Receptors In Brown Adipose Tissue Research Articles

Obesity Represses CYP2R1, the Vitamin D 25-Hydroxylase, in the Liver and Extrahepatic Tissues.

ABSTRACTLow plasma level of 25‐hydroxyvitamin D (25‐OH‐D), namely vitamin D deficiency, is associated with obesity and weight loss improves 25‐OH‐D status. However, the mechanism behind obesity‐induced vitamin D deficiency remains unclear. Here, we report that obesity suppresses the expression of cytochrome P450 (CYP) 2R1, the main vitamin D 25‐hydroxylase, in both mice and humans. In humans, weight loss induced by gastric bypass surgery increased the expression of CYP2R1 in the s.c. adipose tissue suggesting recovery after the obesity‐induced suppression. At the same time, CYP27B1, the vitamin D 1α‐hydroxylase, was repressed by the weight loss. In a mouse (C57BL/6N) model of diet‐induced obesity, the plasma 25‐OH‐D was decreased. In accordance, the CYP2R1 expression was strongly repressed in the liver. Moreover, obesity repressed the expression of CYP2R1 in several extrahepatic tissues, the kidney, brown adipose tissue, and testis, but not in the white adipose tissue. Obesity had a similar effect in both male and female mice. In mice, obesity repressed expression of the vitamin D receptor in brown adipose tissue. Obesity also upregulated the expression of the vitamin D receptor and CYP24A1 in the s.c. adipose tissue of a subset of mice; however, no effect was observed in the human s.c. adipose tissue. In summary, we show that obesity affects CYP2R1 expression both in the mouse and human tissues. We suggest that in mouse the CYP2R1 repression in the liver plays an important role in obesity‐induced vitamin D deficiency. Currently, it is unclear whether the CYP2R1 downregulation in extrahepatic tissues could contribute to the obesity‐induced low plasma 25‐OH‐D, however, this phenomenon may affect at least the local 25‐OH‐D concentrations. © 2020 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.

¿Puede el estudio del gen ADRB3 ayudar a mejorar los programas de pérdida de peso en individuos obesos?

IntroductionObesity is a chronic disease of multifactorial origin characterized by excess weight and excess fat accumulation, and whose etiology includes intrinsic (genetic, physiological, and metabolic) and extrinsic (social and cultural) factors. Fat accumulation is caused by a prolonged imbalance in the energy balance influenced, among other factors, by adaptive thermogenesis, which is triggered by cold environmental conditions, or by hypercaloric intake. Thermogenesis is regulated by the sympathetic nervous system and occurs in the muscle and brown adipose tissue. There are adrenergic receptors in brown adipose tissue, including the beta-3 adrenergic receptor (ADRB3), the main receptor for the regulation of thermogenesis. The presence in heterozygosis of an SNP-type polymorphism in the ADRB3 gene (Trp64Arg; rs4994) is associated with a lower lipolytic activity, a predisposition to obesity, and resistance to weight loss. The objective of this study was to analyze through a systematic review the weight loss program most appropriate for carriers. MethodsA retrospective study of published papers on rs4994 polymorphism in the SNP and PubMed databases was conducted. ResultsMost published studies suggest the presence of obesity and resistance to weight loss in carriers, and report significant improvements in anthropometric parameters when patients receive fat-rich hypocaloric diets. ConclusionsBased on these conclusions, specific nutritional and physical exercise guidelines are proposed for individuals carrying the Trp64Arg allele.

Secretin: An Old Hormone with a Burning Secret

Most theories of meal-induced thermogenesis involve a gut-brain-brown adipose tissue axis driving sympathetic nervous system-mediated thermogenesis. Li etal. demonstrate that secretin released by the gut after a meal binds to abundant receptors in brown adipose tissue to stimulate thermogenesis, inhibiting food intake and thereby suggesting a novel role for secretin regulating satiety.

Modulation of musculoskeletal hyperalgesia by brown adipose tissue activity in mice.

Cold exposure and a variety of types of mild stress increase pain in patients with painful disorders such as fibromyalgia syndrome. Acutely, stress induces thermogenesis by increasing sympathetic activation of beta-3 (β3) adrenergic receptors in brown adipose tissue. Chronic stress leads to the hypertrophy of brown adipose, a phenomenon termed adaptive thermogenesis. Based on the innervation of skeletal muscle by collaterals of nerves projecting to brown adipose, we theorized an association between brown adipose tissue activity and musculoskeletal hyperalgesia and tested this hypothesis in mice. Exposure to a cold swim or injection of BRL37344 (β3 adrenergic agonist) each enhanced musculoskeletal hyperalgesia, as indicated by morphine-sensitive decreases in grip force responses, whereas SR59230A (β3 adrenergic antagonist) attenuated swim-induced hyperalgesia. Chemical ablation of interscapular brown adipose, using Rose Bengal, attenuated the development of hyperalgesia in response to either swim stress or BRL37344. In addition, elimination of the gene expressing uncoupling protein-1 (UCP1), the enzyme responsible for thermogenesis, prevented musculoskeletal hyperalgesia in response to either a swim or BRL37344, as documented in UCP1-knockout (UCP1-KO) mice compared with wild-type controls. Together, these data provide a convergence of evidence suggesting that activation of brown adipose contributes to stress-induced musculoskeletal hyperalgesia.

Synthesis of the dopamine D2/D3 receptor agonist (+)-PHNO via supercritical fluid chromatography: preliminary PET imaging study with [3-11C]-(+)PHNO

Carbon-11 labeled (+)-4-[1-11C]propyl-3,4,4a,5,6,10b-hexahydro-2H-naphtho[1,2-b][1,4]oxazin-9-ol ([1-11C]-(+)-PHNO) is a dopamine D3-preferring agonist radiopharmaceutical used for medical imaging by positron emission tomography (PET). We report the synthesis of (+)-PHNO using supercritical fluid chromatography for enantiomeric resolution of its norpropyl derivative, HNO, followed by propylation. (+)-HNO was used to prepare the radiolabeling precursor, (+)-trans-4-acetyl-9-triisopropylsilyloxy-2,3,4a,5,6,10b-hexahydro-4H-naphth[1,2b][1,4]oxazine, in 12 steps. Modifications to the labeling procedure were made to ensure consistent preparation of [3-11C]-(+)-PHNO via [11C]CH3I. A preliminary PET imaging study was carried out with this tracer in an attempt to image dopamine receptors in brown adipose tissue (brown fat) in vivo.

Thyroid-stimulating hormone receptor in brown adipose tissue is involved in the regulation of thermogenesis

C.RF- Tshr(hyt/hyt) mice have a mutated thyroid-stimulating hormone receptor (TSHR), and, without thyroid hormone supplementation, these mice develop severe hypothyroidism. When hypothyroid Tshr(hyt/hyt) mice were exposed to cold (4 degrees C), rectal temperature rapidly dropped to 23.9 +/- 0.40 degrees C at 90 min, whereas the wild-type mice temperatures were 37.0 +/- 0.15 degrees C. When we carried out functional rat TSHR gene transfer in the brown adipose tissues by plasmid injection combined with electroporation, there was no effect on the serum levels of thyroxine, although rectal temperature of the mice transfected with pcDNA3.1/Zeo-rat TSHR 90 min after cold exposure remained at 34.6 +/- 0.34 degrees C, which was significantly higher than that of Tshr(hyt/hyt) mice. Transfection of TSHR cDNA increased mRNA and protein levels of uncoupling protein-1 (UCP-1) in brown adipose tissues, and the weight ratio of brown adipose tissue to overall body weight also increased. Exogenous thyroid hormone supplementation to Tshr(hyt/hyt) mice restored rectal temperature 90 min after exposure to cold (36.8 +/- 0.10 degrees C). These results indicate that not only thyroid hormone but also thyroid-stimulating hormone (TSH)/TSHR are involved in the expression mechanism of UCP-1 in mouse brown adipose tissue. TSH stimulates thermogenesis and functions to protect a further decrease in body temperature in the hypothyroid state.

Expression profiles of three isoforms of inositol 1,4,5-trisphosphate receptor in brown adipose tissue of the rat

The thermogenic function of brown adipose tissue (BAT) is known to be mainly regulated by a signal transduction cascade via β-adrenoceptor. However, recent studies indicated that the α-adrenoceptor and its downstream signal transduction cascade, causing elevation of the cellular Ca 2+ level, are also important for the regulation of this function of BAT. In the present study, expression profiles of 3 isoforms of the inositol 1,4,5-trisphosphate (IP 3) receptor, known as one of the major components of the machinery regulating the intracellular Ca 2+ concentration in the BAT of rats, were investigated by Northern analysis. Of these three IP 3 receptor isoforms, the type 2 one was found to be the most abundant of the three in BAT. Furthermore, when rats were exposed to the cold, under which condition the thermogenic function of BAT is known to be stimulated, the expression levels of types 1 and 2 isoforms of IP 3 receptor were remarkably elevated. The results of Western analysis supported the predominant expression of the type 2 isoform in BAT. However, different from the results of Northern analysis, the expression levels of types 1 and 2 isoforms of IP 3 receptor protein in BAT were not influenced by exposure of the animals to the cold.

Thyrotropin Receptors in Brown Adipose Tissue: Thyrotropin Stimulates Type II Iodothyronine Deiodinase and Uncoupling Protein-1 in Brown Adipocytes

It has been demonstrated that TSH receptors are expressed not only in thyroid gland but also in extrathyroidal tissues. Brown adipose tissue of guinea pig has been reported to express TSH receptor messenger RNA (mRNA), but the physiological roles of TSH receptors in brown adipose tissue have not been understood. We studied the expression and function of TSH receptors in rat brown adipose tissue and cultured rat brown adipocytes. Northern analysis demonstrated the expression of TSH receptor mRNA in rat brown adipose tissue and cultured rat brown adipocytes. TSH receptor mRNA in rat brown adipose tissue was decreased by cold exposure of the rat, and its mRNA in cultured rat brown adipocytes was also decreased by incubation with TSH or (Bu)2cAMP. TSH increased the intracellular cAMP concentration in cultured rat brown adipocytes in a dosedependent manner. Type II iodothyronine deiodinase mRNA, its activity, and uncoupling protein-1 mRNA in cultured rat brown adipocytes were significantly increased by incubation with TSH in a dose-dependent manner. These results suggest the expression of functional TSH receptors in brown adipose tissue, which may be involved in regulation of the expression of type II iodothyronine deiodinase and uncoupling protein-1.

Thyrotropin receptors in brown adipose tissue: thyrotropin stimulates type II iodothyronine deiodinase and uncoupling protein-1 in brown adipocytes.

It has been demonstrated that TSH receptors are expressed not only in thyroid gland but also in extrathyroidal tissues. Brown adipose tissue of guinea pig has been reported to express TSH receptor messenger RNA (mRNA), but the physiological roles of TSH receptors in brown adipose tissue have not been understood. We studied the expression and function of TSH receptors in rat brown adipose tissue and cultured rat brown adipocytes. Northern analysis demonstrated the expression of TSH receptor mRNA in rat brown adipose tissue and cultured rat brown adipocytes. TSH receptor mRNA in rat brown adipose tissue was decreased by cold exposure of the rat, and its mRNA in cultured rat brown adipocytes was also decreased by incubation with TSH or (Bu)(2)cAMP. TSH increased the intracellular cAMP concentration in cultured rat brown adipocytes in a dose dependent manner. Type II iodothyronine deiodinase mRNA, its activity, and uncoupling protein-1 mRNA in cultured rat brown adipocytes were significantly increased by incubation with TSH in a dose-dependent manner. These results suggest the expression of functional TSH receptors in brown adipose tissue, which may be involved in regulation of the expression of type II iodothyronine deiodinase and uncoupling protein-1.

Thyroid hormone control of thermogenesis and energy balance.

The mechanisms whereby thyroid hormone increases heat production have been analyzed with emphasis in more recent developments. Thyroid hormone increases obligatory thermogenesis as a result of the stimulation of numerous metabolic pathways involved in development, remodeling, and delivery of energy to the tissues. In addition, thyroid hormone may specifically stimulate some thermogenic mechanisms selected during evolution of homeotherms (e.g., Na/K-ATPase, Ca2+ cycling in muscle). Thyroid hormone also plays an essential role in facultative thermogenesis interacting with the sympathetic nervous system (SNS) at various levels. Peripherally, thyroid hormone potentiates the effects of the SNS at the level of the adrenergic receptor and adenylyl cyclase complex as well as distal from this point. Synergistic interactions between T3 and cAMP on the regulation of gene expression have been described. Brown adipose tissue (BAT) T4-5'-deiodinase plays a central role in controlling heat production. When this enzyme is stimulated by norepinephrine in the euthyroid and hypothyroid condition, it provides high concentrations of T3 to BAT; inhibition by T4 in hyperthyroidism may limit brown fat thermogenic responses. Also, thyrotoxicosis uniquely reduces the expression of beta 3-adrenergic receptors in brown adipose tissue, and the increased obligatory thermogenesis of this condition, via afferent neural pathways, may reduce the hypothalamic stimulation of brown fat, providing additional mechanisms to limit brown adipose tissue thermogenesis in hyperthyroidism.

Selective beta 3-adrenergic agonists of brown adipose tissue and thermogenesis. 2. [4-[2-[(2-Hydroxy-3-phenoxypropyl)amino]ethoxy]phenoxy]acetamides.

The ester methyl [4-[2-[(2-hydroxy-3-phenoxypropyl)amino]ethoxy]phenoxy]acetate (1) (R1 = OMe) had previously been identified as the most interesting member of a series of selective beta 3-adrenergic agonists of brown adipose tissue and thermogenesis in the rat. In vivo it acts mainly via the related acid 1 (R1 = OH). Amides have been examined to determine whether they have advantages over the ester. In particular, in the rat and dog the half-lives of amides of appropriate potency were no longer than those of the ester. The amide (S)-4-[2-[(2-hydroxy-3-phenoxypropyl)amino]ethoxy]-N-(2- methoxyethyl)phenoxyacetamide [S-27, ICI D7114] was selected as having properties consistent with a sustained-release formulation should that prove necessary. Unlike the ester it is resistant to hydrolysis in the gut lumen. Further testing of ICI D7114 has shown that in the rat, cat, and dog it stimulates the beta 3-adrenergic receptor in brown adipose tissue at doses lower than those at which it affects beta 1- and beta 2-adrenergic receptors in other tissues. Slimming effects were observed in the dog. ICI D7114 may be a selective thermogenic agent in man and may be useful in the treatment of obesity and diabetes.

Selective beta 3-adrenergic agonists of brown adipose tissue and thermogenesis. 1. [4-[2-[(2-Hydroxy-3-phenoxypropyl)amino]ethoxy]phenoxy]acetates.

The ester methyl [4-[2-[(2-hydroxy-3-phenoxypropyl)amino]ethoxy]phenoxy]acetate (8) has been identified as the most interesting member of a series of selective beta 3-adrenergic agonists of brown adipose tissue and thermogenesis in the rat. In vivo it acts mainly via the related acid 10. Potency was generally markedly reduced by placing substituents on the phenyl ring of the phenoxypropanolamine unit of 8; only the 2-fluoro analogue 16 had comparable potency to 8. Other structure-activity relationships are discussed. Further testing of 8 (ICI 198157) has shown that in the rat it stimulates the beta 3-adrenergic receptor in brown adipose tissue at doses lower than those at which it affects beta 1 and beta 2 adrenergic receptors in other tissues. It increases metabolic rate, as judged by an increase in oxygen consumption, and in the genetically obese Zucker rat it causes a reduced rate of weight gain. This class of compound may be useful in the treatment of obesity in man.

Comparison of the pharmacological profiles of adrenergic drugs (Including BRL-agonists) at [ 3H]prazosin and [ 3H]CGP-12177 binding sites in brown adipose tissue

1. In order to determine the selectivity of classical and novel adrenergic agents for α 1- and β-adrenergic receptors in brown adipose tissue, the ability of these agents to compete for binding sites labelled with [ 3H]prazosin and [ 3H]CGP-12177, respectively, was investigated. 2. The β -antagonist propranolol, known to inhibit norepinephrine-induced respiration in micromolar concentrations, bound to the [ 3H]CGP-12177 site with nanomolar affinity. 3. Among agonists, only isoprenaline showed high selectivity for β-receptors, and only oxymetazoline for ga 1-receptors. 4. Unexpectedly, the novel thermogenic agonists (BRL-agonists), shown to be potent and selective stimulators of brown fat thermogenesis, were unselective and bound only with low affinity to the [ 3H]CGP-12177 binding sites. 5. These results suggest that the β-adrenergic binding site in brown adipose tissue identified here with [ 3H]CGP-12177 may not be the one (or not the only one) coupled to thermogenesis.

α1- and β-adrenergic receptors in brown adipose tissue of lean (Fa/?) and obese (fa/fa) Zucker rats. Effects of cold-acclimation, sucrose feeding and adrenalectomy

1. The populations of alpha 1- and beta-adrenergic receptors in brown adipose tissue (BAT) of genetically obese Zucker rats (fa/fa) were studied with [3H]prazosin and [3H]CGP-12177 respectively. 2. The density of alpha 1-adrenergic receptors in BAT was significantly lower in obese than in lean Zucker rats, both at 2-4 months of age and at 6 weeks of age. The density of beta-adrenergic receptors was identical in BAT of lean and obese 6-week-old Zucker rats. 3. Cold-acclimation increased the alpha 1-receptor density significantly in BAT of both lean and obese Zucker rats, and the number of beta-receptors was also somewhat increased. 4. Sucrose feeding did not affect the density of alpha 1-receptors in BAT of lean or obese Zucker rats, but it increased beta-receptor density. 5. Adrenalectomy restored the density of alpha 1-adrenergic receptors in BAT of obese Zucker rats to the value observed in lean rats. 6. It is concluded that there is a direct correlation between alpha 1-receptor density and tissue recruitment, and that alpha 1-receptor density is thus positively correlated with sympathetic activity. beta-Receptor density is apparently better correlated with feeding conditions.

α 2-Adrenergic receptors in brown adipose tissue of infant rats—I. Identification and characteristics of binding sites in isolated plasma membranes

1. 1. α 2- Adrenoceptor antagonists [ 3H]yohimbine and [ 3H]RX 781094 and the partial α 2- agonist [ 3H]clonidine exhibited specific binding to plasma membrane fragments isolated from interscapular brown fat of 7-day-old rats. 2. 2. Competition studies with epinephrine, yohimbine and practolol revealed that [ 3H]norepinephrine, the principal in vivo agonist acting upon brown adipocytes, can readily bind to α 2- adrenoceptors in brown fat of infant rats. 3. 3. The presence of α 2- adrenoceptor subclass in brown fat of infant rats may play a role in the sympathetic regulation of this rapidly proliferating tissue.

Formula omitted] receptors in brown adipose tissue of infant rats—II. Studies on function and regulation

1. 1.Clonidine inhibited the forskolin- and MIX-induced rate oflipolysis in brown fat adipocytes isolated from interscapular brown fat of 7-day-old rats. Its effect could be prevented by the α 2 - antagonist yohimbine. 2. 2.Pertussis toxin prevented the above effect of clonidine, thus indicating that α 2- adrenoceptors are linked with adenylate cyclase via the N i regulatory subunit. 3. 3.Che4mical sympathectomy of 5-day-old rats by 6-hydroxydopamine increased the number of low-affinity α 2 sites in brown fat. 4. 4.Chronic administration of yohimbine to 2-3-week-old rats also increased the density of α 2- adrenoceptors in brown fat. 5. 5.It is suggested that brown fat of infant rats possesses functional α 2- adrenoceptors .

Nuclear 3,5,3'-triiodothyronine (T3) in brown adipose tissue: receptor occupancy and sources of T3 as determined by in vivo techniques.

The amount and sources of T3 associated with high affinity, low capacity cellular nuclear receptors in brown adipose tissue (BAT) have been estimated by in vivo pulse-labeling techniques. Maximal binding capacity was measured by in vivo saturation analysis. Nuclear receptor occupancy at endogenous levels of T3 and T4 in euthyroid rats was estimated from the equilibrium nuclear to serum ratio of tracer T3, and the locally generated nuclear T3 to serum T4 ratio after injecting tracer T3 and T4. These ratios were multiplied, respectively, by the endogenous concentrations of T3 and T4 as measured by RIA. The maximal binding capacity was 0.65 ng T3/mg DNA, and saturation was 71%. Fifty-five percent of the nuclear T3 was generated locally, and 45% was derived from circulating T3. BAT is, hence, comparable to the liver in number of receptors (approximately 5000/cell) and to the pituitary with regard to saturation and relative contributions of locally generated T3 and plasma T3 to nuclear T3. These results suggest that BAT may be an important target for thyroid hormones and, along with other data, that alterations in the activity of the type II 5'-deiodinase of this tissue may influence the saturation of nuclear T3 receptors.

Increased alpha 1-adrenergic receptor density in brown adipose tissue of cafeteria-fed rats.

A possible general corollary between alpha 1-receptor density in brown adipose tissue and the degree of activation of the tissue was investigated. For this purpose, the effect of cafeteria feeding on alpha 1-adrenergic receptors in brown adipose tissue of seven-week-old female rats was studied by the use of the alpha 1-antagonist (3H)-prazosin. In cafeteria-fed rats, the KD of the alpha 1-receptor for (3H)prazosin was unchanged (about 0.35 nM), but the receptor density was doubled (up to 40 fmol per mg of membrane protein). This was also observed when the results were expressed per unit of a plasma-membrane marker (5'-nucleotidase). It was concluded that an increased alpha 1-receptor density is seen not only in cold-acclimated rats, but also in other conditions where brown fat is activated, and a possible general physiological significance of alpha 1-adrenergic pathways in brown adipose tissue is discussed.

β‐Adrenergic Receptors in Brown‐Adipose Tissue. Characterization and Alteratios during Acclimation of Rats to Cold

The capacity of brown adipose tissue to respond calorigenically to catecholamines increases markedly during cold‐acclimation of adult rats. To investigate this phenomenon, we have used the potent radioactive ligand (‐)‐[3H]dihydroalprenolol to directly estimate the number, the density and the affinity of β‐adrenergic receptors in brown adipose tissue membranes from control, cold‐exposed and cold‐acclimated rats. Binding of (−)‐[3H]dihydroalprenolol to unfractionated membranes was rapid, stable, saturable and reversible. It displayed the affinity, specificity and stereoselectivity expected of binding to adenylate cyclase‐coupled β‐adrenergic receptors. β‐Adrenergic agonists competed for binding sites with an order of potency typical of the β1 subtype of adrenergic receptors: (−)‐Isoproterenol > (−)‐norepinephrine ≥ (−)‐epinephrine. Binding exhibited a remarkable stereoselectivity, the (−)‐isomers of β‐adrenergic agonists and antagonists being 34 to 280 times more potent than the (+)‐isomers in competing for (−)‐[3H]dihydroalprenolol binding sites. Total interscapular brown adipose tissue of the adult, warm‐acclimated rat contained 1.12 ± 0.08 pmol of (−)‐[3H]dihydroalprenolol binding sites. During cold‐acclimation, growth of the tissue was accompanied by a 4–5‐fold increase in the total number of recptor sites. However, this increase did not keep pace with the increse in brown adipose tissue cellularity (as estimated by total tissue DNA content), resulting in a 40–50% reduction in receptor density. The decrease in receptor density was associated with cold‐exposure rather than with cold‐acclimation. The affinity of (−)‐[3H]dihydroalprenolol receptor sites was not significantly altered by cold‐acclimation. The results of this study are interpreted as indicating that catecholamines released via activation of the sympathetic nervous system regulate both the density and the number of their own receptors in brown adipose tissue of cold‐exposed animals. The development of the hyperadrenergic response of this thermogenic tissue during cold‐acclimation may result from a marked organ hyperplasia associated with an increased number of β‐adrenergic receptor sites and cannot be explained by alterations in receptor density or affinity.

Interrelationship of cyclic AMP, lipolysis, and respiration in brown fat cells.

ARTICLESInterrelationship of cyclic AMP, lipolysis, and respiration in brown fat cellsJN Fain, MD Jacobs, and YC Clement-CormierJN Fain, MD Jacobs, and YC Clement-CormierPublished Online:01 Feb 1973https://doi.org/10.1152/ajplegacy.1973.224.2.346MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByNeed for Ca ions in the lipolytic action of 5-hydroxytryptamine in rat brown adipose tissue12 April 2011 | Journal of Pharmacy and Pharmacology, Vol. 30, No. 1Brown Adipose Tissue: Function and Physiological SignificanceBARBARA CANNON, and JAN NEDERGAARD1 January 2004 | Physiological Reviews, Vol. 84, No. 1Effects of cold exposure on cyclic AMP concentration in plasma, liver, and brown and white adipose tissues in cold-acclimated ratsInternational Journal of Biometeorology, Vol. 33, No. 2Temperature Regulation5-HT Receptors Coupled to Adenylate CyclaseBiochemical Mechanisms of ThermogenesisBrown adipose tissue: molecular mechanisms controlling activity and thermogenesisQuantitative differentiation of α- and β-adrenergic respiratory responses in isolated hamster brown fat cells: Evidence for the presence of an α1-adrenergic componentEuropean Journal of Pharmacology, Vol. 93, No. 3-4Cellular Mechanisms of Heat DissipationThyroid Hormones and ThermogenesisRat adipocyte lipoprotein lipase activity is inhibited by theophylline and stimulated by inosine through adenosine-independent mechanismsBiochemical and Biophysical Research Communications, Vol. 107, No. 1Regulation of Lipid Metabolism by Cyclic NucleotidesThe Brown Fat CellInfluence of Cardiac Glycosides on Myocardial Energy MetabolismLipid biochemistry in the cold-acclimated ratComparative Biochemistry and Physiology Part B: Comparative Biochemistry, Vol. 70, No. 4Alpha1-adrenergic activation of phosphatidylinositol labeling in isolated brown fat cellsBiochemical Pharmacology, Vol. 29, No. 24Hormonal Regulation of Lipid Mobilization from Adipose TissueAdrenergic- and cyclic nucleotide-induced glycerol release from brown adipocytesEuropean Journal of Pharmacology, Vol. 56, No. 1-2Effects of colchicine and trimethoxybenzene on glucose oxidation in isolated brown fat cells from ratsGeneral Pharmacology: The Vascular System, Vol. 10, No. 1EFFECTS OF CHLORPROMAZINE ON LIPOLYSIS IN BROWN AND WHITE ADIPOSE TISSUES OF COLD-EXPOSED RATSJapanese Journal of Pharmacology, Vol. 29, No. 4beta-Adrenergic Receptors in Brown-Adipose Tissue. Characterization and Alteratios during Acclimation of Rats to ColdEuropean Journal of Biochemistry, Vol. 92, No. 1Comparison of isoproterenol, salbutamol and talzolol as lipolytic agents with isolated rodent adipocytesBiochemical Pharmacology, Vol. 27, No. 14Effects of Lipolytic and Antilipolytic Drugs on Metabolism of Adenosine 3': 5'-Monophosphate in Brown Adipose Tissue of Cold Acclimated RatsEuropean Journal of Biochemistry, Vol. 69, No. 1Brown adipose tissue mitochondriaBiochimica et Biophysica Acta (BBA) - Reviews on Bioenergetics, Vol. 416, No. 16 Methods Related to Cyclic AMP and Adenylate CyclaseControl of cardiac sarcolemmal adenylate cyclase and sodium, potassium-activated adenosinetriphosphatase activities.Circulation Research, Vol. 36, No. 1Lack of correlation between cyclic amp synthesis and free fatty acid release in brown fat of cold-adapted ratsBiochemical Pharmacology, Vol. 23, No. 20Control of sn-glycerql 3-phosphate oxidation in brown adipose tissue mitochondria by calcium and ACYL-CoABiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 348, No. 1Cyclic AMP metabolism in brown adipocytes of hamsters exposed to different temperaturesBiochimica et Biophysica Acta (BBA) - General Subjects, Vol. 338, No. 2 More from this issue > Volume 224Issue 2February 1973Pages 346-351 Copyright & PermissionsCopyright © 1973 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1973.224.2.346PubMed4346846History Published online 1 February 1973 Published in print 1 February 1973 Metrics