Clinical and Experimental Pharmacology and Physiology最新文献

{"title":"Effect of escitalopram on an acetic acid-induced ulcerative colitis model.","authors":"Negar Firouzabadi,&nbsp;Nahid Alimoradi,&nbsp;Mohammad Najafizadeh,&nbsp;Parvaneh Najafizadeh","doi":"10.1111/1440-1681.13474","DOIUrl":"https://doi.org/10.1111/1440-1681.13474","url":null,"abstract":"<p><p>Ulcerative colitis (UC) is a chronic and recurrent gastrointestinal (GI) disorder with an unknown aetiology and pathogenesis. Regarding the effectiveness of antidepressants on UC in animal models of depression and the known anti-inflammatory effects of escitalopram this study was conducted to evaluate the beneficial effects of escitalopram on an acetic acid-induced UC model without depression. UC model was induced by intra rectal (i.r.) administration of 4% acetic acid in rats after 24 hours of fasting. Animals were treated with three doses of escitalopram (5, 10 and 20 mg/kg). Prednisolone (4 mg/kg) was used as a reference drug in UC. Histological and oxidative stress markers were measured in all groups. Results showed significant increase in superoxide dismutase (SOD) activity and glutathione (GSH) levels, as well as significant decrease in myeloperoxidase (MPO) activity, malondialdehyde (MDA) levels, macroscopic factors (ulcer surface area, ulcer severity and weight-to-colon ratio) and microscopic and histological parameters (severity and extent of inflammation, cryptic destruction and severity of tissue involvement) in escitalopram treated rats (10, 20 mg/kg) compared to the UC group. In conclusion, the results of our study are in support of beneficial anti-inflammatory and antioxidant effects of escitalopram in UC.</p>","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"48 5","pages":"782-790"},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/1440-1681.13474","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25352176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of zinc sulphate and zinc methionine on growth, plasma growth hormone concentration, growth hormone receptor and insulin-like growth factor-I gene expression in mice.","authors":"Ze-Peng Yu,&nbsp;Guo-Wei Le,&nbsp;Yong-Hui Shi","doi":"10.1111/j.1440-1681.2005.04183.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.2005.04183.x","url":null,"abstract":"<p><p>1. The current experiment was conducted to investigate the effect of zinc sulphate (ZnSO4) and zinc methionine (Zn-Met) on growth and their effect on plasma growth hormone (GH) concentration, growth hormone receptor (GHR) and insulin-like growth factor I (IGF-I) mRNA expression in mice. 2. Ninety male KunMing (KM) mice were randomly divided into three treatments. The control group was fed on a basal diet containing 11.67 mg/kg of zinc. The ZnSO4 group and Zn-Met group were fed on the diets supplemented with ZnSO4 or Zn-Met at 30 mg/kg (containing zinc of 40.05 and 40.75 mg/kg, respectively). The mice were offered the test diets for 10 days. Weight gains and food intake were measured at the end of the experiment, zinc contents in liver and serum were determined using atomic absorption spectrophotometry; GH was determined by radioimmunoassay, the levels of GHR and IGF-I mRNA were determined with reverse transcript polymerase chain reaction. 3. Both ZnSO4 and Zn-Met enhanced weight gain and food intake in the mice, Zn-Met improved the growth and food intake more effectively than ZnSO4 did (P < 0.05). The both forms of zinc had no effect on GH and the level of GHR mRNA expression (P > 0.05) and they up-regulated the expression of IGF-I mRNA (P < 0.05). As compared to ZnSO4, Zn-Met enhanced the level of IGF-I mRNA significantly (P < 0.05). 4. Both ZnSO4 and Zn-Met had no effect on plasma GH and the expression of GHR mRNA, but they enhanced the expression of IGF-I mRNA. Zinc methionine enhanced the weight gain and up-regulated IGF-I mRNA expression more effectively than ZnSO4.</p>","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"32 4","pages":"273-8"},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.2005.04183.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25041793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optical imaging of respiratory neuron activity from the dorsal view of the lower brainstem.","authors":"Hiroshi Onimaru,&nbsp;Ikuo Homma","doi":"10.1111/j.1440-1681.2005.04187.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.2005.04187.x","url":null,"abstract":"<p><p>1. We visualized respiratory-related neuron network activity in the dorsal part of the pons and medulla of an in vitro preparation from newborn rats by optical recordings using a voltage-sensitive dye. We measured optical signals from several seconds before to several seconds after the inspiratory phase using the inspiratory motor nerve discharge as the trigger signal and we averaged the optical signals of 20-50 respiratory cycles to obtain an optical image correlating specifically to inspiratory activity. 2. Four areas that were excited or inhibited corresponding to the respiratory cycles were detected. (i) The most rostral activity was in the rostral and lateral parts of the pons, with activity mainly in the inspiratory phase, corresponding to the pontine-respiratory group. (ii) In the midpontine level, inspiratory activity followed by long-lasting hyperpolarization appeared in the midlateral parts. This part was presumed to reflect activity in the locus coeruleus. The hyperpolarization became almost negligible after treatment with the alpha-adrenergic antagonist, phentolamine. (iii) In the dorsal medulla, the predominantly inspiratory activity was detected at the rostral level of the area postrema. This part was considered to reflect activity mainly of the hypoglossal nucleus. (iv) At a similar level, we also detected weak and disperse inspiratory activity extending more laterally and caudally than that of the hypoglossal nucleus activity. This might reflect activity of the dorsal respiratory group. 3. In conclusion, the present optical recording study revealed that the dorsal part of the lower brainstem in the in vitro preparation is noticeably active as well as the ventral part shown in the previous study. This method is very useful for analysis of pharmacological properties, as well as the spatio-temporal pattern of respiratory-related network activity in the brainstem.</p>","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"32 4","pages":"297-301"},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.2005.04187.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25041797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anaphylactic hepatic venoconstriction is attenuated by nitric oxide released via shear stress-dependent and -independent mechanisms in Guinea pig.","authors":"Toshishige Shibamoto,&nbsp;Zonghai Ruan,&nbsp;Sen Cui,&nbsp;Yasutaka Kurata,&nbsp;Tomonobu Koizumi,&nbsp;Keishi Kubo","doi":"10.1111/j.0305-1870.2005.04186.x","DOIUrl":"https://doi.org/10.1111/j.0305-1870.2005.04186.x","url":null,"abstract":"<p><p>1. The role of shear stress in nitric oxide (NO)-mediated attenuation of anaphylactic venoconstriction was studied using an isolated ovalbumin-sensitized guinea pig liver. 2. Guinea pigs were actively sensitized by a subcutaneous injection of 1 mg ovalbumin. Two weeks after sensitization, the livers were perfused with diluted blood under constant flow or constant perfusion pressure. The constant flow could result in increased shear stress during constriction, while the constant perfusion pressure could prevent changes in shear stress. Using the double occlusion technique to estimate the hepatic sinusoidal pressure, pre- and postsinusoidal constriction was evaluated. Hepatic anaphylaxis was induced by an injection of ovalbumin (4 microg) into the perfusate, the volume of which was 40 mL. 3. Under either constant flow or pressure, anaphylaxis caused venoconstriction of predominantly presinusoids over postsinusoids, although anaphylactic venoconstriction under constant pressure was significantly greater than that under constant flow. When shear stress was held constant by maintaining constant perfusion pressure, a NO synthase inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME, 100 micromol/L), potentiated similarly both pre- and postsinusoidal constriction induced by anaphylaxis. This suggests that hepatic anaphylaxis shear stress-independently generates NO, resulting in dilatation of both pre- and postsinusoidal vessels in a similar magnitude. In contrast, when shear stress was allowed to rise under constant flow, anaphylactic presinusoidal constriction was preferentially potentiated by L-NAME. 4. Hepatic anaphylaxis can increase NO production in a shear stress-independent manner and dilates similarly both pre- and postsinusoids, while NO produced in a shear stress-dependent manner attenuates predominantly venoconstriction of the presinusoids where shear stress is preferentially increased.</p>","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"32 4","pages":"288-93"},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.0305-1870.2005.04186.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25041795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glucose phosphorylation as a barrier to muscle glucose uptake.","authors":"Patrick T Fueger","doi":"10.1111/j.1440-1681.2005.04190.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.2005.04190.x","url":null,"abstract":"<p><p>1. Glucose phosphorylation is the first irreversible step of the muscle glucose uptake pathway and is catalysed by a hexokinase isozyme. 2. While glucose transport is the primary barrier to muscle glucose uptake during basal conditions, glucose phosphorylation becomes an important barrier to muscle glucose uptake during stimulated conditions such as hyperinsulinaemia or exercise. 3. High fat feeding markedly impairs insulin- and exercise-stimulated muscle glucose uptake. As hexokinase II overexpression corrects this dietary-induced deficit during exercise, glucose phosphorylation is a site of impairment following high fat feeding. 4. Exercise is an important tool for diagnosing deficits in glucose phosphorylation.</p>","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"32 4","pages":"314-8"},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.2005.04190.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25041800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interaction of physiological mechanisms in control of muscle glucose uptake.","authors":"David H Wasserman,&nbsp;Julio E Ayala","doi":"10.1111/j.1440-1681.2005.04191.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.2005.04191.x","url":null,"abstract":"<p><p>1. Control of glucose uptake is distributed between three steps. These are the rate that glucose is delivered to cells, the rate of transport into cells, and the rate that glucose is phosphorylated within these same cells. The functional limitations to each one of these individual steps has been difficult to assess because they are so closely coupled to each other. Studies have been performed in recent years using complex isotopic techniques or transgenic mouse models to shed new light on the role that each step plays in overall control of muscle glucose uptake. 2. Membrane glucose transport is a major barrier and glucose delivery and glucose phosphorylation are minor barriers to muscle glucose uptake in the fasted, sedentary state. GLUT-4 is translocated to the muscle membrane during exercise and insulin-stimulation. The result of this is that it can become so permeable to glucose that it is only a minor barrier to glucose uptake. 3. In addition to increasing glucose transport, exercise and insulin-stimulation also increase muscle blood flow and capillary recruitment. This effectively increases muscle glucose delivery and by doing so, works to enhance muscle glucose uptake. 4. There is a growing body of data that suggests that insulin resistance to muscle glucose uptake can be because of impairments in any one or more of the three steps that comprise the process.</p>","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"32 4","pages":"319-23"},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.2005.04191.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25041071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comments on journal guidelines for reporting statistics.","authors":"John Ludbrook","doi":"10.1111/j.1440-1681.2005.04221.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.2005.04221.x","url":null,"abstract":"This letter is prompted by 10 detailed guidelines for reporting statistics in journals published by The American Physiological Society. 1 I take issue with several of these guidelines. I also take issue with the two short paragraphs on statistics in the ‘Instructions to Authors’ issued by Clinical and Experimental Pharmacology and Physiology (CEEP). I have tried to resolve these differences. In his ‘Instructions for Authors’, the Editor-in-Chief of CEPP provides two short paragraphs of advice to prospective authors on how to present descriptive and analytical statistics (see the website http://www.blackwellpublishingasia.com). CEPP subscribes to the policies of The International Committee of Medical Journal Editors (ICMJE) (see the website http://www.icmje.org/). Should our Editor-in-Chief or the ICMJE do more? In contrast, the American Journals of Physiology have recently published an Editorial by Douglas Curran-Everett and Dale J. Benos in which they give 10, very detailed, guidelines for reporting statistics in journals published by the American Physiological Society (APS) (see the website http://www.ajpregu.org for details). 1 The APS adheres to the policies of the Council of Science Editors (CSE) (see the website http://www.councilscienceeditors.org). In this letter, I attempt to resolve the differences between minimalists and maximalists. I shall start to do this by considering the recommendations of Curran-Everett and Benos one-by-one.","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"32 4","pages":"324-6"},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.2005.04221.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25041072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resistance to excessive bodyweight gain in risperidone-injected rats.","authors":"Miyuki Ota,&nbsp;Keiji Mori,&nbsp;Akira Nakashima,&nbsp;Yoko S Kaneko,&nbsp;Hisahide Takahashi,&nbsp;Akira Ota","doi":"10.1111/j.1440-1681.2005.04184.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.2005.04184.x","url":null,"abstract":"<p><p>1. The present study was carried out to explain the resistance of rats injected subcutaneously with risperidone, the atypical antipsychotic drug, for 21 consecutive days at 0.1 mg/kg per day (a dose equivalent to the one used for patients) to result in an excessive bodyweight despite the increase in diet-uptake in rats against risperidone-induced decrease in body temperature. 2. Rectal temperature measurements were made in 8-week-old male Sprague-Dawley rats maintained under standard laboratory conditions using a 12 h daylight cycle. A s.c. injection of risperidone (0.05 mg/kg) produced hypothermia in rats, which was observed during the daily injection for 21 consecutive days. 3. Sera, white and brown adipose tissues, skeletal muscle and liver were extracted from 8-week-old male Sprague-Dawley rats injected subcutaneously with risperidone (0.01 or 0.1 mg/kg per day) or a vehicle for 21 consecutive days. Serum levels of lipids, ketones and thyroid hormone were measured. The mRNA expression levels in these tissues and organs of the genes encoding the substances involved in heat production and/or lipid metabolism were investigated by using quantitative real-time polymerase chain reaction amplification. 4. Serum nonesterified fatty acid levels in risperidone 0.1 mg/kg per day s.c. injected rats were significantly lower than those in vehicle-injected ones. Serum beta-hydroxybutyrate levels in risperidone-injected rats tended to decrease compared with those in vehicle-injected ones. The serum level of neither triiodothyronine nor thyroxine was affected by risperidone s.c. injection at the doses examined, although their values were within normal limits. 5. Risperidone injection (0.1 mg/kg per day) for 21 consecutive days upregulated mRNA expressions in white adipose tissue of uncoupling protein 3 which dissipates energy as heat; peroxisome proliferator-activated receptor (PPAR) gamma coactivator 1alpha which activates mitochondrial biogenesis to expand the oxidative machinery; and PPARalpha which is necessary for the fat-depletion of adipocytes for thermogenesis. The mRNA of lipogenic enzymes (acetyl-CoA carboxylase alpha, fatty-acid synthase and glycerol-3-phosphate acyltransferase), hormone sensitive lipase and beta1-adrenoceptor were also enhanced in white adipose tissue by the injection of 0.1 mg/kg per day risperidone. 6. These findings suggest that the materials for heat generation in white adipose tissue would be readily supplied, which in turn would reduce a storage of lipids in white adipose tissue resulting in the lower rate of bodyweight gain of rats.</p>","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"32 4","pages":"279-87"},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.2005.04184.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25041794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Active role for the vasculature in the delivery of insulin to skeletal muscle.","authors":"Michelle A Vincent,&nbsp;Lucy H Clerk,&nbsp;Stephen Rattigan,&nbsp;Michael G Clark,&nbsp;Eugene J Barrett","doi":"10.1111/j.1440-1681.2005.04188.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.2005.04188.x","url":null,"abstract":"<p><p>1. In the 80+ years since insulin's discovery, an enormous amount of literature has accumulated relating to its actions on body fat, glucose and protein metabolism. In particular, skeletal muscle has been extensively studied because of its major role as a site of insulin-mediated glucose disposal. Liver and adipose tissue are two other extensively studied sites of insulin action. Much less investigation has been directed towards delineating insulin's actions on cells other than myocytes, adipocytes and hepatocytes. 2. Over the past 5-10 years it has become increasingly evident that insulin exerts important actions on vascular cells. Here, we review evidence that insulin's action within muscle may be very much regulated by its ability to transit the vasculature to access the interstitial fluid (and hence the myocyte insulin receptor). Surprisingly little is known regarding the regulation of vascular events that first bring insulin to the capillary endothelium within muscle, whence presumably it transits from the vascular to the interstitial space. Recent studies suggest that insulin can increase blood flow and also influence the distribution of blood flow within skeletal muscle, potentially therefore regulating its own delivery to the capillary endothelium. Beyond insulin's ability to access the vascular lumen within skeletal muscle microvasculature lies the issue of its passing the endothelial barrier. Even less is known about the processes involved in insulin's actual transit across the endothelium. Available data do not clearly indicate whether this is a saturable, receptor-mediated process or a passive-diffusion pathway. Also, whether insulin in any manner regulates its own transit across the endothelium or its clearance via the lymphatic system is entirely unknown. 3. The aim of the present review is to identify areas where knowledge is deficient and highlight hypotheses which may lead to a better understanding of the coordinated relationship between insulin's vascular actions within muscle and its metabolic actions in that tissue. Even so, there is now sufficient evidence to indicate that insulin's vascular action within skeletal muscle is a major regulatory locus for its insulin mediated glucose disposal.</p>","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"32 4","pages":"302-7"},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.2005.04188.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25041798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Use of GLUT-4 null mice to study skeletal muscle glucose uptake.","authors":"Maureen J Charron,&nbsp;Naira Gorovits,&nbsp;J Skye Laidlaw,&nbsp;Mollie Ranalletta,&nbsp;Ellen B Katz","doi":"10.1111/j.1440-1681.2005.04189.x","DOIUrl":"https://doi.org/10.1111/j.1440-1681.2005.04189.x","url":null,"abstract":"<p><p>1. The present review focuses on the effects of varying levels of GLUT-4, the insulin-sensitive glucose transporter, on insulin sensitivity and whole body glucose homeostasis. 2. Three mouse models are discussed including myosin light chain (MLC)-GLUT-4 mice which overexpress GLUT-4 specifically in skeletal muscle, GLUT-4 null mice which express no GLUT-4 and the MLC-GLUT-4 null mice which express GLUT-4 only in skeletal muscle. Overexpressing GLUT-4 specifically in the skeletal muscle results in increased insulin sensitivity in the MLC-GLUT-4 mice. In contrast, the GLUT-4 null mice exhibit insulin intolerance accompanied by abnormalities in glucose and lipid metabolism. Restoring GLUT-4 expression in skeletal muscle in the MLC-GLUT-4 null mice results in normal glucose metabolism but continued abnormal lipid metabolism. 3. The results of experiments using these mouse models demonstrates that modifying the expression of GLUT-4 profoundly affects whole body insulin action and consequently glucose and lipid metabolism.</p>","PeriodicalId":10259,"journal":{"name":"Clinical and Experimental Pharmacology and Physiology","volume":"32 4","pages":"308-13"},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1681.2005.04189.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25041799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}