattern of fasting pigeons. In very cold conditions, diurnal Tb of fasted birds also dropped below the normal level of the active phase. Predation risk prevented diurnal hypothermia but also attenuated the depth of nocturnal hypothermia in fasting pigeons. This study provides the first empirical effects of predation risk on hypothermia in starving birds. The study suggests that the presence of crop in pigeons allows adaptive timing of digestion. At thermoneutrality, peak digestion appeared late in the dark phase in birds with fed in the morning. Because the Tb of the birds increases to diurnal levels late in the dark phase, this obligatory heat from digestion can be used to aid re-warming by such timing. On other hand, the results of this study were partly opposite to the classical model of thermoregulatory substitution. In line with the classical model, a postprandial increase in metabolic rate (heat increment of feeding, HIF) was seen at thermoneutrality but not in cold. However, electromyographic measurements showed that there was no postprandial decrease in the intensity of shivering in the fed birds in cold. This indicates that true thermoregulatory substitution may be less common than assumed and suggests a role for facultative thermogenesis in HIF.
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