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At least 19 recordsLinked to original sources
PubMed1977

Nonshivering thermogenesis in the rat. I. The relation between drug-induced changes in thermogenesis and changes in the concentration of plasma cyclic AMP.

Barbital-sedated, cold-acclimated (CA) or warm-acclimated (WA) rats were given different doses and combinations of noradrenaline, theophylline, and the adrenergic-blocking agents propranolol and phentolamine, to stimulate or inhibit calorigenesis in various ways. To see whether the effects of these drugs on calorigenesis could be ascribed to effects on the adenylate cyclase (EC 4.6.1.1) - cyclic AMP system, and to try to assess thereby the significance of this system in the regulation of nonshivering thermogenesis (NST), changes in the concentration of plasma cyclic AMP were measured as an index (Broadus, A.E., Hardman, J.G., Kaminsky, N. I., Ball, J. H., Sutherland, E.W., and Liddle, G. W.: 1971. Ann. N.Y. Acad. Sci. 185, 50-60) of changes in tissue levels of cyclic AMP. In CA rats, which have a severalfold greater capacity for NST than WA rats, calorigenic responses to noradrenaline, theophylline, noradrenaline plus theophylline, or phentolamine plus theophylline were as much as four times larger than in WA rats, However, the changes in level of plasma cyclic AMP produced by each of these and other treatments were virtually the same for both groups. It would appear, therefore, that the difference between WA and CA rats in ability to produce heat by NST is not a function of the amplitude of changes in tissue levels of cyclic AMP. Nevertheless, it was also observed, and was particularly striking in CA rats, that when a drug or combination of drugs had a stimulatory, inhibitory, or synergistic effect on calorigenesis, it had a similar effect with respect to elevation of plasma cyclic AMP. Altogether, the results indicate that adenylate cyclase and cyclic AMP are likely to be participants in the regulation of NST in the rat, but that they would be subservient in this regard to whatever factors are responsible for acclimation-related differences in capacity for NST.

Animals↗
PubMed1978

Thermoregulation and non-shivering thermogenesis in the genetically obese (ob/ob) mouse.

1. The capacity ofr thermoregulation and thermogenesis in lean and genetically obese (ob/ob) mice has been investigated. 2. At 4 degrees C ob/ob mice rapidly die of hypothermia, because of a reduced capacity for cold-induced thermogenesis, but the animals are able to survive if previously adapted to 12 degrees C. 3. At all environmental temperatures between 30 degrees C and 10 degrees C the body temperature of ob/ob mice is 2.0-2.5 degrees C below that of lean animals. This may be due to a lower "setting" for body temperature. 4. At 34 degrees C the oxygen consumption of obese mice is greater than that of the lean animals while at 30 degrees C it is similar. When the environmental temperature is below 30 degrees C the oxygen consumption of the lean mice is greater. The obese animals therefore expend less energy on thermoregulatory thermogenesis. 5. The capacity for non-shivering thermogenesis was measured in lean and obese mice by investigating the effect of an injection of L-nor-adrenaline (1000 microgram/kg body weight) on the metabolic rate at 31 degrees C. Non-shivering thermogenesis was reduced by one-half in the obese animals. 6. One cause of the obesity of the ob/ob mouse is its high metabolic efficiency. We suggest that this high metabolic efficiency is due, at least in part, to less energy being expended on thermoregulatory thermogenesis.

Animals↗
PubMed1978

The central control of shivering and non-shivering thermogenesis in the rat.

1. To test whether the preoptic area controls only non-shivering and the spinal cord only shivering thermogenesis, ten rats were chronically implanted with a preoptic and a spinal cord thermode each. The following were then studied: (a) the effect of propranolol (8 mg/kg.hr) on the metabolic response to cooling the preoptic area, and the spinal cord, (b) the effect of exogenous noradrenaline (0.5 mg/kg) on the metabolic response to cooling the preoptic area, and the spinal cord, and (c) the effect of warming the preoptic area on the metabolic response to cooling the spinal cord, and vice versa. 2. Administration of propranolol inhibited the metabolic response to cooling each of the thermosensitive areas, but the response to cooling the preoptic area was more strongly inhibited than that to cooling the spinal cord. 3. Administration of exogenous noradrenaline did not prevent the metabolic response to cooling either the preoptic area or the spinal cord. 4. Warming the spinal cord completely inhibited the metabolic response to cooling the preoptic area, and warming the preoptic area fully inhibited the metabolic response to cooling the spinal cord. 5. It is concluded that exogenous noradrenaline underestimates the capacity for non-shivering thermogenesis, and that both thermosensitive areas can control both forms of thermogenesis, but that the preoptic area threshold of non-shivering thermogenesis is probably lower than that of shivering, while the spinal cord threshold of shivering is probably lower than that of non-shivering thermogenesis.

Animals↗
PubMed2025

The suprachiasmatic nucleus regulates brown fat thermogenesis in male mice through an adrenergic receptor ADRB3-S100B signaling pathway.

The suprachiasmatic nucleus (SCN), the central circadian pacemaker, orchestrates daily metabolic rhythms, yet its role in substrate selection and thermogenic adaptation under stress remains insufficiently understood. Here, we show that SCN lesioning abolishes the adaptive suppression of brown adipose tissue (BAT) thermogenesis typically observed during time-restricted feeding in subthermoneutral environments (TRF-STE), a paradigm that imposes concurrent nutrient and thermal stress. Contrary to wild-type responses, SCN-lesioned mice maintain elevated BAT thermogenic activity, despite impaired lipolysis, instead shifting toward glucose-driven heat production. This phenotype is accompanied by sustained sympathetic tone and β3-adrenergic receptor (ADRB3) signaling in BAT. Mechanistically, we identify a SCN-regulated ADRB3-S100B signaling axis underlying this metabolic reprogramming. S100B, a nutrient-sensitive calcium-binding protein, is upregulated in BAT following SCN disruption, where it promotes thermogenesis by stimulating brown adipocyte proliferation and suppressing senescence. Functional studies reveal that S100B is both necessary and sufficient for sustaining BAT thermogenesis under TRF-STE. Furthermore, diverse SCN disruption models, including light-induced circadian arrhythmia, N-Methyl-D-aspartic acid (NMDA) excitotoxicity, and Caspase-3-mediated ablation, consistently elevate S100B expression in BAT, reinforcing its role as a convergent effector of SCN-regulated metabolic adaptation. Thus, in intact animal, the SCN restrains the ADRB3-S100B module, gating BAT thermogenic output in accordance with energetic availability. Disruption of SCN output lifts this restraint, unmasking a latent ADRB3-S100B program that preserves thermogenesis when lipid fuel is limited. These findings reveal a previously unrecognized role of the SCN in governing thermogenic flexibility and fuel partitioning, and position the ADRB3-S100B axis as a potential target for mitigating circadian misalignment and metabolic disease.

Animals↗
PubMed1979

Thermoregulation in the diabetic-obese (db/db) mouse. The role of non-shivering thermogenesis in energy balance.

1. Thermoregulation and non-shivering thermogenesis have been studied in the genetically diabetic obese (db/db) mouse. 2. At all environmental temperatures between 33 and 10 degrees C the body temperature of the diabetic mice was lower than that of the normal littermates, the difference varying from 1.1 degrees C at 33 degrees C to 4.5 degrees C at 10 degrees C. 3. At 4 degrees C the diabetic mice rapidly died (3.2h) of hypothermia while the normal mice maintained their body temperature within the normal range. 4. At 23 degrees C the diabetic animals exhibited a diurnal rhythm in body temperature which was similar in both phase and amplitude to the controls, but at every point throughout the 24h cycle the temperature of the mutants was lower by 1--2 degrees C. 5. The resting metabolic rate at thermoneutrality (33 degrees C) was higher per whole animal for the diabetics than for the normals. However, at temperatures below thermoneutrality the converse was observed; between 30 and 4 degrees C the RMR of the mutants was lower than the controls by approximately 25%. 6. The capacity for non-shivering thermogenesis in diabetic mice was only one-half that found in normal animals. 7. The diabetic mouse has abnormalities in thermoregulation and non-shivering thermogenesis which are similar to those found in the genetically obese (ob/ob) mouse. It is concluded that the high metabolic efficiency of the diabetic mouse, like that of the ob/ob mouse, can be explained by a reduced energy expenditure on thermoregulatory thermogenesis; this may represent a primary mechanism for the operation of the "thirfty genotype" associated with obesity and diabetes.

Animals↗
PubMed1976

Cellular thermogenesis.

The principal conclusion presented in this review is that no single mechanism underlies any of the examples of basal or altered cellular thermogenesis. Both increased Na+ pump operation and uncoupling may occur to a greater or lesser extent, as may other heat-producing mechanisms. There are areas in which further information is needed in order to explain fully the composite nature of the mechanisms involved in cellular thermogenesis. The control of mitochondrial oxidations in their natural habitat (i.e. inside cells) by regulatory proteins, fatty acids, ions (Ca2+, Na+, K+), cyclic AMP, protein kinases, prostaglandins, purine nucleotides, and other factors must be elucidated. There is evidence for the participation of all of these substances in the control of cellular thermogenesis, but no scheme has been developed that takes them all into account. Further emphasis on the tissue-specific differences in the regulation of mitochondrial function is desirable. The regulation of the biogenesis of mammalian mitochondria is another area currently under intense study for which no clear hypothesis has as yet emerged. Information in this area is needed in order to understand the mechanism and role of mitochondrial adaptations associated with altered thermogenesis in hyperthyroidism, in acclimation to cold, and in exercise training, as well as the nature of altered mitochondrial biogenesis, such as appears to underlie the Luft hypermetabolic syndrome.

Adenosine Triphosphatases↗
PubMed1978

Hormonal thermogenesis of "non-norepinephrine" type.

Physiological significance and mechanisms controlling thermogenesis due to substances other than norepinephrine (NE) are considered. Epinephrine (E) induces a strong calorigenic effect, which is potentiated by cold adaptation to the level observed after application of NE. Thermogenesis due to E is located to a great extent in visceral organs. Cold acclimation increases the component of epinephrine thermogenesis located in the brown adipose tissue and non-visceral organs, predominantly. Although E and NE act on the same thermogenic effector, their effect is realized via different regulatory sites. Steroid hormones are not necessary for inducing cold resistance and thermogenesis due to NE. The permissive role of steroids and other substances in inducing changes in enzyme activity and synthesis during various cold stress is discussed.

Adipose Tissue, Brown↗
PubMed2025

Cooperative contribution of multiple energy substrate pathways to floral thermogenesis in sacred lotus.

Floral thermogenesis in lotus (Nelumbo nucifera) is a highly energy-intensive process, requiring substantial metabolic reconfiguration and substrate input. However, the mechanisms coordinating energy substrate supply during this process remain unclear. Here, we integrated microscale proteomics, time-series transcriptomics, and mitochondrial feeding assays to elucidate the substrate provisioning strategies supporting thermogenesis in lotus receptacles. Proteomic analysis revealed a concerted upregulation of major energy metabolism pathways at the thermogenic initiation stage, accompanied by enhanced expression of energy dissipation-related proteins (alternative oxidase and uncoupling proteins), indicative of a metabolic shift favoring heat production over ATP synthesis. Our results highlight the cooperative contribution of multiple pyruvate sources to mitochondrial respiration. Both the mitochondrial pyruvate carrier (MPC)-mediated cytosolic pyruvate import and the NAD-dependent malic enzyme (NAD-ME)-derived intramitochondrial pyruvate flux were significantly elevated at the thermogenic stage. Notably, isotopic feeding experiments revealed that NAD-ME-derived pyruvate may contribute more substantially than MPC-derived pyruvate under thermogenic conditions, reflecting a highly flexible substrate utilization strategy. In addition, increased expression of alanine aminotransferase (AlaAT) and β-oxidation-related genes suggested that alanine transamination and fatty acid degradation may further expand the respiratory substrate pool. Collectively, this study uncovers a diverse and dynamic landscape of energy substrate supply that underpins heat production in thermogenic lotus tissues. These findings offer insights into how plants coordinate metabolic flexibility to meet the high energetic demands of floral thermogenesis.

Flowers↗
PubMed1976

Pathways of carbohydrate oxidation during thermogenesis by the spadix of Arum maculatum.

1. The aims of this work were to discover the pathways of carbohydrate oxidation prior to and during thermogenesis by the club of the spadix of Arum maculatum, and whether there was coarse control of these pathways. 2. 14C02 production from [1-14C]-, [3,4-14C]-, and [6-14C]glucose, the detailed distribution of 14C from [1-14C]- and [6-14C]glucose, and the maximum catalytic activities of phosphofructokinase, fructose-1,6-diphosphate aldolase, glucose-6-phosphate dehydrogenase, and phosphogluconate dehydrogenase were determined at different stages in the development of the spadix. The results indicate that in the early stages carbohydrate is oxidized via both the pentose phosphate pathway and glycolysis, and that a shift to glycolysis occurs during development so that just before and during thermogenesis glycolysis predominates almost exclusively. 3. During development the activities of phosphofructokinase and glucose-6-phosphate dehydrogenase per club increased 100- ans during spadix development, and indicated that the onset of rapid glycolysis at thermogenesis is regulated by fine control or availability of substrate.

Fructose-Bisphosphate Aldolase↗
PubMed1978

Plasma membrane involvement in brown fat thermogenesis.

Recent experiments indicate that plasma membranes of brown adipocytes contain distinct alpha- and beta-adrenergic receptors able to recognize norepinephrine. Although activation of either receptor leads to brown fat thermogenesis via pathways that have some, but not all, events in common, the beta-induced calorigenesis appears quantitatively greater than that elicited by the alpha-pathway. The sensitivity of the adrenergic-evoked respiration to Na+/K+ pump blockade as well as to atractyloside supports the view that a significant portion of brown fat thermogenesis reflects increased ATP turnover and enhanced mitochondrial ATP synthesis.

Adipose Tissue, Brown↗
PubMed1978

Hibernation as a model for studies on thermogenesis and its control.

Mammalian hibernation is characterized by the alternation of prolonged periods of hypothermia and spontaneous arousals with a temporary return to euthermia. Of special interest to the physiology of effectors of thermogenesis are the following points: a) In the second part of the arousal process, the metabolic rate reaches 6 to 8 times BMR, with a body temperature about 10 degrees C lower. Enzymatic adaptations provide for the maintenance of normal reaction rates and regulatory potentials at low temperatures, but how very high thermogenetic rates can be achieved still remains largely unexplained. b) Entrance into hibernation involves a resetting of the hypothalamic thermostat to a lower level, but this is probably not the only intervening regulation. Evidence is presented in favor of a control of thermogenesis at the effector level, in terms both of baseline levels and of loop gains. One likely control factor is acid-base state, which can be changed rapidly and reversibly by ventilation and is characterized by a strong acidosis in hibernation.

Animals↗
PubMed1979

Thermogenesis and thermolysis during sleeping and waking in the rat.

Thermogenesis (VO2), sensible heat loss and subcutaneous back temperature were recorded simultaneously during sleeping and waking in both intact and depilated rats at Ra ranging from 21--28 degrees C. VO2 increased during wakefulness (W), decreased and plateaued during slow wave sleep (SWS) and then decreased 10% with each paradoxical sleep (PS) phase. Sensible heat loss, which represented about 90% of the heat production, increased and plateaued during SWS, decreased in W and generally rose abruptly (+40%) during PS. After removal of the fur the mean levels of VO2 and sensible heat loss were increased by 20--50% and returned to normal values within two weeks, although their variations related to stages of sleep were unchanged. These results concerning thermogenesis and thermolysis are in agreement with the variations of body temperature (brain excluded) during sleeping and waking.

Animals↗
PubMed1979

A role for brown adipose tissue in diet-induced thermogenesis.

Measurement of energy balance during voluntary overeating in rats unequivocally establishes the quantitative importance of diet-induced thermogenesis in energy balance. Like cold-induced thermogenesis, this form of heat production involves changes in the activity of the sympathetic nervous system and brown adipose tissue which suggest that this tissue may determine metabolic efficiency and resistance to obesity.

Adipose Tissue, Brown↗
PubMed1976

Norepinephrine thermogenesis in seasonally acclimatized and cold acclimated red-backed voles in Alaska.

The calorigenic response (millilitres O2 per gram pre hour) to injected norepinephrine (NE) was compared as an index of nonshivering thermogenesis (NST) in the following groups of the Alaska red-backed vole (Clethrionomys rutilus): (1) summer, (2) fall acclimatized, (3) winter acclimatized, (4) 20 degrees C acclimated and (5) 5 degrees C acclimated. The metabolic response was tested at thermoneutrality (25 degrees C) and during cold exposure (5 degrees C). Winter acclimatized voles showed a significantly greater metabolic response to NE than summer voles at both 25 degrees C and 5 degrees C. In summer or winter voles the total metabolic rate after NE (Mne) was similar at 25 degrees C and 5 degrees C but the fraction of the total caused by exogenous NE was lower at 5 degrees C. Thus, thermogenesis during cold exposure and resulting from exogenous NE appear to be based on the same mechanism, and NE has thermoregulatory significance in these voles. The magnitude of the NE response in winter voles was comparable to he highest values reported for bats and exceeded levels reported for other adult small mammal species. Summer acclimatized voles and those acclimatized to 20 degrees C in the laboratory were comparable in their response to NE but winter acclimatized voles were significantly more sensitive to NE than voles acclimated to 5 degrees C. The seasonal winter peak in MNE coincided with peaks previously found for maximum metabolic capacity (MMAX), maximum brown fat, and the period of coldest temperature in December-January. the ratio of MNE to Mmax was similar throughout the year. The results suggest that small arctic-subarctic rodents have a greater capacity for NE stimulated NST than rodents from temperate latitudes probably because they are acclimatized to colder seasonal condtions.

Acclimatization↗
PubMed1978

Differential impairment of thermogenesis in the pigeon after chemical sympathectomy.

A dose-controlled chemical sympathectomy with 6-hydroxydopamine (6-OHDA) did not disrupt thermostasis in the pigeon at +38 degrees C. At +6 degrees C, thermogenesis was impaired, but the lower body temperature and oxygen consumption were stable and vasoconstriction was normal. The stability may partly be explained by a massive release of adrenaline from the adrenals (50% in 20 min). Despite a deficit in heat production both after sympathectomy and after acute 6-OHDA, no change in muscle electrical activity was observed. Plasma free fatty acid (FFA) concentration was significantly elevated after sympathectomy, but no changes occurred in blood glucose or plasma lactate levels. The results indicate a major compensatory role for the adrenals in avian thermogenesis. They also suggest a sympathetically mediated auxiliary thermogenic mechanism independent of muscle electrical activity and coupled to FFA metabolism.

Adrenal Glands↗
PubMed1978

Controlled cellular energy conversion in brown adipose tissue thermogenesis.

Brown adipose tissue serves as a model system for nonshivering thermogenesis (NST) since a) it has as a primary physiological function the conversion of chemical energy to heat; and b) preliminary data from other tissues involved in NST (e.g., muscle) indicate that parallel mechanisms may be involved. Now that biochemical pathways have been proposed for brown fat thermogenesis, cellular models consistent with a thermodynamic representation can be formulated. Stated concisely, the thermogenic mechanism in a brown fat cell can be considered as an energy converter involving a sequence of cellular events controlled by signals over the autonomic nervous system. A thermodynamic description for NST is developed in terms of a nonisothermal system under steady-state conditions using network thermodynamics. Pathways simulated include mitochondrial ATP synthesis, a Na+/K+ membrane pump, and ionic diffusion through the adipocyte membrane.

Adipose Tissue, Brown↗
PubMed1979

Thermoregulatory nonshivering thermogenesis in men, with special reference to lipid metabolism.

The existence of thermoregulatory nonshivering thermogenesis, with special reference to lipid metabolism, was investigated in men. Acute cold exposure (10 degrees C, 60 min) produced a marked increase in heat production, with concomitant elevation of plasma free fatty acid (FFA) level, modest increase of ketone body concentration and lowered respiratory quotient (R.Q.). The correlation of heat production to plasma FFA levels was significantly positive; that is, subjects with higher heat production showed higher plasma FFA levels. Moreover, correlation of either heat production or plasma FFA levels to R.Q. was significantly negative, respectively. On the other hand, exposure to cold after an administration of nicotinic acid, which has a suppressive effect on FFA mobilization from adipose tissue, resulted in less cold-elevated heat production, a significant fall of plasma FFA and ketone body concentrations, and no change in R.Q. Although no visible or only slight shivering was observed in control cold exposure study, greater shivering occurred in the nicotinic acid cold exposure study. These results appear to indicate that nonshivering thermogenesis as a source of heat production achieved by enhanced utilization of lipids is also present in men.

Adult↗