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At least 19 recordsLinked to original sources
PubMed2002

Thermogenesis associated with fermentable carbohydrate in humans, validity of indirect calorimetry, and implications of dietary thermogenesis for energy requirements, food energy and body weight.

BACKGROUND: Animal studies and theory show fermentable carbohydrate (FC) intake causes appreciably thermogenesis, but a similar occurrence in humans is controversial. HYPOTHESES: (a) That indirect calorimetry (IDC) is a valid method to assess thermogenesis during fermentation. (b) That a consistent and rigorous approach to the analysis of published IDC data from human studies will establish a representative thermogenic response to FC. (c) That conventional estimates of food energy and energy requirements can mismatch appreciably, more especially when thermogenesis is ignored. PURPOSE: To derive information and understanding of IDC, thermogenesis and energy balance in relation to food energy and energy requirement estimates. METHODS: (a) The validities of IDC equations that estimate the heat of reaction and carbohydrate utilization were assessed for various types of FCs under various circumstances. (b) Pooled analysis of eight published randomized cross-over studies in humans with elevation of FC intake. Studies were analysed for the first time or reanalysed according to a consistent approach with appropriate corrections for confounders. (c) Some 1500 regular and 'special' diet compositions were examined to assess the extent to which Atwater general food energy factors and updated estimates of energy requirements mismatch due to variation in substrate-associated thermogenesis and substrate-associated faecal+urinary energy losses. Impact of such mismatches on BMI was assessed under conditions of all else being equal. RESULTS: (a) Indirect calorimetry was valid, providing robust estimates of heat production during various types of fermentation; only small correction factors were necessary. By contrast, IDC equations for carbohydrate utilization sometimes applied poorly to FC. (b) A best estimate of thermogenesis in humans due to fermentation, above that due to oral glucose as a reference standard, was 0.39 (s.e.m. 0.14) kJ per kJ net metabolizable energy (NME; P<0.05, n=8 studies, total 72 humans) compared with 0.34 kJ/kJ from theory. Six sources of bias were identified; all had potential to underestimate FC thermogenesis. (c) Mismatches in energy availability and requirement estimates were often marked and translated into long-term differences in body mass index from approximately 20 to 33 kg/m(2) in average-height middle-aged initially obese women, and from approximately 22 to a non-survivable 13 kg/m(2) in initially slim women. CONCLUSIONS: (a) Indirect calorimetry is valid for the present purpose. (b) Thermogenesis in response to FC is real in humans and is comparable to that in animals and in theory. (c) Mismatches between estimates of energy requirements and dietary energy as metabolizable energy means the two expressions are not directly comparable, which has implications for the expression of food energy, energy requirements and the conduct and interpretation of research related to body weight.

Body Weight↗
PubMed2000

The effect of short-term fasting on shivering thermogenesis in Japanese quail chicks (Coturnix coturnix japonica): indications for a significant role of diet-induced/growth related thermogenesis.

(1) The effect of short-term fasting on metabolism and shivering thermogenesis was studied in 9-day-old Japanese quail. (2) After 31 h of fasting, heat production decreased 39% and body temperature over 2 degrees C in the thermoneutral zone. The difference in heat production between control and fasting groups decreased with decreasing ambient temperature. (3) Despite the lower metabolic rate, the amplitudes of shivering EMGs were higher in fasted chicks, especially in pectoralis. This indicates that fasted quails used shivering to compensate the decrease in diet-induced/growth related thermogenesis. (4) In cold, conductance of control birds decreased simultaneously with increasing heat production while in fasted chicks, conductance decreased to its minimum before heat production was activated. (5) Japanese quail chicks adapt quickly to short-term fasting by decreasing metabolism but they maintain their ability to thermoregulate in cold. Diet-induced/growth related thermogenesis has a significant role in thermoregulation since it reduces the need of shivering thermogenesis.

Journal Article↗
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↗
PubMed2003

Thermogenesis inhibition in brown adipocytes is a specific property of volatile anesthetics.

BACKGROUND: This investigation examined the possibility that the inhibitory effect of halothane on nonshivering thermogenesis (heat production) in brown adipocytes is not a universal effect of all anesthetic agents but related to the type of anesthetic. METHODS: Brown adipocytes from hamster were isolated with a collagenase digestion method and incubated with anesthetic agents. The rate of oxygen consumption was measured with an oxygen electrode. The effect of clinically relevant (and higher) doses of anesthetics of different classes on basal and norepinephrine-induced thermogenesis (oxygen consumption) was tested. RESULTS: Two distinct groups of anesthetics could be distinguished: thermogenesis inhibitors and noninhibitors. Thermogenesis inhibitors include volatile anesthetics such as halothane (IC(50), 1.1 mm), ether (IC(50), 20 mm), and chloroform (IC(50), 2.2 mm) (nominal concentrations), but also tribromoethanol (IC(50), 0.6 mm), all inducing inhibition of norepinephrine-induced thermogenesis without affecting the EC for norepinephrine. Thermogenesis noninhibitors include the nonvolatile anesthetics pentobarbital, propofol, ketamine, and urethane, the inhalation anesthetic nitrous oxide, and, notably, also the volatile nonanesthetics (nonimmobilizers) 1,2-dichlorohexafluorocyclobutane and 2,3-dichlorooctafluorobutane; none of these compounds had any effect on norepinephrine-induced thermogenesis at any concentration tested. CONCLUSIONS: There are two distinct classes of anesthetics with regard to effects on thermogenesis, thermogenesis inhibitors and thermogenesis noninhibitors. The results are important for the interpretation of studies in thermal biology in general; specifically, they indicate that conclusions concerning regulation of nonshivering thermogenesis during anesthesia depend on the type of anesthetic used. Of clinical importance is that the volatile anesthetics are inhibitory for nonshivering thermogenesis and thus for an alternative heat production when myorelaxants prevent shivering. As the distinction between thermogenesis inhibitors and thermogenesis noninhibitors corresponds to the distinction between volatile and nonvolatile anesthetics, it may be related to the mode of action of the volatile anesthetics.

Adipocytes↗
PubMed1989

Role of thermogenesis in the regulation of energy balance in relation to obesity.

Obligatory thermogenesis is a necessary accompaniment of all metabolic processes involved in maintenance of the body in the living state, and occurs in all 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.

Adipose Tissue, Brown↗
PubMed2001

An adipose-specific control of thermogenesis in body weight regulation.

Much of our understanding about 'adaptive thermogenesis' as a control system in mammalian weight regulation derives from studies of experimental starvation and overfeeding, and these have served to characterize its functional role as an 'attenuator' of energy imbalance. By applying a system-analysis approach in evaluating data on the energetics of starvation and refeeding, evidence is presented here in support of the hypothesis that there are in fact two distinct control systems underlying adaptive thermogenesis. In one of them, the efferent limb is primarily under the control of the sympathetic nervous system (SNS), whose functional state is dictated by overlapping or interacting signals arising from a variety of environmental stresses, including food deprivation, deficiency of essential nutrients, excess energy intake and exposure to cold or to infections; it is hence referred to as the non-specific control of thermogenesis, and is likely to occur primarily in organs/tissues with a high specific metabolic rate (eg liver, kidneys, brown fat). The other is independent of the functional state of the SNS and is dictated solely by signals arising from the state of depletion of the adipose tissue fat stores; it is hence referred to as the adipose-specific control of thermogenesis, and is postulated to occur primarily in the skeletal muscle. While suppression of this adipose-specific thermogenesis during both starvation and refeeding leads to energy conservation, the energy spared during refeeding is directed specifically at the replenishment of the fat stores, so that it functions as an 'accelerator' of fat recovery. These two distinct control systems for adaptive thermogenesis have been incorporated in a compartmental model of body weight and body composition regulation. This is used to provide a mechanistic explanation as to how, during weight recovery, they can operate simultaneously but in opposite directions--with activation of thermogenesis under non-specific control being energy-dissipating, while suppression of thermogenesis under adipose-specific control being energy-conserving--and could hence explain the paradox of a high efficiency of fat recovery co-existing with an overall state of enhanced thermogenesis and hypermetabolism. Elucidating the components of the adipose-specific control of thermogenesis (ie its sensors, signals and effector mechanisms) will have important implications for our understanding of body composition regulation, and hence for the development of more effective strategies in the management of cachexia and obesity.

Adipose Tissue↗
PubMed1998

Development of infrared imaging to measure thermogenesis in cell culture: thermogenic effects of uncoupling protein-2, troglitazone, and beta-adrenoceptor agonists.

PURPOSE: Although the effects of thermogenic agents in cell culture can be measured by direct microcalorimetry, only a few samples can be analyzed over several hours. In this report, we describe a robust non-invasive technique to measure real-time thermogenesis of cells cultured in microtiter plates using infrared thermography. METHODS: Yeast were transformed with uncoupling protein-2 (UCP2) or exposed to carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP) or rotenone. Adipocytes were exposed to rotenone, FCCP, cycloheximide. troglitazone, or CL316243. Thermogenesis was measured using infrared thermography. RESULTS: Thermogenesis increased after exposing yeast to the mitochondrial uncoupler, FCCP, or transforming the cells with UCP2. Further, thermogenesis in adipocytes was stimulated by CL316243, a beta3-adrenoceptor agonist being developed to treat obesity. The protein synthesis inhibitor, cycloheximide, did not inhibit CL316243-mediated thermogenesis. In contrast, the mitochondrial proton transport inhibitor, rotenone, inhibited thermogenesis in yeast and adipocytes. Similarly, the antidiabetic agent, troglitazone, suppressed thermogenesis in adipocytes. Although increased UCP synthesis resulted in increased thermogenesis in yeast, UCP expression did not correlate with thermogenesis in adipocytes. CONCLUSIONS: The results, taken together with the high resolution (0.002 degrees C) and robustness (384-well format) of the approach, indicate infrared-imaging is a rapid and effective method for measuring thermogenesis in vitro.

Adipocytes↗
PubMed1991

Influence of mild cold on the components of 24 hour thermogenesis in rats.

1. The influence of two weeks' acclimation to either 28 degrees C (thermal neutrality) or 21 degrees C (mild cold) on 24 h heat production and motor activity has been investigated in male Wistar rats. Food intake was controlled and provided as a single meal of approximately 170 kJ per day. Mathematical modelling was used to relate metabolic rate to measured movement and time of day. 2. For animals at thermal neutrality it was clear that metabolic rate increased during periods of substantial measured movement and returned to baseline during periods of minimal activity. Total heat production could therefore be divided into two components: underlying and movement-induced thermogenesis. 3. At 21 degrees C, a more complex model was needed. During periods of substantial activity, the relation between metabolic rate and movement was similar to that at 28 degrees C and total heat production could be divided into the same two components of underlying and movement-induced thermogenesis. However, during periods of prolonged inactivity, a different model was required, which included a component of extra metabolic activity, termed supplementary thermogenesis. By fitting this model to data at 28 and 21 degrees C, it was possible to partition 24 h heat production into the three possible sources of underlying, movement-induced and supplementary thermogenesis. 4. Total 24 h heat production was approximately 25% higher for rats at 21 compared with 28 degrees C (P less than 0.01) and underlying thermogenesis was approximately 20% higher for those in the mild cold (P less than 0.01). Measured movement was significantly reduced in the mild cold (P less than 0.05) although it was energetically less efficient since there was no difference in movement-induced thermogenesis, which accounted for 18 and 15% of total heat production at 28 and 21 degrees C respectively. Supplementary thermogenesis was observed only in the mild cold and it accounted for approximately 6% of 24 h heat production, while the peak value accounted for 20% of total heat production. Circadian variations in thermogenesis were also different at 28 compared with 21 degrees C. Possible mechanisms accounting for the components of underlying thermogenesis and supplementary thermogenesis are discussed.

Animals↗
PubMed1985

[Thermogenesis induced by nutrients in man: its role in weight regulation].

The maintenance of body weight at a stable level for an adult man requires the involvement of mechanisms which should adapt energy intake to energy expenditure (or vice versa). Energy balance is thus maintained near equilibrium. However, the nature of these mechanisms is poorly understood. The control of food intake has been studied often and will not be discussed in this presentation. This paper concerns the control of energy expenditure, particularly the control of nutrient-induced thermogenesis. The recent interest in this field has arisen following the demonstration of the role of nutrient-induced thermogenesis in rats and mice having free access to the "cafeteria diet". Under these conditions, these animals overeat, but the major part of the excess energy intake above maintenance, is dissipated as heat through the sympathetic activation of brown adipose tissue. By contrast, a thermogenic defect in brown adipose tissue is involved in the development of genetic or hypothalamic obesity in rats and mice. In man, diet-induced thermogenesis seems to play a smaller role in the control of energy balance than in small mammals. This is probably related to the partial atrophy of brown adipose tissue in adult man. Studies on thermogenesis induced by the intravenous infusion of glucose and insulin (euglycemic hyperinsulinemic clamp technique) in man have allowed us to identify two components: the first, the obligatory thermogenesis is due to the energetic cost of glucose storage (which mainly occurs as glycogen); the second has been called facultative thermogenesis, and is dependent upon stimulation of the sympathetic nervous system. Facultative thermogenesis can be suppressed by propranolol, a drug which blocks the beta-receptors of the sympathetic nervous system. The effector tissue which is responsible for the facultative thermogenesis in man is unknown. Overfeeding studies with carbohydrates in man have also shown the occurrence of facultative thermogenesis. The contribution of a thermogenesis defect to the development of obesity in predisposed individuals is shown by studies using the technique of the respiration chamber. About one third of obese subjects who have been studied in the chamber have shown a decreased postprandial thermogenic response. A thermogenic defect could explain a weight gain of about 10 kg. Other mechanisms which include eating behaviour and low physical activity are needed to explain weight gains greater than 10 kg.(ABSTRACT TRUNCATED AT 400 WORDS)

Adipose Tissue, Brown↗
PubMed2002

Vago-sympathoadrenal reflex in thermogenesis induced by osmotic stimulation of the intestines in the rat.

Duodenal infusion of hypertonic solutions elicits osmolality-dependent thermogenesis in urethane-anaesthetized rats. Here we investigated the involvement of the autonomic nervous system, adrenal medulla and brain in the mechanism of this thermogenesis. Bilateral subdiaphragmatic vagotomy greatly attenuated the first hour, but not the later phase, of the thermogenesis induced by 3.6 % NaCl (10 ml kg(-1)). Neither atropine pretreatment (10 mg kg(-1), I.P.) nor capsaicin desensitization had any effect on the osmotically induced thermogenesis, suggesting the involvement of non-nociceptive vagal afferents. Bilateral splanchnic denervation caudal to the suprarenal ganglia also had no effect, suggesting a lack of involvement of spinal afferents and sympathetic efferents to the major upper abdominal organs. Adrenal demedullation greatly attenuated the initial phase, but not the later phase, of thermogenesis. Pretreatment with the beta-blocker propranolol (20 mg kg(-1), I.P.) attenuated the thermogenesis throughout the 3 h observation period. The plasma adrenaline concentration increased significantly 20 min after osmotic stimulation but returned to the basal level after 60 min. The plasma noradrenaline concentration increased 20 min after osmotic stimulation and remained significantly elevated for 120 min. Therefore, adrenaline largely mediated the initial phase of thermogenesis, and noradrenaline was involved in the entire thermogenic response. Moreover, neither decerebration nor pretreatment with the antipyretic indomethacin (10 mg kg(-1), S.C.) had any effect. Accordingly, this thermogenesis did not require the forebrain and was different from that associated with fever. These results show the critical involvement of the vagal afferents, hindbrain and sympathoadrenal system in the thermogenesis induced by osmotic stimulation of the intestines.

Adrenal Glands↗
PubMed1984

Nonshivering thermogenesis.

Nonshivering thermogenesis was originally defined as a cold-induced increase in heat production not associated with the muscle activity of shivering. Recent research shows it to be a metabolic process located primarily in brown adipose tissue and controlled by the activity of the sympathetic nervous supply of this tissue. Another stimulus to sympathetic nervous activity, the ingestion of food, promotes diet-induced thermogenesis in brown adipose tissue. Brown adipose tissue grows and regresses in accordance with the extent to which it is stimulated, either by cold or by diet, and the capacity of the animal for cold-induced nonshivering thermogenesis and diet-induced thermogenesis increases or decreases accordingly. In certain hibernators another stimulus, photoperiod, promotes growth or regression of brown adipose tissue. The neural regulation of thermogenesis in brown adipose tissue is thus not only part of the central control mechanisms involved in thermoregulation but also part of those involved in the regulation of energy balance. In hibernators , such as the hamster, the neural regulation of thermogenesis in brown adipose tissue includes, in addition, central components that control the function of brown adipose tissue during entry into and arousal from hibernation and pineal or melatonin-related components that control its growth in response to photoperiod. In animals which become intermittently torpid, such as the mouse, the regulation includes in addition central components that control the function of brown adipose tissue during entry into and arousal from torpor. The central neural components involved in control of thermoregulation are better understood than are those involved in the regulation of energy balance. Studies of animal with hypothalamic obesity indicate that the control of diet-induced thermogenesis in brown adipose tissue requires the participation of the ventromedial region of the hypothalamus whereas the control of cold-induced nonshivering thermogenesis does not. The importance of comparative studies in different species is emphasized since any neural model for the control of brown adipose tissue thermogenesis is likely to apply in detail only to the species for which it was developed.

Acclimatization↗
PubMed1989

The endocrine control of the onset of thermogenesis at birth.

The experimental studies in the fetal sheep demonstrate that the central hypothalamic mechanisms for responding to a cold stress have differentiated well before birth. There are several major determinants of the initiation of maximal thermogenesis at birth. These are cutaneous cooling, oxygenation and separation from the placenta. Firstly the stimulation of cutaneous cold receptors regulates sympathetic nervous system activity, primarily local noradrenaline release from sympathetic nerve termini to the brown adipocyte adrenoreceptors. Circulating catecholamines, the euthyroid state and other hormones also play a role. Secondly an increase in oxygen delivery to brown adipose tissue through increased oxygen content and increased blood flow is required. Finally, our observations suggest that separation from the placenta is necessary for maximal nonshivering thermogenesis. The effects on thermogenesis of interrupting and reestablishing placental flow are rapid and reversible. Umbilical cord occlusion is the signal for a rapid increase in thermogenesis, while the release of cord occlusion is followed by an equally rapid fall in thermogenesis. This strongly suggests the presence of a placental inhibitor of brown adipose tissue thermogenesis. The problem of the regulation of growth and recruitment of brown adipose tissue in the fetus despite the lack of thermal stress in utero may be resolved by this evidence for an inhibitory factor of thermogenesis produced by the placenta. The withdrawal of the inhibitor at birth by separation from the placenta will allow the rapid initiation of thermogenesis in response to sympathetic nervous system stimulation of the brown adipose tissue.

Animals↗
PubMed1980

Increased proton conductance pathway in brown adipose tissue mitochondria of rats exhibiting diet-induced thermogenesis.

It has recently been demonstrated that in rats induced to overeat by being fed a varied and palatable diet (the 'cafeteria diet') there is a marked increase in heat production which serves to reduce, or prevent, the development of obesity. This diet-induced thermogenesis is associated with increases in sympathetic activity, and with changes in brown adipose tissue. Following cafeteria feeding, brown adipose tissue hypertrophies and and exhibits increased lipolysis and an apparently greater thermogenesis in response to noradrenaline. These metabolic changes resemble those seen during non-shivering thermogenesis in cold-adapted rats, and it was proposed that non-shivering thermogenesis and diet-induced thermogenesis have a similar metabolic origin which depends on the unique capacity of brown adipose tissue for thermogenesis. During non-shivering thermogenesis heat is produced in brown adipose tissue through a proton conductance pathway across the inner mitochondrial membrane that dissipates the proton gradient generated by respiration. The activity of the proton conductance pathway can be modulated by purine nucleotides, and changes in the pathway seem to be related to the level of purine nucleotide binding to brown adipose tissue mitochondria. We now report results which indicate that the proton conductance pathway is augmented in cafeteria-fed rats, and suggest that it operates to dissipate their excess energy intake through diet-induced thermogenesis

Adipose Tissue↗
PubMed1984

Brown adipose tissue thermogenesis, energy balance, and obesity.

The concept that thermogenesis in brown adipose tissue can play a role as an energy buffer has developed during the last 5 years. The history of this development is reviewed. Control of brown adipose tissue thermogenesis resides in regions of the brain, located primarily but not exclusively in the hypothalamus, that control the activity of the sympathetic nervous system in response to diet and to environmental temperature. Brown adipose tissue mitochondria are uniquely specialized for thermogenesis, possessing a specific proton leakage mechanism that is regulated by the concentration of fatty acids in the cells of the brown adipose tissue. The level of fatty acids is in turn controlled by the lipolytic action of noradrenaline on the tissue. Sympathetic stimulation also exerts a trophic influence on brown adipose tissue. Effective thermogenesis in brown adipose tissue is associated with leanness and decreased metabolic efficiency, as in the rat rendered hyperphagic and hypermetabolic, by either cold acclimation or cafeteria feeding. Conversely, food restriction is associated with suppressed thermogenesis in brown adipose tissue and increased metabolic efficiency. Defective brown adipose tissue thermogenesis is associated with obesity in a number of different types of obese animals. In three of these (the genetically obese fa/fa Zucker rat, the mouse with hypothalamic damage induced by gold thioglucose, the rat with a surgically induced hypothalamic lesion), diet-induced thermogenesis is defective in brown adipose tissue, but cold-induced thermogenesis is normal. In another type of obese animal, the genetically obese (ob/ob) mouse, control of brown adipose tissue is defective. Studies of this control are complicated by the frequency of torpor in the fed state.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue, Brown↗
PubMed1984

Potentiation of in vivo thermogenesis in rat brown adipose tissue by stimulation of alpha 1-adrenoreceptors is associated with increased release of cyclic AMP.

Release of cyclic AMP (cAMP) from the interscapular brown adipose tissue (IBAT) of barbital-anesthetized, cold-acclimated rats given activators and inhibitors of brown adipose tissue (BAT) thermogenesis was assessed by measuring IBAT blood flow (microsphere method) and the arteriovenous difference in plasma cAMP across the tissue. The release was taken as an index of the generation of cAMP in the IBAT. During thermogenesis induced by infusion of graded doses of noradrenaline (NA), release of cAMP increased from no significant release without NA to 68 pmol/min at a NA dose that effected maximal thermogenesis. The alpha-adrenoreceptor antagonist dihydroergotoxin inhibited NA-induced BAT thermogenesis and markedly reduced the release of cAMP. The alpha 1-adrenoreceptor agonist phenylephrine potentiated the in vivo thermogenic response of BAT to isoproterenol or to a suboptimal dose of NA and enhanced the release of cAMP elicited by these catecholamines. But given alone, phenylephrine or dihydroergotoxin had very little or no effect on thermogenesis and cAMP release. These results suggest that stimulation of the alpha 1-adrenoreceptors on BAT adipocytes potentiates the thermogenic response originating from stimulation of the adenylate cyclase-coupled beta 1-adrenoreceptors by increasing, in some indirect way, the generation of cAMP, the intracellular messenger for activation of thermogenesis. However, in the absence of proof that adipocytes are the principal source of the cAMP released from IBAT, during catecholamine-induced thermogenesis, this explanation for the effect of alpha 1-adrenoreceptor stimulation on thermogenesis remains tentative.

Adipose Tissue, Brown↗
PubMed1982

Effect of diet and exercise on norepinephrine-induced thermogenesis in male and female rats.

Male and female rats were fed standard laboratory chow or a highly palatable diet (cafeteria diet) for 10 wk. The cafeteria diet caused an increase in caloric intake and in body weight, and it induced thermogenesis that was associated with elevated plasma triiodothyronine (T3) levels, increased brown adipose tissue size, and enhanced metabolic response to norepinephrine. For a comparable caloric intake, body-weight gain was significantly greater in female than in male rats possibly because of difference in thermogenesis as suggested by the response to norepinephrine. Exercise training (swimming 2 h/day for 10 wk) reduced food intake and body-weight gain and failed to increase norepinephrine-induced thermogenesis in rats fed laboratory chow. In animals fed the cafeteria diet, food intake and body-weight gain were also reduced by exercise training, which at the same time diminished the diet-induced thermogenesis as evidenced by the diminution of 1) brown fat hypertrophy, 2) the elevation of plasma T3, and 3) the hyperthermic response to injected norepinephrine. It is suggested that the thyroid hormone and catecholamines through their actions on the brown adipose tissue are the important regulatory of thermogenesis. Exercise training would reduce the diet-induced thermogenesis by preventing increased T3 production. Enhanced thermogenesis may be considered an adaptive reaction as it serves to reduce fat deposition in animals fed cafeteria diet and to promote nonshivering heat production in the cold. On the other hand, exercise training reduces thermogenesis and thus prevents energy wasting.

Adipose Tissue↗