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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↗
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↗
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

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↗
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↗
PubMed2025

Bidirectional shifts in Pm20d1 expression impact thermogenesis and metabolism.

BACKGROUND: Peptidase M20 domain containing 1 (PM20D1) is a secreted N-fatty acyl amino synthase and hydrolase that controls tissue and blood levels of N-fatty acyl amino acids. In brown adipocytes, N-fatty acyl amino acids bind to mitochondria and act as uncouplers of mitochondria, independent of UCP1. Interventions aimed at increasing or inhibiting PM20D1 expression considerably impact energy balance and metabolism; however, little is known about naturally occurring variants of the PM20D1/Pm20d1 gene and their impact on phenotype. METHODS: In vivo, gene expression of Pm20d1 in BALB/c, C57BL/6, and Ucp1 KO in brown adipose tissue and other metabolic tissues was measured. In vitro, transcriptional activity of Pm20d1 and brown adipocytes' oxygen consumption in primary culture were assessed. Human PM20D1 circulating levels were quantified. In silico analysis of the Pm20d1 gene sequencing and human polymorphisms associated with PM20D1 was performed. RESULTS: Here, we identified a gain-of-function variant in the Pm20d1 promoter region present in BALB/c mice and absent in C57BL/6 mice. The presence of this variant is accompanied by increased expression of Pm20d1 in brown and white adipose tissues, muscle, liver, and hypothalamus; moreover, it leads to increased cold tolerance and UCP1-independent brown adipose tissue mitochondrial respiration. Inhibition of Pm20d1 in brown adipose tissue results in defective cold tolerance in BALB/c, whereas the brown adipose tissue overexpression of Pm20d1 results in increased cold tolerance in C57BL/6 mice. In humans, variants of the PM20D1 gene are associated with changes in body mass index, whereas at least one variant in the promoter region is associated with increased body mass index and metabolic syndrome. CONCLUSION: Thus, PM20D1 plays a bidirectional role in regulating thermogenesis and body mass, and, at least in part, variants in the promoter region can partially explain the differences in PM20D1 expression and its impact on the metabolic phenotype.

Thermogenesis↗
PubMed1978

Brown adipose tissue: the dominant site of nonshivering thermogenesis in the rat.

Measurements with tracer microspheres of changes in tissue blood flow associated with noradrenaline (NA)-induced calorigenesis in warm-acclimated and in cold-acclimated (CA) rats revealed very large increases in flow to brown adipose tissue (BAT). The data on flow together with measurements of the arteriovenous difference in blood O2 across interscapular BAT indicate that BAT accounts for at least 60% of the NA-induced nonshivering thermogenesis (NST) of CA rats. Skeletal muscle was found to be only minimally, if at all, involved in this NST.

Acclimatization↗
PubMed1978

Non shivering thermogenesis and implication of the thyroid in cold labile and cold resistant populations of the golden spiny mouse (Acomys russatus).

The golden spiny mouse is dependent on non shivering thermogenesis (N.S.T.) for thermoregulation at cool ambient temperatures. Mice from the shores of the Dead Sea (Ein-Gedi, EG-mice) lose body heat when exposed to 6 degrees C. Their rate of cooling is linearly correlated to the magnitude of N.S.T. This is true for mice acclimated to 28 degrees C, born in the laboratory or freshly captured. Mice from the high mountains of South Sinai (S-mice) resist cooling under the same conditions and their N.S.T. is about twice that of EG-mice. EG-mice did not acclimate to cold. However thyroxine injections made them cold resistant and their N.S.T. rose to values close to that of S-mice. Light and electronmicroscopy of the thyroids in mice acclimated to 28 degrees C and exposed to 6 degrees C, or injected with TRH suggested intense activity in S-mice and little activity in EG-mice.

Acclimatization↗
PubMed1978

Control of non-shivering thermogenesis in a hibernator.

Present experiments indicate that in hedgehogs two different control mechanisms of non-shivering thermogenesis (NST) exist. During arousal from hibernation catecholamines control heat production in the interscapular brown adipose tissue. In a non-hibernating state, cold-induced NST is controlled by a desoxycorticosterone-like acting compound. The effector system of this second mode of NST is obviously not the interscapular brown fat but a layer of brown adipose tissue which covers the whole back of the hedgehog.

Animals↗
PubMed1977

Corticotropin and nonshivering thermogenesis.

Chronic treatment with corticotropin led to reduced calorigenic effect of norepinephrine in cold acclimatized rats, but potentiated its effect in controls. This inhibitory effect was not due to the observed decrease in corticosterone plasma level, as it was shown by metopirone administration. It is concluded that corticotropin could have a competitive action on receptor sites mediating the calorigenic effect of norepinephrine in nonshivering thermogenesis.

Acclimatization↗
PubMed1979

A source of nonshivering thermogenesis in fur seal skeletal muscle.

The mitochondria from the subscapular muscle of naturally cold-stressed 10- to 15-year-old northern fur seals (Callorhinus ursinus) were loosely coupled upon isolation, whereas the mitochondria from the same muscle of warm-acclimated pups of the same age were tightly coupled. Thus, loose-coupled muscle mitochondria might provide an important vehicle for nonshivering thermogenesis in this species.

Adenine Nucleotides↗
PubMed1977

[Influence of conditions of the acclimatization to cold on the thermogenesis without shivering in rats].

As indicated by a theophylline administration previously to a norepinephrine infusion, the nonshivering thermogenesis does not seem to be mediated by the cyclic AMP system in constant cold acclimated rats, in opposite to rats acclimated to discontinuous cold. However, in that last thermal condition, the cyclic AMP mediation was not observed in the brown adipose tissue and in the liver.

Acclimatization↗