Relevant bibliographies by topics / Muscles Metabolism Animal models

Academic literature on the topic 'Muscles Metabolism Animal models'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Muscles Metabolism Animal models"

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Feraco, Alessandra, Stefania Gorini, Andrea Armani, Elisabetta Camajani, Manfredi Rizzo, and Massimiliano Caprio. "Exploring the Role of Skeletal Muscle in Insulin Resistance: Lessons from Cultured Cells to Animal Models." International Journal of Molecular Sciences 22, no. 17 (August 28, 2021): 9327. http://dx.doi.org/10.3390/ijms22179327.

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Skeletal muscle is essential to maintain vital functions such as movement, breathing, and thermogenesis, and it is now recognized as an endocrine organ. Muscles release factors named myokines, which can regulate several physiological processes. Moreover, skeletal muscle is particularly important in maintaining body homeostasis, since it is responsible for more than 75% of all insulin-mediated glucose disposal. Alterations of skeletal muscle differentiation and function, with subsequent dysfunctional expression and secretion of myokines, play a key role in the pathogenesis of obesity, type 2 diabetes, and other metabolic diseases, finally leading to cardiometabolic complications. Hence, a deeper understanding of the molecular mechanisms regulating skeletal muscle function related to energy metabolism is critical for novel strategies to treat and prevent insulin resistance and its cardiometabolic complications. This review will be focused on both cellular and animal models currently available for exploring skeletal muscle metabolism and endocrine function.
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Benton, Carley R., Xiao-Xia Han, Maria Febbraio, Terry E. Graham, and Arend Bonen. "Inverse relationship between PGC-1α protein expression and triacylglycerol accumulation in rodent skeletal muscle." Journal of Applied Physiology 100, no. 2 (February 2006): 377–83. http://dx.doi.org/10.1152/japplphysiol.00781.2005.

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PGC-1α is a key regulator of tissue metabolism, including skeletal muscle. Because it has been shown that PGC-1α alters the capacity for lipid metabolism, it is possible that PGC-1α expression is regulated by the intramuscular lipid milieu. Therefore, we have examined the relationship between PGC-1α protein expression and the intramuscular fatty acid accumulation in hindlimb muscles of animals in which the capacity for fatty acid accumulation in muscle is increased (Zucker obese rat) or reduced [FAT/CD36 null (KO) mice]. Rates of palmitate incorporation into triacylglycerols were determined in perfused red (RG) and white gastrocnemius (WG) muscles of lean and obese Zucker rats and in perfused RG and WG muscles of FAT/CD36 KO and wild-type (WT) mice. In obese Zucker rats, the rate of palmitate incorporation into triacylglycerol depots in RG and WG muscles were 28 and 24% greater than in lean rats ( P < 0.05). In FAT/CD36 KO mice, the rates of palmitate incorporation into triacylglycerol depots were lower in RG (−50%) and WG muscle (−24%) compared with the respective muscles in WT mice ( P < 0.05). In the obese animals, PGC-1α protein content was reduced in both RG (−13%) and WG muscles (−15%) ( P < 0.05). In FAT/CD36 KO mice, PGC-1α protein content was upregulated in both RG (+32%, P < 0.05) and WG muscles (+50%, P < 0.05). In conclusion, from studies in these two animal models, it appears that PGC-1α protein expression is inversely related to components of intramuscular lipid metabolism, because 1) PGC-1α protein expression is downregulated when triacylglycerol synthesis rates, an index of intramuscular lipid metabolism, are increased, and 2) PGC-1α protein expression is upregulated when triacylglycerol synthesis rates are reduced. Therefore, we speculate that the intramuscular lipid sensing may be involved in regulating the protein expression of PGC-1α in skeletal muscle.
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Flis, Damian Jozef, Katarzyna Dzik, Jan Jacek Kaczor, Karol Cieminski, Malgorzata Halon-Golabek, Jedrzej Antosiewicz, Mariusz Roman Wieckowski, and Wieslaw Ziolkowski. "Swim Training Modulates Mouse Skeletal Muscle Energy Metabolism and Ameliorates Reduction in Grip Strength in a Mouse Model of Amyotrophic Lateral Sclerosis." International Journal of Molecular Sciences 20, no. 2 (January 9, 2019): 233. http://dx.doi.org/10.3390/ijms20020233.

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Metabolic reprogramming in skeletal muscles in the human and animal models of amyotrophic lateral sclerosis (ALS) may be an important factor in the diseases progression. We hypothesized that swim training, a modulator of cellular metabolism via changes in muscle bioenergetics and oxidative stress, ameliorates the reduction in muscle strength in ALS mice. In this study, we used transgenic male mice with the G93A human SOD1 mutation B6SJL-Tg (SOD1G93A) 1Gur/J and wild type B6SJL (WT) mice. Mice were subjected to a grip strength test and isolated skeletal muscle mitochondria were used to perform high-resolution respirometry. Moreover, the activities of enzymes involved in the oxidative energy metabolism and total sulfhydryl groups (as an oxidative stress marker) were evaluated in skeletal muscle. ALS reduces muscle strength (−70% between 11 and 15 weeks, p < 0.05), modulates muscle metabolism through lowering citrate synthase (CS) (−30% vs. WT, p = 0.0007) and increasing cytochrome c oxidase and malate dehydrogenase activities, and elevates oxidative stress markers in skeletal muscle. Swim training slows the reduction in muscle strength (−5% between 11 and 15 weeks) and increases CS activity (+26% vs. ALS I, p = 0.0048). Our findings indicate that swim training is a modulator of skeletal muscle energy metabolism with concomitant improvement of skeletal muscle function in ALS mice.
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Miyamoto, Licht, Tatsuro Egawa, Rieko Oshima, Eriko Kurogi, Yosuke Tomida, Koichiro Tsuchiya, and Tatsuya Hayashi. "AICAR stimulation metabolome widely mimics electrical contraction in isolated rat epitrochlearis muscle." American Journal of Physiology-Cell Physiology 305, no. 12 (December 15, 2013): C1214—C1222. http://dx.doi.org/10.1152/ajpcell.00162.2013.

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Physical exercise has potent therapeutic and preventive effects against metabolic disorders. A number of studies have suggested that 5′-AMP-activated protein kinase (AMPK) plays a pivotal role in regulating carbohydrate and lipid metabolism in contracting skeletal muscles, while several genetically manipulated animal models revealed the significance of AMPK-independent pathways. To elucidate significance of AMPK and AMPK-independent signals in contracting skeletal muscles, we conducted a metabolomic analysis that compared the metabolic effects of 5-aminoimidazole-4-carboxamide-1-β-d-ribonucleoside (AICAR) stimulation with the electrical contraction ex vivo in isolated rat epitrochlearis muscles, in which both α1- and α2-isoforms of AMPK and glucose uptake were equally activated. The metabolomic analysis using capillary electrophoresis time-of-flight mass spectrometry detected 184 peaks and successfully annotated 132 small molecules. AICAR stimulation exhibited high similarity to the electrical contraction in overall metabolites. Principal component analysis (PCA) demonstrated that the major principal component characterized common effects whereas the minor principal component distinguished the difference. PCA and a factor analysis suggested a substantial change in redox status as a result of AMPK activation. We also found a decrease in reduced glutathione levels in both AICAR-stimulated and contracting muscles. The muscle contraction-evoked influences related to the metabolism of amino acids, in particular, aspartate, alanine, or lysine, are supposed to be independent of AMPK activation. Our results substantiate the significance of AMPK activation in contracting skeletal muscles and provide novel evidence that AICAR stimulation closely mimics the metabolomic changes in the contracting skeletal muscles.
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Avin, Keith G., Julian A. Vallejo, Neal X. Chen, Kun Wang, Chad D. Touchberry, Marco Brotto, Sarah L. Dallas, Sharon M. Moe, and Michael J. Wacker. "Fibroblast growth factor 23 does not directly influence skeletal muscle cell proliferation and differentiation or ex vivo muscle contractility." American Journal of Physiology-Endocrinology and Metabolism 315, no. 4 (October 1, 2018): E594—E604. http://dx.doi.org/10.1152/ajpendo.00343.2017.

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Skeletal muscle dysfunction accompanies the clinical disorders of chronic kidney disease (CKD) and hereditary hypophosphatemic rickets. In both disorders, fibroblast growth factor 23 (FGF23), a bone-derived hormone regulating phosphate and vitamin D metabolism, becomes chronically elevated. FGF23 has been shown to play a direct role in cardiac muscle dysfunction; however, it is unknown whether FGF23 signaling can also directly induce skeletal muscle dysfunction. We found expression of potential FGF23 receptors ( Fgfr1–4) and α-Klotho in muscles of two animal models (CD-1 and Cy/+ rat, a naturally occurring rat model of chronic kidney disease-mineral bone disorder) as well as C2C12 myoblasts and myotubes. C2C12 proliferation, myogenic gene expression, oxidative stress marker 8-OHdG, intracellular Ca2+ ([Ca2+]i), and ex vivo contractility of extensor digitorum longus (EDL) or soleus muscles were assessed after treatment with various amounts of FGF23. FGF23 (2–100 ng/ml) did not alter C2C12 proliferation, expression of myogenic genes, or oxidative stress after 24- to 72-h treatment. Acute or prolonged FGF23 treatment up to 6 days did not alter C2C12 [Ca2+]i handling, nor did acute treatment with FGF23 (9–100 ng/ml) affect EDL and soleus muscle contractility. In conclusion, although skeletal muscles express the receptors involved in FGF23-mediated signaling, in vitro FGF23 treatments failed to directly alter skeletal muscle development or function under the conditions tested. We hypothesize that other endogenous substances may be required to act in concert with FGF23 or apart from FGF23 to promote muscle dysfunction in hereditary hypophosphatemic rickets and CKD.
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Singh, Himadri, Samuel Joshua Pragasam, and Vijayalakshmi Venkatesan. "Emerging Therapeutic Targets for Metabolic Syndrome: Lessons from Animal Models." Endocrine, Metabolic & Immune Disorders - Drug Targets 19, no. 4 (June 12, 2019): 481–89. http://dx.doi.org/10.2174/1871530319666181130142642.

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Background: Metabolic syndrome is a cluster of medical conditions that synergistically increase the risk of heart diseases and diabetes. The current treatment strategy for metabolic syndrome focuses on treating its individual components. A highly effective agent for metabolic syndrome has yet to be developed. To develop a target for metabolic syndrome, the mechanism encompassing different organs - nervous system, pancreas, skeletal muscle, liver and adipose tissue - needs to be understood. Many animal models have been developed to understand the pathophysiology of metabolic syndrome. Promising molecular targets have emerged while characterizing these animals. Modulating these targets is expected to treat some components of metabolic syndrome. Objective: o discuss the emerging molecular targets in an animal model of metabolic syndrome. Methods: A literature search was performed for the retrieval of relevant articles. Conclusion: Multiple genes/pathways that play important role in the development of Metabolic Syndrome are discussed.
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Katta, Anjaiah, Sunil Kakarla, Miaozong Wu, Satyanarayana Paturi, Murali K. Gadde, Ravikumar Arvapalli, Madhukar Kolli, Kevin M. Rice, and Eric R. Blough. "Altered Regulation of Contraction-Induced Akt/mTOR/p70S6k Pathway Signaling in Skeletal Muscle of the Obese Zucker Rat." Experimental Diabetes Research 2009 (2009): 1–9. http://dx.doi.org/10.1155/2009/384683.

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Increased muscle loading results in the phosphorylation of the 70 kDa ribosomal S6 kinase (p70S6k), and this event is strongly correlated with the degree of muscle adaptation following resistance exercise. Whether insulin resistance or the comorbidities associated with this disorder may affect the ability of skeletal muscle to activate p70S6k signaling following an exercise stimulus remains unclear. Here, we compare the contraction-induced activation of p70S6k signaling in the plantaris muscles of lean and insulin resistant obese Zucker rats following a single bout of increased contractile loading. Compared to lean animals, the basal phosphorylation of p70S6k (Thr389;37.2% and Thr421/Ser424;101.4%), Akt (Thr308;25.1%), and mTOR (Ser2448;63.0%) was higher in obese animals. Contraction increased the phosphorylation of p70S6k (Thr389), Akt (Ser473), and mTOR (Ser2448) in both models however the magnitude and kinetics of activation differed between models. These results suggest that contraction-induced activation of p70S6k signaling is altered in the muscle of the insulin resistant obese Zucker rat.
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Romeu Montenegro, Karina, Milene Amarante Pufal, and Philip Newsholme. "Vitamin D Supplementation and Impact on Skeletal Muscle Function in Cell and Animal Models and an Aging Population: What Do We Know So Far?" Nutrients 13, no. 4 (March 28, 2021): 1110. http://dx.doi.org/10.3390/nu13041110.

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Aging is associated with impairment in skeletal muscle mass and contractile function, predisposing to fat mass gain, insulin resistance and diabetes. The impact of Vitamin D (VitD) supplementation on skeletal muscle mass and function in older adults is still controversial. The aim of this review was to summarize data from randomized clinical trials, animal dietary intervention and cell studies in order to clarify current knowledge on the effects of VitD on skeletal muscle as reported for these three types of experiments. A structured research of the literature in Medline via PubMed was conducted and a total of 43 articles were analysed (cells n = 18, animals n = 13 and humans n = 13). The results as described by these key studies demonstrate, overall, at cell and animal levels, that VitD treatments had positive effects on the development of muscle fibres in cells in culture, skeletal muscle force and hypertrophy. Vitamin D supplementation appears to regulate not only lipid and mitochondrial muscle metabolism but also to have a direct effect on glucose metabolism and insulin driven signalling. However, considering the human perspective, results revealed a predominance of null effects of the vitamin on muscle in the ageing population, but experimental design may have influenced the study outcome in humans. Well-designed long duration double-blinded trials, standardised VitD dosing regimen, larger sample sized studies and standardised measurements may be helpful tools to accurately determine results and compare to those observed in cells and animal dietary intervention models.
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Chen, Yi-Wen, Chris M. Gregory, Mark T. Scarborough, Rongye Shi, Glenn A. Walter, and Krista Vandenborne. "Transcriptional pathways associated with skeletal muscle disuse atrophy in humans." Physiological Genomics 31, no. 3 (November 2007): 510–20. http://dx.doi.org/10.1152/physiolgenomics.00115.2006.

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Disuse atrophy is a common clinical phenomenon that significantly impacts muscle function and activities of daily living. The purpose of this study was to implement genome-wide expression profiling to identify transcriptional pathways associated with muscle remodeling in a clinical model of disuse. Skeletal muscle biopsies were acquired from the medial gastrocnemius in patients with an ankle fracture and from healthy volunteers subjected to 4–11 days of cast immobilization. We identified 277 misregulated transcripts in immobilized muscles of patients, of which the majority were downregulated. The most broadly affected pathways were involved in energy metabolism, mitochondrial function, and cell cycle regulation. We also found decreased expression in genes encoding proteolytic proteins, calpain-3 and calpastatin, and members of the myostatin and IGF-I pathway. Only 26 genes showed increased expression in immobilized muscles, including apolipoprotein (APOD) and leptin receptor (LEPR). Upregulation of APOD (5.0-fold, P < 0.001) and LEPR (5.7-fold, P < 0.05) was confirmed by quantitative RT-PCR and immunohistochemistry. In addition, atrogin-1/MAFbx was found to be 2.4-fold upregulated ( P < 0.005) by quantitative RT-PCR. Interestingly, 96% of the transcripts differentially regulated in immobilized limbs also showed the same trend of change in the contralateral legs of patients but not the contralateral legs of healthy volunteers. Information obtained in this study complements findings in animal models of disuse and provides important feedback for future clinical studies targeting the restoration of muscle function following limb disuse in humans.
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Nadeau, Kristen J., Lindsay B. Ehlers, Lina E. Aguirre, Russell L. Moore, Korinne N. Jew, Heidi K. Ortmeyer, Barbara C. Hansen, Jane E. B. Reusch, and Boris Draznin. "Exercise training and calorie restriction increase SREBP-1 expression and intramuscular triglyceride in skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 291, no. 1 (July 2006): E90—E98. http://dx.doi.org/10.1152/ajpendo.00543.2005.

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Intramuscular triglyceride (IMTG) deposition in skeletal muscle is associated with obesity and type 2 diabetes (T2DM) and is thought to be related to insulin resistance (IR). Curiously, despite enhanced skeletal muscle insulin sensitivity, highly trained athletes and calorie-restricted (CR) monkeys also have increased IMTG. Sterol regulatory element-binding proteins (SREBPs) are transcription factors that regulate the biosynthesis of cholesterol and fatty acids. SREBP-1 is increased by insulin in skeletal muscle in vitro and in skeletal muscle of IR subjects, but SREBP-1 expression has not been examined in exercise training or calorie restriction. We examined the relationship between IMTG and SREBP-1 expression in animal models of exercise and calorie restriction. Gastrocnemius and soleus muscle biopsies were obtained from 38 Sprague-Dawley rats (18 control and 20 exercise trained). Triglyceride content was higher in the gastrocnemius and soleus muscles of the trained rats. SREBP-1c mRNA, SREBP-1 precursor and mature proteins, and fatty acid synthase (FAS) protein were increased with exercise training. Monkeys ( Macaca mulatta) were CR for a mean of 10.4 years, preventing weight gain and IR. Vastus lateralis muscle was obtained from 12 monkeys (6 CR and 6 controls). SREBP-1 precursor and mature proteins and FAS protein were higher in the CR monkeys. In addition, phosphorylation of ERK1/ERK2 was increased in skeletal muscle of CR animals. In summary, SREBP-1 protein and SREBP-1c mRNA are increased in interventions that increase IMTG despite enhanced insulin sensitivity. CR and exercise-induced augmentation of SREBP-1 expression may be responsible for the increased IMTG seen in skeletal muscle of highly conditioned athletes.
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Dissertations / Theses on the topic "Muscles Metabolism Animal models"

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Kump, David S. "Physical inactivity induced dysregulation of skeletal muscle and adipose tissue metabolism." Diss., Columbia, Mo. : University of Missouri-Columbia, 2005. http://hdl.handle.net/10355/4154.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2005.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "May 2005" Includes bibliographical references.
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Andersen, Ditte K. "The role of microRNAs in skeletal muscle insulin resistance." Thesis, Royal Veterinary College (University of London), 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701676.

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Brenner, Eiliv. "Glutamate related metabolism in animal models of schizophrenia." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for nevromedisin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-13875.

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Schizophrenia is a clinical syndrome of variable psychopathology, which involves thought, perception, emotion, movement and behavior. The cumulative effect of the illness is always severe and usually long lasting. Epidemiologic studies indicate that the lifetime expectancy is 0.5-1% worldwide. The etiology and pathophysiology of schizophrenia are unknown. The two predominant pathophysiological hypotheses of schizophrenia are the dopamine hypothesis and the glutamate hypothesis. The former hypothesis states that dopamine neurotransmission is hyperactive in schizophrenia, the latter – that there is a hypofunction of glutamatergic neurotransmission in some areas of the brain. Recent studies also suggest that schizophrenia is associated with cytoskeletal alterations in neuronal architecture, e.g. differences in micro tubule associated proteins (MAP). The symptoms of schizophrenia are mostly unique to human behavior. Consequently, the exact reproduction of schizophrenia in an animal is not possible. However, animal models are important tools for exploring the underlying mechanisms of schizophrenia and for designing new therapies. The present thesis is based on four publications on animal models of schizophrenia. We used the NMDA receptor antagonist MK-801 to induce a state of hypoglutamatergia in rats in the three of them. Three different designs were used: injection of a single high dose, repeated high dose injections over several days and repeated injections of a lower dose. The fourth study was designed to investigate glutamate related metabolism in a state of microtubule instability. Knock out mice were used as a model, in which the gene coding for the microtubule associated protein STOP (Stable Tubule Only Peptide) was deleted. Glutamate related metabolism was investigated in these models by analyzing brain extracts from multiple brain areas, using HPLC (High Performance Liquid Chromatography) and 13C and1H nuclear magnetic resonance spectroscopy. By injecting animals with 1-13C labeled glucose and 1,2-13C labeled acetate, the preferential substrates of neurons and astrocytes, respectively, it was possible to follow metabolic interactions between astrocytes and neurons. A single dose of 0.5 mg/kg MK-801 produced predominantly changes in the temporal lobe with increased total amounts of glutamate and glutamine, and increased labeling from [1-13C]glucose. Similar changes were observed when MK-801 was administered repeatedly at 0.1 mg/kg for 6 consecutive days and all the metabolic alterations were confined to the temporal lobe. However, while 0.5 mg/kg MK-801 was used repeatedly instead of 0.1 mg/kg MK-801, changes were found in the cingulate, retrosplenial and frontal cortices. The total amount of glutamate increased in those areas together with a decrease in labeling from both [1-13C]glucose and [1,2-13C]acetate in several metabolites. In Paper 4 decreased levels of both total glutamine and labeled [4,5-13C]glutamine were reported in the cerebrum of STOP knock out mice. Compared to data from studies of schizophrenic patients, our results indicate that repeated injections of MK-801 in high doses may be a good model for first episode schizophrenia and the STOP KO mouse model show similarities to and may be a good model chronic schizophrenia. Results show that both the NMDA receptor hypofunction and the loss of microtubule stability seem to disrupt the glutamate-glutamine cycle, and it can be stated that astrocytic-neuronal interactions probably are underestimated in schizophrenia research.
Glutamat-relatert metabolisme i dyremodeller for schizofreni Schizofreni er en alvorlig psykisk lidelse som preges av psykotiske symptomer som vrangforestillinger, hallusinasjoner og andre symptomer som sosial tilbaketrekning og svekket sosial fungering. Epidemiologiske studier har vist at livstidsrisikoen er 0,5-1% i det meste av verdens befolkning. Etiologien og patofysiologien til schizofreni er ikke kjent. De to viktigste patofysiologiske teoriene for schizofreni har vart den såkalte dopaminteorien og glutamatteorien. Disse predikerer henholdsvis økt aktivitet i dopaminerge systemer og redusert aktivitet i visse glutamaterge systemer. Resultater fra studier i den senere tid tyder også på at det finnes forandringer i cytoskjellettet ved schizofreni, for eksempel i mikrotubuliassosierte proteiner. De fleste schizofrenisymptomer er unike for menneskelig atferd. Å kunne reprodusere schizofreni i en dyremodell er derfor vanskelig. Dyremodeller er likevel et viktig verktøy for a identifisere patofysiologiske mekanismener bak schizofreni, og for a komme fram til nye medisiner. Denne avhandlingen inneholder fire publikasjoner hvor vi studerte dyremodeller for schizofreni. I tre av dem ble NMDA-reseptorantagonisten MK-801 brukt til a redusere glutamaterg nevrotransmisjon i rotter. Tre forskjellige forsøksoppsett ble brukt: En enkelt injeksjon av en høy dose MK-801, daglige injeksjoner med høy konsentrasjon i til sammen seks dager, og daglige injeksjoner med en lavere dose MK-801 i seks dager. Den fjerde studien beskriver glutamatrelatert metabolisme ved ustabile mikrotubili. Dette gjorde vi ved å undersøke ”knock out” mus hvor genet for det mikrotubiliassosierte proteinet STOP (Stable Tubule Only Peptide) var satt ut av funksjon. Vi undersøkte glutamatrelatert metabolisme i alle disse modellene. Hjerneekstrakter fra flere hjerneomrader ble analysert med HPLC (High Performance Liquid Chromatography), 13C- og1H-magnetisk resonansspektroskopi. Ved a injisere 1-13 C merket glukose og 1,2- 13 C merket acetat kunne vi se forskjell pa nevron- og astrocyttmetabolisme. En enkelt dose med 0,5 mg/kg kroppsvekt MK-801 skapte flest metabolske forskjeller i temporal lappen. Her var det okte totale mengder av glutamat og glutamin, og dessuten okt innmerkning fra [1-13C]glukose. Vi så liknende forskjeller da vi injiserte 0,1 mg/kg MK-801 i flere påfølgende dager. Da rottene derimot ble injisert med 0,5 mg/ MK-801, fant vi metabolske forskjeller i cingulate-, retrosplenial- og frontalcortex. Her var det ogsa en økt totalmengde av glutamat, men innmerkning fra bade [1-13C]glukose og [1,2-13C]acetat var redusert i flere metabolitter sammenlignet med kontrolldyrene. Reultater i artikkel 4 viser reduserte mengder av bade totalglutamin og glutamin merket fra [1,2-13C]acetat i cerebrum til STOP ”knock out” mus. Når vi sammenligner resultatene våre med data fra studier av pasienter med schizofreni, ser det ut til at repeterte injeksjoner av en høy dose MK-801, kan vare en god dyremodell for schizofreni i et tidlig stadium. STOP ”knock out” modellen viser lignende metabolske forskjeller som hos pasienter med kronisk schizofreni, og derfor kanskje en god dyremodell for mer langtkommen schizofreni. Resultatene fra studiene i denne oppgaven viser at både blokkering av NMDA-reseptoren og ustabile mikrotubili, forstyrrer glutamatglutamin syklus, og det er fristende a påstå at interaksjonen mellom astrocytter og nevroner er undervurdert i schizofreniforskning.
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Ling, Zong-Chao. "Islet glucose metabolism and insulin release in two animal models of glucose intolerance /." Stockholm, 1999. http://diss.kib.ki.se/1999/19990517ling/.

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Chisholm, Jeffrey W. "Abnormal lipoprotein metabolism in animal models of intrahepatic cholestasis induced by Ã-naphthylisothiocyanate." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq24769.pdf.

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Takemura, Ai. "Effects of exposure to mild hyperbaric oxygen on metabolism-related diseases in animal models." Kyoto University, 2019. http://hdl.handle.net/2433/242722.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(人間・環境学)
甲第21845号
人博第874号
新制||人||210(附属図書館)
2018||人博||874(吉田南総合図書館)
京都大学大学院人間・環境学研究科共生人間学専攻
(主査)教授 石原 昭彦, 教授 久代 恵介, 教授 神﨑 素樹
学位規則第4条第1項該当
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Abass, K. M. (Khaled M. ). "Metabolism and interactions of pesticides in human and animal in vitro hepatic models." Doctoral thesis, University of Oulu, 2010. http://urn.fi/urn:isbn:9789514262999.

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Abstract Risk assessment of chemicals needs reliable scientific information and one source of information is the characterization of the metabolic fate and toxicokinetics of a chemical. Metabolism is often the most important factor contributing to toxicokinetics. Cytochrome P450 (CYP) enzymes are a superfamily of microsomal proteins playing a pivotal role in xenobiotic metabolism. In the present study, pesticides were used as representative xenobiotics since exposure to pesticides is a global challenge to risk assessment. Human and animal in vitro hepatic models were applied with the advantage of novel analytical techniques (LC/TOF-MS and LC/MS-MS) to elucidate the in vitro metabolism and interaction of selected pesticides. The results of these studies demonstrate that CYP enzymes catalyze the bioactivation of profenofos, diuron and carbosulfan into their more toxic metabolites desthiopropylprofenofos, N-demethyldiuron and carbofuran, respectively. The suspected carcinogenic metabolite of metalaxyl, 2,6-dimethylaniline, was not detected. CYP3A4 and CYP2C19 activities may be important in determining the toxicity arising from exposure to profenofos and carbosulfan. Individuals with high CYP1A2 and CYP2C19 activities might be more susceptible to diuron toxicity. Qualitative results of in vitro metabolism were generally in agreement with the results obtained from the published in vivo data, at least for the active chemical moiety and major metabolites. Considerable differences in the quantities of the metabolites produced within the species, as well as in the ratios of the metabolites among the species, were observed. These findings illustrate that in vitro screening of qualitative and quantitative differences are needed to provide a firm basis for interspecies and in vitro-in vivo extrapolations. Based on our findings, in vitro-in vivo extrapolation based on the elucidation of the in vitro metabolic pattern of pesticides in human and animal hepatic models could be a good model for understanding and extending the results of pesticides metabolism studies to human health risk assessment.
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Abolghasemi, Armita. "Lipid mediators as regulators of lipid and energy metabolism during energy balance derangement in animal models." Doctoral thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/67011.

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Thèse en cotutelle : Université Laval, Québec, Canada et Università Studi Cagliari, Cagliari, Italie
Les facteurs environnementaux jouent un rôle clé dans le développement du syndrome métabolique et de l'obésité, qui sont maintenant de véritables épidémies soulevant des problèmes de santé publique. Les excès de graisse corporelle dans l'obésité et la perte de masse grasse et maigre dans les conditions de dénutrition ou d'anorexie mentale sont le résultat d'un déséquilibre énergétique. Par conséquent, le maintien de l'équilibre énergétique est crucial à la fois pour la prévention de l'obésité et pour le traitement de l'anorexie mentale et d'autres formes de dénutrition. Les signaux lipidiques tels que ceux médiés par les médiateurs des endocannabinoidomes sont profondément impliqués dans le contrôle du métabolisme énergétique. Dans cette thèse, au sein de deux projets différents, nous avons étudié comment différents facteurs environnementaux, y compris la restriction calorique, l'activité physique, la supplémentation en vitamine D et les médicaments antipsychotiques, peuvent conduire à une modification du métabolisme énergétique par la modulation de la signalisation des endocannabinoïdomes. Les résultats des travaux expérimentaux montrent comment les différentes conditions étudiées provoquent des changements dans les niveaux tissulaires du médiateur lipidique endocannabinoïdome ainsi que dans l'expression de leurs récepteurs et enzymes métaboliques, ce qui peut contribuer aux changements observés de la masse grasse corporelle et du métabolisme énergétique au sein des modèles. Nous concluons que les conditions étudiées peuvent provoquer des changements dans le bilan énergétique par altération de l'endocannabinoidome.
Environmental factors play a key role in the development of obesity-induced metabolic syndrome and obesity, which are now true epidemics raising public health concerns. Both excess body fat in obesity, and fat and lean mass loss in undernutrition conditions or anorexia nervosa, are the result of energy imbalance. Therefore, maintaining energy balance is crucial for both the prevention of obesity and the treatment of anorexia nervosa and other forms of undernutrition. Lipid signals such as those mediated by endocannabinoidome mediators are deeply involved in the control of energy metabolism. In this thesis, within two different projects, we studied how different environmental factors including calorie restriction, physical activity, vitamin D supplementation and antipsychotic drugs, may lead to energy metabolism modification through modulation of the endocannabinoidome signaling. The results of the experimental work show how the different studied conditions cause changes in the tissue levels of endocannabinoidome lipid mediator as well as in the expression of their receptors and metabolic enzymes, which may contribute to the observed changes in body fat mass and energy metabolism within the models. We conclude that the investigated conditions may cause changes in energy balance through alteration of the endocannabinoidome.
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Glenn, L. Lee, and Brad G. Samojla. "A Critical Reexamination of the Morphology, Neurovasculature, and Fiber Architecture of Knee Extensor Muscles in Animal Models and Humans." Digital Commons @ East Tennessee State University, 2002. https://dc.etsu.edu/etsu-works/7526.

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The purposes of the present study were to resolve a number of major inconsistencies found in the literature on the structure of the quadriceps femoris muscle and to extend knowledge of its structure using descriptive, qualitative methodology. The quadriceps femoris muscle was investigated in 41 cats, and the findings were confirmed in 6 human cadavers. Two aponeuroses with major biomechanical functions (rectus-vastus and vastus aponeurosis), neither of which had been previously described in the literature, were characterized in both species. The study also resolved many major inconsistencies in the literature: The muscle sometimes described as vastus intermedius (VI) was found to be the articularis genu, the muscle sometimes described as vastus medialis (VM) was found to be the VI, the rectus femoris head was found to have an additional proximal nerve branch not previously recognized, no anomalous 5th head was ever found, and the distal VM were not found to have 2 heads (in either cats or humans). The authors’ anatomical descriptions and bimechanical models of the muscles, tendons, and neurovascular should provide a helpful foundation for future studies on the quadriceps. Two general recommendations are made: 1) that the feline model be considered a viable model to elucidate human knee pathomechanics; and 2) that regardless of the anatomical structure of interest, orthopedic nurses, orthopedic surgeons, and research investigators should routinely use the research literature for anatomical guidance instead of standard anatomical textbooks. © 2002, Sage Publications. All rights reserved.
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Ng, Kit-ying, and 吳潔瑩. "Neuroprotective effects of adiponectin in focal cerebral ischemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634371.

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Books on the topic "Muscles Metabolism Animal models"

1

Asher, Ornoy, ed. Animal models of human related calcium metabolic disorders. Boca Raton, Fla: CRC Press, 1995.

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Fanning, Lorna. Factors influencing chemically induced myotonia in rat muscles. Dublin: University College Dublin, 1995.

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International, Symposium on Biological Reactive Intermediates (3rd 1985 University of Maryland College Park). Biological reactive intermediates III: Mechanisms of action in animal models and human disease. New York: Plenum Press, 1986.

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1930-, Sparkes Robert S., and Lusis Aldons J. 1947-, eds. Genetic factors in atherosclerosis: Approaches and model systems. Basel: Karger, 1989.

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Trivedi, A. Percutaneous absorption and metabolism of tritiated oil i. urinary excretion of tritium in rats. Mississauga, Ont: Ontario Hydro, 1992.

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1941-, McCandless David W., ed. Metabolic encephalopathy. New York: Springer, 2009.

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International, Symposium for Biomedical Research on Alcoholism (1988 Taipei Taiwan). Molecular mechanisms of alcohol: Neurobiology and metabolism. Clifton, N.J: Humana Press, 1989.

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Babu, Uma S., and Paddy L. Wiesenfeld. Interactions of rice components and obesity-lipid biomarkers and immune function. Trivandrum, Kerala, India: Transworld Research Network, 2007.

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1951-, Marescaux C., Vergnes M. 1935-, and Bernasconi R. 1929-, eds. Generalized non convulsive epilepsy: Focus on GABA-B receptors. Wien: Springer-Verlag, 1992.

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Morozov, Vladimir I. Exercise and cellular mechanisms of muscle injury. Hauppauge, N.Y: Nova Science, 2009.

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Book chapters on the topic "Muscles Metabolism Animal models"

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Banu, Jameela, and Gabriel Fernandes. "Animal Models of Menopausal Metabolism." In Nutrition and Diet in Menopause, 395–406. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-373-2_29.

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Kritchevsky, D. "Animal Models of Lipoprotein Metabolism." In Handbook of Experimental Pharmacology, 207–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78426-2_7.

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Wissler, R. W., and D. Vesselinovitch. "Animal Models for Hyperlipidemia-Induced Atherosclerosis." In Drugs Affecting Lipid Metabolism, 111–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71702-4_20.

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Beynen, A. C. "Animal Models for Cholesterol Metabolism Studies." In New Developments in Biosciences: Their Implications for Laboratory Animal Science, 279–88. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-3281-4_43.

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M. Lyons, Karen. "Animal Models: Genetic Manipulation." In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 69–75. Ames, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118453926.ch8.

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Harrison, Lawrence E. "Animal Models of Cancer Cachexia." In Protein and Amino Acid Metabolism in Cancer Cachexia, 1–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22346-8_1.

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Susa, John B. "Methodology for the Study of Metabolism: Animal Models." In Principles of Perinatal-Neonatal Metabolism, 48–60. New York, NY: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-0400-5_3.

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Jäger, Walter, and Martina Höferl. "Metabolism of Terpenoids in Animal Models and Humans." In Handbook of Essential Oils, 275–301. Third edition. | Boca Raton : CRC Press, [2020]: CRC Press, 2020. http://dx.doi.org/10.1201/9781351246460-10.

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D. Blank, Robert. "Animal Models: Allelic Determinants for BMD." In Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 76–81. Ames, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118453926.ch9.

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Ishida, A., A. Ashihara, K. Nakashima, and M. Katsumata. "Expression of amino acid transporter in porcine skeletal muscles during postnatal development." In Energy and protein metabolism and nutrition in sustainable animal production, 395–96. Wageningen: Wageningen Academic Publishers, 2013. http://dx.doi.org/10.3920/978-90-8686-781-3_141.

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Conference papers on the topic "Muscles Metabolism Animal models"

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Humble, M., M. Palmér, and H. Hansson. "3. How is farm animal welfare internalized in consumers’ mental models at point of purchase?" In 6th EAAP International Symposium on Energy and Protein Metabolism and Nutrition. The Netherlands: Wageningen Academic Publishers, 2019. http://dx.doi.org/10.3920/978-90-8686-892-6_3.

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Tseng, Jen-Chieh, and Jeffrey Peterson. "Abstract 5124: Molecular imaging of tumor energy metabolism as an early indicator of anticancer drug efficacy in small animal models." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5124.

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Ji, Cheng. "P237 Enzyme complexes of alcohol metabolism protect against liver injury in animal models fed acute alcohol and anti-HIV drugs." In Abstracts for the STI & HIV World Congress (Joint Meeting of the 23rd ISSTDR and 20th IUSTI), July 14–17, 2019, Vancouver, Canada. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/sextrans-2019-sti.373.

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Rizzuto, E., A. Musarò, A. Catizone, and Z. Del Prete. "Morpho-Functional Interaction Between Muscle and Tendon in Hypertrophic MLC/mIGF-1 Mice." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19332.

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Tendons and ligaments are uniaxial viscoelastic connective tissues and, during normal activity, tendons transmit forces from muscles to bones, while ligaments stabilize the joints. Many experiments have been carried out to study ligaments and tendons mechanical properties [1], and the effects of training protocols [2] or specific pathologies. Recently, different transgenic mice models have been proposed as a new way to study in depth tendons’ function and development [3]. Within this context, we made use of pathological and transgenic animal models to investigate the morpho-functional interaction between muscles with an altered functionality and their tendons. In a previous work, by using the animal model of human Duchenne dystrophy, mdx, we found out that tendons connected to muscles with functional defects present reduced mechanical properties and an altered balance between alive and dead cells [4]. Here, we evaluated whether hypertrophic muscles would also involve alterations in tendon biomechanical properties. To do this, we used the transgenic animal model MLC/mIgf-1, were the local form of Igf-1 is over-expressed under a muscle specific promoter [5] inducing an increase in skeletal muscle mass and a proportional increment of force. To determine tendons’ elastic and viscous response separately, complex compliance has been computed with a new experimental method [6] which uses a pseudorandom Gaussian noise (PGN) to stimulate all the frequencies of interest within its bandwidth. Elasticity determines the tissue response to loading while viscous dissipation affects the likelihood of injuries to tendons. Indeed, knowing tendinous tissue viscoelasticity is central to better understand the mechanism between energy dissipation and tissue injuries. Finally, the hypothesis that changes in tendons’ mechanical properties could be correlated with alterations in the balance between alive and dead cells has been tested with an in situ cellular analysis.
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Marshall, Lauren, Andra Frost, Tim Fee, and Joel Berry. "Assembly and Characterization of 3D, Vascularized Breast Cancer Tissue Mimics." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14199.

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Drug development platforms such as two-dimensional (2D) in vitro cell culture systems and in vivo animal studies do not accurately predict human in vivo effectiveness of candidate therapeutics [1]. Cell culture systems have limited similarities to primary human cells and tissues as only one cell type is employed and animal studies have a generally limited ability to recapitulate human drug response as different species have differences in metabolism, physiology, and behavior. Mike Leavitt, a former U.S. Secretary of Health and Human Services, has stated that “currently, nine out of ten experimental drugs fail in clinical studies because we cannot accurately predict how they will behave in people based on laboratory and animal studies” [2]. Therefore, this research project is focused on developing an in vitro platform to test candidate therapeutics for more efficacious predictions of human response. We have fabricated a three-dimensional (3D) breast cancer tissue volume containing a vascular network. This vascular network is necessary because current in vitro systems (e.g., rotating bioreactors, suspension of spheroids, and growth on a porous scaffold) are limited in size (1–2 mm) by their absence of micrometer-scale blood flow micro-channels that allow for oxygen and nutrient diffusion into the tissue [4]. The extracellular matrix scaffold has been developed to mimic the native extracellular matrix and includes relevant cell types (e.g., human breast cancer epithelial cells and human breast fibroblasts) along with the prefabricated vascular network (prevascularization). These systems are intended to support long-term growth, recapitulate physiological tissue function, and accurately model response to treatment. It is hypothesized that the development of reproducible tissue volumes will transform breast cancer drug development by providing reliable, cost-effective models that can more accurately predict therapeutic efficacy than current preclinical in vivo and in vitro models.
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Kindel, G., and J. Fareed. "MODULATORY EFFECT OF SERINE PROTEASES AND RELATED ENZYMES ON ISOLATED SMOOTH MUSCLE PREPARATIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644602.

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Thrombin and related proteases produce varying pharmacologic responses in animal models. To more specifically study the in vivo actions of thrombin and related proteases, we have used isolated tissue preparations of the rabbit aortic strip (RAS), isolated guinea pig ileum (GPI) and isolated rat uterus (RU). Standard tissue-agonist regimens include epinephrine, thromboxane B2 with RAS; bradykinin, acetylcholine, histamine and serotonin with GPI; and acetylcholine, bradykinin and angiotensin with RU. The smooth muscle modulant action of numerous proteinases were screened in these regimens by bracketing the median dose response of the individual agonists. Protease complexes such as serum (rabbit, human and guinea pig), activated and nonactivated prothrombin complex concentrates and pancreatin were shown to produce varying but similar contractile responses as obtained by the standard agonists. Sera produced a dose-dependent contraction of the RAS, GPI and RU preparations. Various forms of thrombin produced different degrees of contraction of RAS accompanied by a desensitization process. On a molar basis the order of contractile activity ranged α > β>γ > nitro > DIP. All thrombins were found to augment the epinephrine and thromboxane B2 induced contraction of the RAS. Bovine and human factor Xa produced marked dilatation of the RAS but did not have any effect on the GPI and RU preparations. These results suggest that proteases exert direct musculotropic actions on smooth muscles. This should be taken into consideration in the pathophysiology of vascular spasms.
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Zhou, Yilu, Lauren Resutek, Liyun Wang, and X. Lucas Lu. "Effects of Bisphosphonate on Long-Term Culture of Cartilage Allografts." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14635.

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Zoledronic acid (ZA), an FDA approved bisphosphonate (BP) medicine, is widely used for the treatment of osteoclast-related bone loss diseases [1]. Our previous study has found that systemic administration of ZA could dramatically suppress the development of post-traumatic osteoarthritis (PTOA) in the DMM (destabilization of the medial meniscus) mouse model, a model recapitulating the altered joint loading associated with PTOA [2]. This finding is consistent with a few similar studies using different animal models [3]. However, little is known about the cellular and biochemical mechanisms of BP mediated chondro-protection in PTOA pathogenesis. Studies have shown that PTOA often initiates from the apoptosis and altered metabolism of cartilage chondrocytes. In this study, we will investigate the direct effects of ZA on the metabolisms of chondrocytes using long-term in vitro culture of cartilage allografts. As one of the earliest responses of chondrocytes to mechanical stimulation, intracellular calcium ([Ca 2+] i) signaling is the upstream of numerous mechanotransduction pathways [4]. We hypothesize that the chondro-protective mechanisms of ZA could be represented by the characteristics of [Ca 2+] i signaling of in situ chondrocytes. Our specific aims were to: (i) compare the in situ spontaneous [Ca 2+] i responses of chondrocytes cultured in non-ZA and ZA supplemented environments, and (ii) compare the biomechanical properties of cartilage allografts under the two culture conditions.
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Kumar, A., J. Fareed, W. H. Wehrmacher, D. Hoppensteadt, O. Ulutin, and J. M. Walenga. "ENDOTHELIAL FUNCTION MODULATION AND CONTROL OF VASCULAR AND THROMBOTIC DISORDERS: EXPERIMENTAL RESULTS WITH A POLYDEOXY RIBONUCLEOTIDE AGENT DEFIBROTIDE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643149.

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Numerous approaches with single and multiple drugs modulating protease cascade, platelet function and blood viscosity and to reduce blood lipids to manage thrombotic processes have been tried. Defibrotide, a polydeoxyribonucleotide, (Mr =17,000) offers a new approach to vascular and related thrombotic processes as it acts via modulation of endothelial cell function. We have used a primate model (Macaca mulatta) to study the endogenous action of this agent after the oral (10-25 mg/kg) and intravenous (5-10 mg/kg) administration. This agent produced no effect on clotting tests and ex vivo laboratory findings but rather it elevated the t-PA (antigen and functional), protein C (antigen and functional), prostacyclin and decreased thromboxane, 01.2-antiplasmin (functional) and t-PA inhibitor (functional) in both studies. These observations suggest that Defibrotide modulates endothelial function. Hepatic isolation in rabbits totally blocked the antithrombotic actions of Defibrotide suggesting that this agent is converted into an active product endogenously. Pretreatment of Defibrotide with nucleases also resulted in a complete loss of its actions. Defibrotide produced dose dependent antithrombotic actions in animal models (rabbit venous stasis and rat vena caval ligation) after either intravenous or oral administration. Blood pressure, heart rate, respiration and kidney function were not altered by it. No effect on bleeding time was noted in any studies. Upon oral administration this drug produced pharmacologic action after 2 hours whereas after intravenous administration, the action peaked at 30 minutes. Defibrotide exhibited cytoprotective effects towards endothelial lining of the vascular smooth muscles characterized by microscopic studies. In summary Defibrotide is an endothelial support agent whose multicomponent actions are primarily mediated via the physical and functional modulation of the endothelial cells in the vascular system.
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Reports on the topic "Muscles Metabolism Animal models"

1

Boisclair, Yves R., and Arieh Gertler. Development and Use of Leptin Receptor Antagonists to Increase Appetite and Adaptive Metabolism in Ruminants. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697120.bard.

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Objectives The original project had 2 major objectives: (1) To determine the effects of centrally administered leptin antagonist on appetite and adaptive metabolism in the sheep; (2) To develop and prepare second-generation leptin antagonists combining high binding affinity and prolonged in vivo half-life. Background Periods of suboptimal nutrition or exaggerated metabolic activity demands lead to a state of chronic energy insufficiency. Ruminants remain productive for a surprisingly long period of time under these circumstances by evoking adaptations sparing available energy and nutrients. The mechanism driving these adaptations in ruminant remains unknown, but could involve a reduction in plasma leptin, a hormone acting predominantly in the brain. In laboratory animals, reduced leptin signaling promotes survival during nutritional insufficiency by triggering energy sparing adaptations such as reduced thyroid hormone production and insulin resistance. Our overall hypothesis is that similar adaptations are triggered by reduced leptin signaling in the brain of ruminants. Testing of this hypothesis in ruminants has not been possible due to inability to block the actions of endogenous leptin and access to ruminant models where leptin antagonistic therapy is feasible and effective. Major achievements and conclusions The Israeli team had previously mutated 3 residues in ovine leptin, with no effect on receptor binding. This mutant was renamed ovine leptin antagonist (OLA) because it cannot activate signaling and therefore antagonizes the ability of wild type leptin to activate its receptor. To transform OLA into an effective in vivo antagonist, the Israeli made 2 important technical advances. First, it incorporated an additional mutation into OLA, increasing its binding affinity and thus transforming it into a super ovine leptin antagonist (SOLA). Second, the Israeli team developed a method whereby polyethylene glycol is covalently attached to SOLA (PEG-SOLA) with the goal of extending its half-life in vivo. The US team used OLA and PEG-SOLA in 2 separate animal models. First, OLA was chronically administered directly into the brain of mature sheep via a cannula implanted into the 3rdcerebroventricule. Unexpectedly, OLA had no effect of voluntary feed intake or various indicators of peripheral insulin action but reduced the plasma concentration of thyroid hormones. Second, the US team tested the effect of peripheral PEG-SOLA administration in an energy sensitive, rapidly growing lamb model. PEG-SOLA was administered for 14 consecutive days after birth or for 5 consecutive days before sacrifice on day 40 of life. Plasma PEG-SOLA had a half-life of over 16 h and circulated in 225- to 288-fold excess over endogenous leptin. PEG-SOLA administration reduced plasma thyroid hormones and resulted in a higher fat content in the carcass at slaughter, but had no effects on feed intake, body weight, plasma glucose or insulin. These results show that the team succeeded in developing a leptin antagonist with a long in vivo half-life. Moreover, in vivo results show that reduced leptin signaling promotes energy sparing in ruminants by repressing thyroid hormone production. Scientific and agricultural implications The physiological role of leptin in ruminants has been difficult to resolve because peripheral administration of wild type leptin causes little effects. Our work with leptin antagonists show for the first time in ruminants that reduced leptin signaling induces energy sparing mechanisms involving thyroid hormone production with little effect on peripheral insulin action. Additional work is needed to develop even more potent leptin antagonists, to establish optimal administration protocols and to narrow down phases of the ruminant life cycle when their use will improve productivity.
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