Respiration In Adipose Tissue Research Articles

Nr4a3 Loss Impairs Adipose Mitochondrial Respiration Through Downregulaion of Mek1

Type 2 diabetes mellitus (T2D) is a chronic condition affecting nearly half a billion people worldwide. Symptoms of T2D include impaired glucose tolerance, decreased insulin secretion and significant weight gain. While the symptoms of T2D are well-documented, the underlying pathology remains unclear. Recent research has indicated the critical role of the nuclear receptor Nr4a3 in the development of glucose intolerance and weight gain. In individuals with T2D, the Nr4a3 promoter is hypermethylated, leading to decreased Nr4a3 expression. Elucidating the role of Nr4a3 in mitochondrial respiration in adipose will help define the mechanism of T2D onset and treatment. Here we demonstrate the effect of systemic Nr4a3 loss. Full body Nr4a3 KO animals were fed a standard diet. Male, but not female, Nr4a3 KO mice demonstrate impaired glucose and insulin tolerance. Male Nr4a3 KO mice have normal muscle, liver, and kidney respiration rates, while adipose tissue respiration is impaired. The impaired adipose respiration corresponds with increased mass of all adipose depots, increased adipocyte size, and increased lipid droplet size. The analysis of electron transport chain and tricarboxylic acid complex proteins did not reveal significant differences. Instead, the altered respiration is attributed to a decreased Mek1 protein level, and decreased phosphorylation and activation of its downstream target DRP1. Our data demonstrate the critical role of Nr4a3 in adipose tissue through regulating mitochondrial function. NIH R15DK124835-01A1. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Adverse bioenergetic effects of N-acyl amino acids in human adipocytes overshadow beneficial mitochondrial uncoupling

ObjectiveEnhancing energy turnover via uncoupled mitochondrial respiration in adipose tissue has great potential to improve human obesity and other metabolic complications. However, the amount of human brown adipose tissue and its uncoupling protein 1 (UCP1) is low in obese patients. Recently, a class of endogenous molecules, N-acyl amino acids (NAAs), was identified as mitochondrial uncouplers in murine adipocytes, presumably acting via the adenine nucleotide translocator (ANT). Given the translational potential, we investigated the bioenergetic effects of NAAs in human adipocytes, characterizing beneficial and adverse effects, dose ranges, amino acid derivatives and underlying mechanisms. MethodNAAs with neutral (phenylalanine, leucine, isoleucine) and polar (lysine) residues were synthetized and assessed in intact and permeabilized human adipocytes using plate-based respirometry. The Seahorse technology was applied to measure bioenergetic parameters, dose-dependency, interference with UCP1 and adenine nucleotide translocase (ANT) activity, as well as differences to the established chemical uncouplers niclosamide ethanolamine (NEN) and 2,4-dinitrophenol (DNP). ResultNAAs with neutral amino acid residues potently induce uncoupled respiration in human adipocytes in a dose-dependent manner, even in the presence of the UCP1-inhibitor guanosine diphosphate (GDP) and the ANT-inhibitor carboxyatractylate (CAT). However, neutral NAAs significantly reduce maximal oxidation rates, mitochondrial ATP-production, coupling efficiency and reduce adipocyte viability at concentrations above 25 μM. The in vitro therapeutic index (using induced proton leak and viability as determinants) of NAAs is lower than that of NEN and DNP. ConclusionNAAs are potent mitochondrial uncouplers in human adipocytes, independent of UCP1 and ANT. However, previously unnoticed adverse effects harm adipocyte functionality, reduce the therapeutic index of NAAs in vitro and therefore question their suitability as anti-obesity agents without further chemical modifications.

Prolonged Endurance Exercise Increases Macrophage Content and Mitochondrial Respiration in Adipose Tissue in Trained Men.

The aim of this study was to investigate the effect of prolonged endurance exercise on adipose tissue inflammation markers and mitochondrial respiration in younger and older men. "Young" (aged 30 years, n = 7) and "old" (aged 65 years, n = 7) trained men were exposed to an exercise intervention of 15 consecutive days biking 7 to 9 hours/day at 63% and 65% of maximal heart rate (young and old, respectively), going from Copenhagen, Denmark to Palermo, Italy. Adipose tissue was sampled from both the gluteal and abdominal depot before and after the intervention. Mitochondrial respiration was measured by high-resolution respirometry, and adipose inflammation was assessed by immunohistochemical staining of paraffin embedded sections. An increased number of CD163+ macrophages was observed in both the gluteal and abdominal depot (P < .01). In addition, an increased mitochondrial respiration was observed in the abdominal adipose tissue from men in the young group with complex I (CIp) stimulated respiration, complex I + II (CI+IIp) stimulated respiration and the capacity of the electron transport system (ETS) (P < .05), and in the older group an increase in CIp and CI+IIp stimulated respiration (P < .05) was found. Overall, we found a positive effect of prolonged endurance exercise on adipose tissue inflammation markers and mitochondrial respiration in both young and old trained men, and no sign of attenuated function in adipose tissue with age.

Impact of GLP-1 receptor agonist versus omega-3 fatty acids supplement on obesity-induced alterations of mitochondrial respiration.

To compare administration of the glucagon-like peptide-1 (GLP-1) analogue, exenatide, versus dietary supplementation with the omega-3 fatty acid-rich Calanus oil on obesity-induced alterations in mitochondrial respiration. Six-week-old female C57BL/6JOlaHSD mice were given high fat diet (HFD, 45% energy from fat) for 12 weeks to induce obesity. Thereafter, they were divided in three groups where one received exenatide (10 μg/kg/day) via subcutaneously implanted mini-osmotic pumps, a second group received 2% Calanus oil as dietary supplement, while the third group received HFD without any treatment. Animals were sacrificed after 8 weeks of treatment and tissues (skeletal muscle, liver, and white adipose tissue) were collected for measurement of mitochondrial respiratory activity by high-resolution respirometry, using an Oroboros Oxygraph-2k (Oroboros instruments, Innsbruck, Austria). It was found that high-fat feeding led to a marked reduction of mitochondrial respiration in adipose tissue during all three states investigated - LEAK, OXPHOS and ETS. This response was to some extent attenuated by exenatide treatment, but not with Calanus oil treatment. High-fat feeding had no major effect on hepatic mitochondrial respiration, but exenatide treatment resulted in a significant increase in the various respiratory states in liver. Mitochondrial respiration in skeletal muscle was not significantly influenced by high-fat diet or any of the treatments. The precise evaluation of mitochondrial respiration considering absolute oxygen flux and ratios to assess flux control efficiency avoided misinterpretation of the results. Exenatide increased hepatic mitochondrial respiration in high-fat fed mice, but no clear beneficial effect was observed in skeletal muscle or fat tissue. Calanus oil did not negatively affect respiratory activity in these tissues, which maintains its potential as a dietary supplement, due to its previously reported benefits on cardiac function.

CoQ Regulates Brown Adipose Tissue Respiration and Uncoupling Protein 1 Expression.

Coenzyme Q (CoQ, aka ubiquinone) is a key component of the mitochondrial electron transport chain (ETC) and membrane-incorporated antioxidant. CoQ10 deficiencies encompass a heterogeneous spectrum of clinical phenotypes and can be caused by hereditary mutations in the biosynthesis pathway or result from pharmacological interventions such as HMG-CoA Reductase inhibitors, and statins, which are widely used to treat hypercholesterolemia and prevent cardiovascular disease. How CoQ deficiency affects individual tissues and cell types, particularly mitochondrial-rich ones such as brown adipose tissue (BAT), has remained poorly understood. Here we show that pharmacological and genetic models of BAT CoQ deficiency show altered respiration that can only in part be explained by classical roles of CoQ in the respiration chain. Instead, we found that CoQ strongly impacts brown and beige adipocyte respiration via the regulation of uncoupling protein 1 (UCP1) expression. CoQ deficiency in BAT robustly decreases UCP1 protein levels and uncoupled respiration unexpectedly, resulting in increased inner mitochondrial membrane potential and decreased ADP/ATP ratios. Suppressed UCP1 expression was also observed in a BAT-specific in vivo model of CoQ deficiency and resulted in enhanced cold sensitivity. These findings demonstrate an as yet unappreciated role of CoQ in the transcriptional regulation of key thermogenic genes and functions.

Maternal Transmission of Human OGG1 Protects Mice Against Genetically- and Diet-Induced Obesity Through Increased Tissue Mitochondrial Content

Obesity and related metabolic disorders are pressing public health concerns, raising the risk for a multitude of chronic diseases. Obesity is multi-factorial disease, with both diet and lifestyle, as well as genetic and developmental factors leading to alterations in energy balance. In this regard, a novel role for DNA repair glycosylases in modulating risk for obesity has been previously established. Global deletion of either of two different glycosylases with varying substrate specificities, Nei-like endonuclease 1 (NEIL1) or 8-oxoguanine DNA glycosylase-1 (OGG1), both predispose mice to diet-induced obesity (DIO). Conversely, enhanced expression of the human OGG1 gene renders mice resistant to obesity and adiposity. This resistance to DIO is mediated through increases in whole body energy expenditure and increased respiration in adipose tissue. Here, we report that hOGG1 expression also confers resistance to genetically-induced obesity. While Agouti obese (Ay/a) mice are hyperphagic and consequently develop obesity on a chow diet, hOGG1 expression in Ay/a mice (Ay/aTg) prevents increased body weight, without reducing food intake. Instead, obesity resistance in Ay/aTg mice is accompanied by increased whole body energy expenditure and tissue mitochondrial content. We also report for the first time that OGG1-mediated obesity resistance in both the Ay/a model and DIO model requires maternal transmission of the hOGG1 transgene. Maternal, but not paternal, transmission of the hOGG1 transgene is associated with obesity resistance and increased mitochondrial content in adipose tissue. These data demonstrate a critical role for OGG1 in modulating energy balance through changes in adipose tissue function. They also demonstrate the importance of OGG1 in modulating developmental programming of mitochondrial content and quality, thereby determining metabolic outcomes in offspring.

Response of Mitochondrial Respiration in Adipose Tissue and Muscle to 8 Weeks of Endurance Exercise in Obese Subjects.

Exercise training improves glycemic control and increases mitochondrial content and respiration capacity in skeletal muscle. Rodent studies suggest that training increases mitochondrial respiration in adipose tissue. To assess the effects of endurance training on respiratory capacities of human skeletal muscle and abdominal subcutaneous adipose tissue and to study the correlation with improvement in insulin sensitivity. Using high-resolution respirometry, we analyzed biopsies from 25 sedentary (VO2 peak 25.1 ± 4.0 VO2 mL/[kg*min]) subjects (16 female, 9 male; 29.8 ± 8.4 years) with obesity (body mass index [BMI] 31.5 ± 4.3 kg/m2), who did not have diabetes. They performed a supervised endurance training over 8 weeks (3 × 1 hour/week at 80% VO2 peak). Based on change in insulin sensitivity after intervention (using the Matsuda insulin sensitivity index [ISIMats]), subjects were grouped in subgroups as responders (>15% increase in ISIMats) and low-responders. The response in ISIMats was correlated to a reduction of subcutaneous and visceral adipose tissue volume. Both groups exhibited similar increases in fitness, respiratory capacity, and abundance of mitochondrial enzymes in skeletal muscle fibers. Respiratory capacities in subcutaneous adipose tissue were not altered by the intervention. Compared with muscle fibers, adipose tissue respiration showed a preference for β-oxidation and complex II substrates. Respiratory capacities were higher in adipose tissue from female participants. Our data show that the improvement of peripheral insulin sensitivity after endurance training is not directly related to an increase in mitochondrial respiratory capacities in skeletal muscle and occurs without an increase in the respiratory capacity of subcutaneous adipose tissue.

Reversible temperature-dependent differences in brown adipose tissue respiration during torpor in a mammalian hibernator

Although seasonal modifications of brown adipose tissue (BAT) in hibernators are well documented, we know little about functional regulation of BAT in different phases of hibernation. In the 13-lined ground squirrel, liver mitochondrial respiration is suppressed by up to 70% during torpor. This suppression is reversed during arousal and interbout euthermia (IBE), and corresponds with patterns of maximal activities of electron transport system (ETS) enzymes. Uncoupling of BAT mitochondria is controlled by free fatty acid release stimulated by sympathetic activation of adipocytes, so we hypothesized that further regulation at the level of the ETS would be of little advantage. As predicted, maximal ETS enzyme activities of isolated BAT mitochondria did not differ between torpor and IBE. In contrast to this pattern, respiration rates of mitochondria isolated from torpid individuals were suppressed by ~60% compared with rates from IBE individuals when measured at 37°C. At 10°C, however, mitochondrial respiration rates tended to be greater in torpor than IBE. As a result, the temperature sensitivity (Q10) of mitochondrial respiration was significantly lower in torpor (~1.4) than IBE (~2.4), perhaps facilitating energy savings during entrance into torpor and thermogenesis at low body temperatures. Despite the observed differences in isolated mitochondria, norepinephrine-stimulated respiration rates of isolated BAT adipocytes did not differ between torpor and IBE, perhaps because the adipocyte isolation requires lengthy incubation at 37°C, potentially reversing any changes that occur in torpor. Such changes may include remodeling of BAT mitochondrial membrane phospholipids, which could change in situ enzyme activities and temperature sensitivities.

Salsalate (Salicylate) Uncouples Mitochondria, Improves Glucose Homeostasis, and Reduces Liver Lipids Independent of AMPK-β1

Salsalate is a prodrug of salicylate that lowers blood glucose in patients with type 2 diabetes (T2D) and reduces nonalcoholic fatty liver disease (NAFLD) in animal models; however, the mechanism mediating these effects is unclear. Salicylate directly activates AMPK via the β1 subunit, but whether salsalate requires AMPK-β1 to improve T2D and NAFLD has not been examined. Therefore, wild-type (WT) and AMPK-β1-knockout (AMPK-β1KO) mice were treated with a salsalate dose resulting in clinically relevant serum salicylate concentrations (∼1 mmol/L). Salsalate treatment increased VO2, lowered fasting glucose, improved glucose tolerance, and led to an ∼55% reduction in liver lipid content. These effects were observed in both WT and AMPK-β1KO mice. To explain these AMPK-independent effects, we found that salicylate increases oligomycin-insensitive respiration (state 4o) and directly increases mitochondrial proton conductance at clinical concentrations. This uncoupling effect is tightly correlated with the suppression of de novo lipogenesis. Salicylate is also able to stimulate brown adipose tissue respiration independent of uncoupling protein 1. These data indicate that the primary mechanism by which salsalate improves glucose homeostasis and NAFLD is via salicylate-driven mitochondrial uncoupling.

Adipose tissue mitochondrial respiration: Key insights from RYGB-induced weight loss.

It has become increasingly well accepted that adipose tissue mitochondria are important regulators of whole body glucose and lipid metabolism (1). Reductions in adipose tissue mitochondrial proteins occur early during the pathogenesis of insulin resistance (2), while adipose mitochondrial content is increased following treatment with the insulin-sensitizing compounds thiazolidinediones (3). In this issue of Obesity, Hansen et al. (4) provide intriguing insight into the regulation of mitochondrial content and function in adipose tissue samples from obese subjects with or without type 2 diabetes following Roux-en-Y gastric bypass surgery (RYGB). A key take-home message of this study is the importance of identifying the proper means with which to normalize adipose tissue respiration data. In both groups of subjects, adipose tissue respiration was increased following RYGB-induced weight loss when expressed relative to tissue weight. However, an important point is that RYGB leads to massive weight loss (>30 kg) and decreases in adipocyte size due to reductions in lipid content. Consequently, for a given amount of tissue analyzed, there are a greater number of cells, and thus mitochondria, per unit tissue. When normalizing to either cell, or mitochondrial number, the weight loss-induced increases in adipose tissue respiration were lost. These findings clearly highlight the need for careful consideration when analyzing adipose tissue respiration, as the choice of denominator can greatly influence the interpretation of the data. A second important finding of this article is that increases in adipose tissue mitochondrial content do not appear to be required for the RYGB-mediated improvements in glucose homeostasis. In this regard, mitochondrial density was not increased with weight loss despite robust increases in systemic insulin sensitivity. However, there were slight but significant increases in the ratio between maximally coupled and uncoupled respiration, i.e., the phosphorylation system control ratio (P/E ratio), suggesting improvements in mitochondrial function following weight loss. It should be stressed, however, that it is not evident from the current data set how quickly the increase in the P/E ratio occurs as this data was only reported from respiration experiments at the inclusion of the study and 18 months following RYGB. Thus, it is not clear whether the improvement in mitochondrial function in adipose tissue is a cause or a consequence of improvements in insulin sensitivity. This is a particularly important point to consider as previous work has demonstrated a role for insulin in the regulation of skeletal muscle mitochondrial function (5). The current investigation is unique in that it examines, longitudinally, changes in adipose tissue respiration and mitochondrial density following RYGB. With this being said, the conclusions that can be drawn regarding the role of adipose tissue mitochondria in RYGB-mediated improvements in insulin sensitivity are limited as only subcutaneous adipose tissue was examined. While procuring visceral adipose tissue samples in a pre–post intervention design would be difficult to execute, these studies would prove to be beneficial in confirming the association of alterations in adipose tissue mitochondrial content and/or function in a more metabolically active fat depot to changes in whole body glucose metabolism.

Measurements of adipose tissue respiration in a closed chamber using an oxygen sensor: methodological considerations.

A new polarographic system for measurement of oxygen consumption in vitro has been constructed to minimize different types of errors. The system was built of polyamide-6, Monax glass, stainless steel, and rubber to diminish oxygen leakage and gas capacitance properties. With these materials the system was gas-tight. Nevertheless, the incubation chambers had oxygen capacitance properties that had to be corrected for mathematically. Thus, in order to obtain more exact absolute values of the respiratory rate, the apparent respiratory slopes were continuously corrected for delta pO2. Furthermore, the initial slope observed in the absence of biological material was also taken into account. Using these variables, the apparent slope (mm Hg/min) could be adjusted by subtracting the following correction factor: correction factor = 0.00306 X delta pO2 + 0.198 X (initial slope). This correction gave a high degree of linearity and an overall error on the order of 10%. Without the described correction for the oxygen capacitance, the true respiratory rate may be underestimated by up to 50%.

Effect of fetal thyroidectomy on newborn thermogenesis in lambs.

We investigated the effect of the transient neonatal hyperthyroid state on thermogenesis at birth by measuring rectal temperature, plasma free fatty acids, plasma catecholamines, and in vitro brown adipose tissue respiration in thyroidectomized (n = 6) and sham operated (n = 5) fetal sheep. Surgery was performed at an average of 133 days of gestation followed by cesarean delivery at 146 days. Fetuses were delivered into a constant room temperature of 25 degrees C. Serial measurements were made in utero before delivery and at timed intervals after birth. Serum 3,3',5 triiodothyronine and thyroxine concentrations in the neonatal period were normal in sham operated and nondetectable in thyroidectomized fetuses. Rectal temperatures and serum free fatty acid levels were reduced in thyroidectomized newborns. Plasma epinephrine concentrations were increased and the hypothyroid neonates were acidotic when compared to control animals. In vitro basal and norepinephrine stimulated brown adipose tissue respiration were reduced in thyroidectomized compared to control animals. These results indicate that thyroid hormone deficiency impairs nonshivering thermogenesis in brown adipose tissue and leads to hypothermia despite augmented plasma epinephrine values.

Mechanisms of stimulus-calorigenesis coupling in brown adipose tissue.

The sequence of metabolic events leading to increased calorigenesis in brown adipose tissue has been reviewed. The first step of this sequence consists in the binding of norepinephrine to adrenergic receptors of the beta1 subtype. This results in the stimulation of adenylate cyclase and activation of lipolysis via the system of protein kinases. Hormone-sensitive lipases represent the "flux-generating" step regulating mitochondrial respiration. Fatty acids released from intracellular triglyceride droplets in consequence of lipase activation play a messenger role between lipolysis and mitochondrial respiration. They stimulate respiration by serving as substrates for beta oxidation (via carnitine-dependent pathways) and (or) by simultaneously increasing mitochondrial permeability to protons (physiological "loose coupling"). The control of brown adipose tissue respiration by lipolysis represents a self-regulatory process, as excessive concentrations of fatty acids retroinhibit lipolysis. At the mitochondrial level, fatty acids appear to interact with an "uncoupling" protein (thermogenin or 32 000 relative mass protein) localized in the inner membrane that confers upon brown adipose mitochondria a unique sensitivity for fatty acid uncoupling. This explains that, contrary to other tissues, respiration is principally controlled in brown adipose tissue by substrate supply (mainly long-chain fatty acids), rather than by the phosphorylation state ratio.

Control of brown adipose tissue lipolysis and respiration by adenosine.

Adenosine competitively inhibited the stimulatory effects of (-)-isoproterenol on lipolysis and respiration in hamster brown adipocytes. The low value of the apparent ki for respiratory inhibition by adenosine (7 nM) indicated that the nucleoside may control brown adipocyte function under physiological concentrations. Significantly, the dose-response curves for isoproterenol stimulation of lipolysis and respiration were both shifted by adenosine to higher agonist concentrations by the same order of magnitude, providing additional evidence for a tight coupling between lipolysis and respiration. The inhibitory effects of adenosine were rapidly reversed by a) adenosine deaminase, b) agents known to increase intracellular cyclic AMP levels (isoproterenol, isobutylmethylxanthine, dibutyryl cyclic AMP), and c) direct stimulation of respiration with palmitic acid. These results, combined with the fact that adenosine failed to affect respiration evoked either by dibutyryl cyclic AMP or by palmitic acid, strongly indicate that adenosine regulates brown adipose tissue respiration at an early metabolic step of the stimulus-thermogenesis sequence, most probably at the level of the adenylate cyclase complex.

Thyroid hormone-sensitive brown adipose tissue respiration in the newborn rabbit

The effects of thyroid hormone treatment on brown adipose tissue (BAT) and liver metabolism were assessed by measuring oxygen consumption, sodium-potassium adenosine triphosphatase (Na-K-ATPase), and mitochondrial alpha-glycerophosphate dehydrogenase (alpha-GPD) activities in tissues from triiodothyronine- (T3) and vehicle-injected (for 3 days) newborn and adult rabbits. In the newborns, basal BAT cellular respiration was increased [mean (%/- SE) = 119 +/- 18 vs. 65 +/- 4 microliter O2/10(6) cells-1 . h in controls (P less than 0.005)], whereas hepatic respiration was unchanged. Ouabain had no effect on basal BAT cellular respiration, but suppressed hepatic respiration by 30% in both newborn groups. T3 treatment had no effect on NE- (10(-6) M) stimulated BAT respiration, whereas adult hepatic respiration was increased almost twofold. alpha-GPD activities were increased in both newborn BAT and adult liver but not in newborn liver. Na-K-ATPase activity was significantly increased only in newborn liver. In conclusion, 1) both BAT and liver are thyroid-hormone sensitive in the newborn rabbit, but the responses to T3 treatment are different in the two tissues; 2) the failure to stimulate both hepatic alpha-GPD and respiration in the newborn appears to be a developmental phenomenon characteristic of the rabbit; 3) thyroid hormones have little effect on sodium transport-dependent respiration in either BAT of liver in the newborn rabbit.

Influence of thyroid hormone on homeothermic development of the rat.

ARTICLESInfluence of thyroid hormone on homeothermic development of the ratRE Steele, and DR WeksteinRE Steele, and DR WeksteinPublished Online:01 Jun 1972https://doi.org/10.1152/ajplegacy.1972.222.6.1528MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByPhysical, Endocrine, and Growth Factors in Lung DevelopmentEvaluation of possible modes of action for acute effects of methyl iodide in laboratory animals23 March 2008 | Inhalation Toxicology, Vol. 21, No. 6Regulation of alveologenesis clinical implications of impaired growthPathology, Vol. 40, No. 2Invited Review: Pulmonary alveoli: formation, the “call for oxygen,” and other regulatorsDonald Massaro, and Gloria D. Massaro1 March 2002 | American Journal of Physiology-Lung Cellular and Molecular Physiology, Vol. 282, No. 3Comparison of heat and cold stress to assess thermoregulatory dysfunction in hypothyroid ratsChristopher J. Gordon, Peggy Becker, and Beth Padnos1 December 2000 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 279, No. 6Multistage enhancement of surface recordings of canine gastric electrical signalsAnnals of Biomedical Engineering, Vol. 21, No. 4Lipid composition of brown adipose tissue mitochondria and microsomes in hyperthyroid ratsInternational Journal of Biochemistry, Vol. 21, No. 3Perinatal Activation of Brown Adipose TissueEuthyroid status is essential for the perinatal increase in thermogenin mRNA in brown adipose tissue of rat pupsBiochemical and Biophysical Research Communications, Vol. 148, No. 1Effect of hyperthyroidism on lipogenesis in brown adipose tissue of young ratsBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 751, No. 3Triiodothyronine-dietary interrelationships in the modulation of brown adipose tissue and liver lipogenesis in the ratInternational Journal of Biochemistry, Vol. 15, No. 7Lipogenesis at the suckling-weaning transition in liver and brown adipose tissue of the ratBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 713, No. 3Thyroid hormone-sensitive brown adipose tissue respiration in the newborn rabbitA. H. Klein, J. J. Jenkins, A. Reviczky, and D. A. Fisher1 December 1981 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 241, No. 6Changes in body temperature after administration of antipyretics, LSD, Δ9-THC, CNS depressants and stimulants, hormones, inorganic ions, gases, 2,4-DNP and miscellaneous agentsNeuroscience & Biobehavioral Reviews, Vol. 5, No. 1Development of olfactory and thermal responsiveness in hypothyroid and hyperthyroid rat pupsDevelopmental Psychobiology, Vol. 13, No. 3The responses of the developing endocrine system to hormones and drugsPharmacology & Therapeutics, Vol. 10, No. 3Heat and Cold Tolerance7 July 2016 | Postgraduate Medicine, Vol. 55, No. 4Changes in interscapular brown adipose tissue of the rat during perinatal and early postnatal development and after cold acclimation VI. Effect of hormones and ambient temperatureInternational Journal of Biochemistry, Vol. 5, No. 1 More from this issue > Volume 222Issue 6June 1972Pages 1528-1533 Copyright & PermissionsCopyright © 1972 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1972.222.6.1528PubMed5030213History Published online 1 June 1972 Published in print 1 June 1972 Metrics

Effect of cold shock on respiration and glycolysis in swine arterial tissue.

ARTICLESEffect of cold shock on respiration and glycolysis in swine arterial tissueRF Scott, ES Morrison, and M KromsRF Scott, ES Morrison, and M KromsPublished Online:01 Nov 1970https://doi.org/10.1152/ajplegacy.1970.219.5.1363MoreSectionsPDF (784 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByRole of Digital Artery Adrenoceptors in Raynaud's Disease24 June 2016 | Vascular Medicine, Vol. 2, No. 1Metabolism of Fibromuscular and Atheromatous Plaques in an Experimental Model: Causal Mechanisms for the Development of Intimal NecrosisMeasurements of adipose tissue respiration in a closed chamber using an oxygen sensor: methodological considerations.Journal of Lipid Research, Vol. 27, No. 9Aortic wall metabolism in relation to susceptibility and resistance to experimental atherosclerosisJournal of Vascular Surgery, Vol. 7, No. 5Existence of fatty acyl-CoA oxidizing system in (micro)peroxisomes of rabbit aortaBiochemical Medicine and Metabolic Biology, Vol. 38, No. 2Metabolism of the arterial wall—influence of atherosclerosis and drugsPharmacology & Therapeutics, Vol. 32, No. 3Histochromatographical determination of cholesteryl ester composition in the human atherosclerotic aortaActa Histochemica, Vol. 76, No. 1Focal alterations in metabolic capabilities associated with development of cholesterol-induced atheromatous lesions: A quantitative cytochemical studyExperimental and Molecular Pathology, Vol. 36, No. 2Pasteur effect in human arterial tissueActa Physiologica Scandinavica, Vol. 114, No. 4Glycolytic activity of rat aorta after exerciseEuropean Journal of Applied Physiology and Occupational Physiology, Vol. 48, No. 2Metabolism of the Arterial WallMetabolic changes in modified smooth muscle cells of rabbit carotid arteriesBasic Research in Cardiology, Vol. 77, No. 1Chemical Energetics of Vascular Smooth Muscle1 January 2011Physical Factors of Regulation1 January 2011Significance of glucose for mechanical activity, flavin and pyridine nucleotide oxidation-reduction changes in isolated rat portal veins under ACh-stimulationBasic Research in Cardiology, Vol. 75, No. 6Enhanced oxygen uptake and lactate production of smooth muscle cell proliferates of rabbit carotid arteriesPfl�gers Archiv European Journal of Physiology, Vol. 387, No. 1Vascular Smooth Muscle: Aerobic Glycolysis Linked to Sodium and Potassium Transport ProcessesScience, Vol. 206, No. 4425Carnitine palmitoyltransferase activity in mitochondrial fractions isolated from aortas of rabbits fed cholesterol-supplemented dietsAtherosclerosis, Vol. 34, No. 1Metabolic Activities in the Arterial WallHemodynamic Contribution to AtherosclerosisThe effects of O2 concentration and albumin on respiration and aerobic glycolysis in rabbit aortic intima-mediaBiochemical Medicine, Vol. 20, No. 2Changes in chemical and metabolic properties of rabbit aorta by dietary cholesterol, and saturated and polyunsaturated fatsAtherosclerosis, Vol. 29, No. 4In vitro tissue oxygen tensions in the rabbit aortic archAtherosclerosis, Vol. 28, No. 3Effect of Lipid Accumulation on Arterial Wall BioenergeticsThe aerobic metabolism of porcine carotid artery and its relationship to isometric forcePfl�gers Archiv European Journal of Physiology, Vol. 370, No. 1Influence of oxygen tension on the metabolism of vascular smooth muscle Demonstration of a Pasteur effectAtherosclerosis, Vol. 25, No. 2-3Abnormalities of the arterial wall and its metabolism in atherogenesisProgress in Cardiovascular Diseases, Vol. 18, No. 5Inherited depression of arterial lipoamide dehydrogenase activity associated with susceptibility to atherosclerosis in pigeons.Circulation Research, Vol. 36, No. 5Vascular Metabolism, Vascular Enzymes, and the Effect of DrugsUptake, oxidation, and esterification of free fatty acids in normal and atherosclerotic rabbit aortaBiochemical Medicine, Vol. 11, No. 2Vascular Enzymes and the Relevance of Their Study to Problems of AtherogenesisMedical Clinics of North America, Vol. 58, No. 2Aortic mitochondrial function in experimentally induced atherosclerosis in swine and rabbitsBiochemical Medicine, Vol. 7, No. 2Glucose degradation in normal and atherosclerotic aortic intima-mediaAtherosclerosis, Vol. 16, No. 2Effect of Hypoxia on Reactivity of Cutaneous and Mesenteric Veins of the Dog More from this issue > Volume 219Issue 5November 1970Pages 1363-1365 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.219.5.1363PubMed5473119History Published online 1 November 1970 Published in print 1 November 1970 Metrics