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Expression of nitric oxide synthase in skeletal muscle: a novel role for nitric oxide as a modulator of insulin action.
Abstract
Previous studies have shown that nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO), is expressed in skeletal muscle. The aim of the present study was to test the hypothesis that NO can modulate glucose metabolism in slow- and fast-twitch skeletal muscles. Calcium-dependent NOS was detected in skeletal muscle, and the enzyme activity was greater in fast-type extensor digitorum longus (EDL) muscles than in slow-type soleus muscles. Both the neuronal-type (nNOS) and endothelial-type (eNOS) enzymes are expressed in resting skeletal muscles. However, nNOS protein was only detected in EDL muscles, whereas eNOS protein contents were comparable in soleus and EDL muscles. NOS expression in muscle cryosections (diaphorase histochemistry) was located in vascular endothelium and in muscle fibers, and the staining was greater in type IIb than in type I and IIa fibers. The macrophage-type inducible NOS (iNOS) was not detected in resting muscle, but endotoxin treatment induced its expression, concomitant with elevated NO production. iNOS induction was associated with impaired insulin-stimulated glucose uptake in isolated rat muscles. In vitro, NOS blockade with specific inhibitors did not affect basal or insulin-stimulated glucose transport in EDL or soleus muscles. In contrast, the NO donors GEA 5024 and sodium nitroprusside induced dose-dependent inhibition (up to 50%) of maximal insulin-stimulated glucose transport in both muscles with minor effects on basal uptake values. GEA 5024 also blunted insulin-stimulated glucose transport and amino acid uptake in cultured L6 muscle cells without affecting insulin binding to its receptor. On the other hand, the permeable cGMP analogue dibutyryl cGMP did not affect muscle glucose transport. These results strongly suggest that NO modulates insulin action in both slow- and fast-type skeletal muscles. This novel autocrine action of NO in muscle appears to be mediated by cGMP-independent pathways.
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“In several situations of insulin resistance, such as diet-induced or genetic obesity, and endotoxaemia, iNOS is induced in tissues classically related to insulin signalling (Bedard et al. 1997; Kapur et al. 1997; Kapur et al. 1999).”
From Acute physical exercise reverses S‐nitrosation of the insulin receptor, insulin receptor substrate 1 and protein kinase B/Akt in diet‐induced obese Wistar rats (2008) · cites this paper as Kapur et al. 1997
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Items 101–200 of 219
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Self-citationFrost, R. A., Nystrom, G. J., & Lang, C. H. (2009) · Shock · doi:10.1097/shk.0b013e3181a034d2 · Cited by 45
Perreault, M., Dombrowski, L., & Marette, A. (2000) · Diabetologia · doi:10.1007/s001250051325 · Cited by 44
“It is interesting to note, in this regard, that nNOS is enriched in fasttwitch compared with slow-twitch fibres [12, 26].”
BackgroundMethodResultInfluentialSelf-citationInsulin resistance, a new target for nitric oxide‐delivery drugs
Cook, S., & Scherrer, U. (2002) · Fundamental and Clinical Pharmacology · doi:10.1046/j.1472-8206.2002.00130.x · Cited by 44
Lee, J. H., Palaia, T. A., & Ragolia, L. (2008) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00254.2008 · Cited by 44
“Although the mechanism of how iNOS causes or exacerbates insulin resistance remains largely unknown, it has been shown that the overproduction of NO causes S-nitroslyation of insulin-responsive molecules such as Akt, insulin receptor- , and insulin receptor substrate-1 in ob/ob diabetic mice, resulting in insulin resi…”
BackgroundFlati, V., Pasini, E., D’Antona, G., Speca, S., Toniato, E., & Martinotti, S. (2008) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2008.02.075 · Cited by 43
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“[37] and Schmidt and Walter [38] a further potential explanation arises for the diminished glycogen resynthesis of the DOMS compared to the CONTROL group.”
ResultMcGrowder, D., Ragoobirsingh, D., & Dasgupta, T. (2001) · Nitric Oxide · doi:10.1006/niox.2001.0360 · Cited by 39
Effect of Phosphodiesterase Inhibition on Insulin Resistance in Obese Individuals
Ho, J. E., Arora, P., Walford, G. A., Ghorbani, A., Guanaga, D. P., Dhakal, B. P., Nathan, D. I., Buys, E. S., Florez, J. C., Newton‐Cheh, C., et al. (2014) · Journal of the American Heart Association · doi:10.1161/jaha.114.001001 · Cited by 39
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“As NO-mediated processes are likely more evident in muscle with greater NO synthase activity (Kobzik et al., 1994; Hussain et al., 1997; Kapur et al., 1997), all experiments were performed using fast-twitch extensor digitorum longus (EDL) muscle fibres.”
MethodInsulin resistance: potential role of the endogenous nitric oxide synthase inhibitor ADMA
Sydow, K., Mondon, C. E., & Cooke, J. P. (2005) · Vascular Medicine · doi:10.1191/1358863x05vm604oa · Cited by 39
Sarcolemmal targeting of nNOSμ improves contractile function ofmdxmuscle
Rebolledo, D. L., Kim, M. J., Whitehead, N. P., Adams, M. E., & Froehner, S. C. (2015) · Human Molecular Genetics · doi:10.1093/hmg/ddv466 · Cited by 35
Oxidative stress in hypertensive children before and after 1 year of antihypertensive therapy
Śladowska-Kozłowska, J., Litwin, M., Niemirska, A., et al. (2012) · Pediatric Nephrology · doi:10.1007/s00467-012-2193-x · Cited by 34
“Independent of vascular action, impaired nitric acid (NO) bioavailability can be related to a cellular defect in skeletal muscles, where NO regulates metabolic and contractile processes including among others, basal glucose transport [40].”
BackgroundNitric oxide synthase-1 is enriched in fast-twitch oxidative myofibers
Planitzer, G., Miethke, A. G., & Baum, O. (2001) · Cell and Tissue Research · doi:10.1007/s004410100449 · Cited by 34
Muscular nitric oxide synthase (muNOS) and utrophin
Chaubourt, E., Voisin, V., Fossier, P., Baux, G., Israël, M., & de la Porte, S. (2002) · Journal of Physiology-Paris · doi:10.1016/s0928-4257(01)00079-1 · Cited by 36
Henstridge, D. C., Kingwell, B. A., Formosa, M. F., Drew, B. G., McConell, G. K., & Duffy, S. J. (2005) · Diabetologia · doi:10.1007/s00125-005-0018-1 · Cited by 33
“transport in skeletal muscle [13, 16–19].”
BackgroundResultEffects of insulin on regional blood flow and glucose uptake in Wistar and Sprague-Dawley rats
Gaudreault, N., Santuré, M., Pǐtre, M., Nadeau, A., Marette, A., & Bachelard, H. (2001) · Metabolism · doi:10.1053/meta.2001.18569 · Cited by 33
Self-citationBlocking iNOS and endoplasmic reticulum stress synergistically improves insulin resistance in mice
Zanotto, T. M., Quaresma, P. G. F., Guadagnini, D., Weissmann, L., Santos, A. C., Vecina, J. F., Calisto, K. L., Santos, A., Prada, P. O., & Saad, M. J. A. (2016) · Molecular Metabolism · doi:10.1016/j.molmet.2016.12.005 · Cited by 32
“Activation of iNOS, which can be induced by proinflammatory cytokines [3,4], has also been described as a potential cause of insulin resistance, a condition which often precedes these metabolic disorders [5e7].”
BackgroundHouse, L. M., Morris, R. T., Barnes, T. M., Lantier, L., Cyphert, T. J., McGuinness, O. P., & Otero, Y. F. (2015) · Cardiovascular Diabetology · doi:10.1186/s12933-015-0223-2 · Cited by 34
Stephens, T., Canny, B., Snow, R., & McConell, G. K. (2004) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/j.1440-1681.2004.04014.x · Cited by 32
Nitric Oxide Is a Downstream Mediator of Agrin-Induced Acetylcholine Receptor Aggregation
Jones, M. A., & Werle, M. J. (2000) · Molecular and Cellular Neuroscience · doi:10.1006/mcne.2000.0901 · Cited by 32
Chagnon, M. J., Elchebly, M., Uetani, N., et al. (2006) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/y06-020 · Cited by 31
“Glucose transport was measured using the glucose analogue 2-[3H]-2-deoxy-D-glucose as previously described (Kapur et al. 1997).”
MethodSelf-citationPicard, F., Kapur, S., Perreault, M., et al. (2001) · The FASEB Journal · doi:10.1096/fj.00-0830fje · Cited by 31
Self-citationInsulin and nitric oxide stimulates glucose transport in human placenta
Acevedo, C. G., Márquez, J. L., Rojas, S., & Bravo, I. (2005) · Life Sciences · doi:10.1016/j.lfs.2004.09.039 · Cited by 30
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Triggle, C. R., Howarth, A. G., Cheng, Z. J., & Ding, H. (2005) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/y05-069 · Cited by 29
“…a clustering of cardiovascular risk factors in young mice that are very similar to those seen in humans with the metabolic syndrome. eNOS, however, is also expressed in skeletal muscle and a role for skeletal musclederived NO in the regulation of insulin action has been argued (Kapur et al. 1997).”
BackgroundZhang, J., Massmann, G. A., Mirabile, C. P., et al. (1999) · Biology of Reproduction · doi:10.1095/biolreprod60.5.1198 · Cited by 30
Ghasemi, A., Syedmoradi, L., Momenan, A. A., Zahediasl, S., & Azizi, F. (2010) · Scandinavian Journal of Clinical and Laboratory Investigation · doi:10.3109/00365511003611282 · Cited by 29
Orzechowski, A., Łokociejewska, M., Muras, P., et al. (2002) · Life Sciences · doi:10.1016/s0024-3205(02)01942-2 · Cited by 28
“One should bear in mind the considerable negative role of iNOS present in muscle fibers [19,36].”
BackgroundHenstridge, D. C., Drew, B. G., Formosa, M. F., Natoli, A. K., Cameron‐Smith, D., Duffy, S. J., & Kingwell, B. A. (2009) · Nitric Oxide · doi:10.1016/j.niox.2009.06.002 · Cited by 27
“One previous paper has reported that the NO donors GEA 5024 and SNP caused a dose-dependent decrease in the insulin-mediated glucose uptake in soleus muscles of rats [6].”
BackgroundYoshimura, T., Hisatomi, A., Kajihara, S., Yasutake, T., Ogawa, Y., Mizuta, T., Ozaki, I., Utsunomiya, T., & Yamamoto, K. (2003) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.10.43 · Cited by 25
Hlinský, T., Kumstát, M., & Vajda, P. (2020) · Nutrients · doi:10.3390/nu12092734 · Cited by 26
Dua, A. K., Dua, N., & Murrant, C. L. (2009) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00216.2009 · Cited by 25
“Vascular cell NOS is involved in the dilatory pathways for other vasodilators implicated in muscle contraction such as ACh and ADO (8, 23), and L-NAME application may, therefore, also be blunting the dilatory response imposed by these dilators during contraction.”
BackgroundInfluentialIssa, N. G., Lachance, G., Bellmann, K., Laplante, M., Stadler, K., & Marette, A. (2018) · Journal of Lipid Research · doi:10.1194/jlr.m086504 · Cited by 27
Self-citationPatel, P. N., Qi, W., Allen, D. M., et al. (2004) · Microsurgery · doi:10.1002/micr.20029 · Cited by 25
“Neuronal NOS (nNOS) in skeletal muscle can regulate contractility and glucose uptake.(7,8)”
BackgroundIncreased Extravasation of Macromolecules in Skeletal Muscles of the Zucker Rat Model
St‐Pierre, P., Bouffard, L., Papirakis, M., & Maheux, P. (2006) · Obesity · doi:10.1038/oby.2006.91 · Cited by 24
Exogenous nitric oxide increases basal leg glucose uptake in humans
Durham, W. J., Yeckel, C. W., Miller, S. L., Gore, D. C., & Wolfe, R. R. (2003) · Metabolism · doi:10.1016/s0026-0495(03)00062-3 · Cited by 23
Insulin inhibits inducible nitric oxide synthase in skeletal muscle cells
Bédard, S., Marcotte, B., & Marette, A. (1998) · Diabetologia · doi:10.1007/s001250051100 · Cited by 21
“Furthermore, only iNOS can produce NO in the L6 myocytes since neither control nor cytokine/ LPS-treated cells express the other nitric oxide synthase isoforms eNOS and nNOS [2, 5].”
BackgroundInfluentialSelf-citationVecoli, C., Novelli, M., Pippa, A., Giacopelli, D., Beffy, P., Masiello, P., L’Abbate, A., & Neglia, D. (2014) · PLoS ONE · doi:10.1371/journal.pone.0104156 · Cited by 20
Effect of metformin on the vascular and glucose metabolic actions of insulin in hypertensive rats
Santuré, M., Pǐtre, M., Gaudreault, N., Marette, A., Nadeau, A., & Bachelard, H. (2000) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.2000.278.5.g682 · Cited by 20
Self-citationHwang, J.-H., Moon, S. A., Lee, C. H., Byun, M. R., Kim, A. R., Sung, M., Park, H., Hwang, E. S., Sung, S. H., & Hong, J. (2012) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2012.04.018 · Cited by 19
St‐Pierre, P., Bouffard, L., & Maheux, P. (2004) · Biochemical Pharmacology · doi:10.1016/j.bcp.2004.02.008 · Cited by 19
Regulation of diaphragmatic nitric oxide synthase expression during hypobaric hypoxia
Javeshghani, D., Sakkal, D., Mori, M., et al. (2000) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.2000.279.3.l520 · Cited by 19
“Indeed, basal and insulin- and contraction-stimulated glucose uptakes are enhanced by endogenous NO synthesis (4, 18).”
BackgroundRedox regulation of skeletal muscle glucose transport
Balon, T. W., & Yerneni, K. K. V. (2001) · Medicine & Science in Sports & Exercise · doi:10.1097/00005768-200103000-00008 · Cited by 19
Insulin Signaling in Skeletal Muscle and Liver of Neonatal Pigs During Endotoxemia
Orellana, R. A., Suryawan, A., Kimball, S. R., et al. (2008) · Pediatric Research · doi:10.1203/pdr.0b013e318183fd4c · Cited by 18
“Furthermore, induction of iNOS activity either by LPS treatment (11) or by obesity (20) has been linked to the impairment of glucose transport in skeletal muscle that contributes to the whole body insulin resistance for glucose metabolism.”
Baum, O., Miethke, A. G., Wöckel, A., et al. (2002) · Acta Histochemica · doi:10.1078/0065-1281-00625 · Cited by 18
Nitric oxide synthase inhibition impairs muscle regrowth following immobilization
Aguiar, A. F., Vechetti, I. J., de Souza, R. W. A., Piedade, W. P., Pacagnelli, F. L., Leopoldo, A. S., Casonatto, J., & Dal‐Pai‐Silva, M. (2017) · Nitric Oxide · doi:10.1016/j.niox.2017.07.006 · Cited by 19
Obesity-linked Insulin Resistance: Is Nitric Oxide the Missing Link?
Dallaire, P., & Marette, A. (2004) · Cited by 17
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“Its expression is upregulated by many inducers of insulin resistance, such as hyperglycemia (16,17), free fatty acids (11), and cytokines (18,19).”
BackgroundPunkt, K., Zaitsev, S., Park, J. K., et al. (2001) · The Histochemical Journal · doi:10.1023/a:1017994108174 · Cited by 16
“Moreover, several authors (Balon & Nadler 1994, Bedard et al. 1997, Kapur et al. 1997, Reid 1998) showed, that basal glucose metabolism in rat skeletal muscles is regulated by NO.”
BackgroundRole of nitric oxide in myotoxic activity induced by crotoxin in vivo
Miyabara, E. H., Tostes, R. C., Selistre-de-Araújo, H. S., et al. (2004) · Toxicon · doi:10.1016/j.toxicon.2004.02.012 · Cited by 15
“Although we have not excluded the possibility that the endothelial NOS (eNOS) isoform is also involved in myoprotection against CTX, previous studies have shown that this isoform is very poorly expressed in skeletal muscle (Kapur et al., 1997) and up to date there is no specific inhibitor available.”
BackgroundNgala, R. A., O’Dowd, J. F., Stocker, C. J., Cawthorne, M. A., & Arch, J. R. S. (2013) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-013-0860-5 · Cited by 15
“This result is consistent with reports that other inhibitors of nitric oxide synthase prevent stimulation of glucose uptake in muscle in vivo in response to insulin (Kapur et al. 1997; Roy et al. 1998; Vincent et al. 2003), but previous work has not shown an effect of nitric oxide synthase inhibitors in isolated muscl…”
BackgroundResultEffects of altered hepatic lipid metabolism on regulation of hepatic iNOS
Stanimirović, J., Obradovic, M. M., Zafirovic, S. S., Resanović, I., Bogdanović, N., Gluvic, Z. M., Mousa, S. A., & Isenović, E. R. (2015) · Clinical Lipidology · doi:10.2217/clp.15.8 · Cited by 14
Recent Advances in the Development of Agents for the Treatment of Type 2 Diabetes
Cobb, J. E., & Dukes, I. D. (1998) · Annual reports in medicinal chemistry · doi:10.1016/s0065-7743(08)61086-6 · Cited by 14
Muscle Fiber Type-Predominant Promoter Activity in Lentiviral-Mediated Transgenic Mouse
Suga, T., Kimura, E., Morioka, Y., Ikawa, M., Li, S., Uchino, K., Uchida, Y., Yamashita, S., Maeda, Y., Chamberlain, J. S., et al. (2011) · PLoS ONE · doi:10.1371/journal.pone.0016908 · Cited by 12
“As nNOS is predominantly expressed in the type IIB fibers [39], the loss of nNOS activity caused by the dystrophin deficiency is considered to play an important role in the pathogenesis of muscle degeneration in DMD, although there is discrepancy (difference) of nNOS localization in muscle fiber types between human an…”
BackgroundKoshinaka, K., Oshida, Y., Han, Y.-Q., Ohsawa, I., & Sato, Y. (2003) · Metabolism · doi:10.1016/j.metabol.2003.08.006 · Cited by 13
Effects of Nitric Oxide on Glucose Transport: in vivo and in vitro Studies
McGrowder, D. A., & Brown, P. D. (2006) · Asian Journal of Biochemistry · doi:10.3923/ajb.2007.1.18 · Cited by 12
Picard, F., Arsenijevic, D., Richard, D., & Deshaies, Y. (2002) · Clinical and Vaccine Immunology · doi:10.1128/cdli.9.4.771-776.2002 · Cited by 12
“It is well known that besides its impact on lipid metabolism, LPS also affects glucose uptake, which becomes resistant to the action of insulin during endotoxemia (6, 26).”
BackgroundŚladowska-Kozłowska, J., Litwin, M., Niemirska, A., Wierzbicka, A., Roszczynko, M., & Szperl, M. (2015) · Pediatric Nephrology · doi:10.1007/s00467-015-3164-9 · Cited by 12
“related to a cellular defect in skeletal muscle tissue, where NO regulates many metabolic and contractile processes, such as basal glucose transport [8].”
BackgroundInsulin sensitivity and resistin expression in nitric oxide-deficient rats
Juan, C., Chang, C. L., Chuang, T., Huang, S., Kwok, C., & Ho, L. T. (2006) · Diabetologia · doi:10.1007/s00125-006-0403-4 · Cited by 12
“[13] reported that NO donors induce dosedependent inhibition of maximal insulin-stimulated glucose transport in L6 muscle cells.”
BackgroundDietary L-arginine supplementation reduces fat mass in diet-induced obese rats
Jobgen, W. S. (2009) · OakTrust (Texas A&M University Libraries) · Cited by 12
Acute Nitric Oxide Synthase Inhibition Accelerates Transendothelial Insulin Efflux In Vivo
Williams, I. M., McClatchey, P. M., Bracy, D. P., Valenzuela, F. A., & Wasserman, D. H. (2018) · Diabetes · doi:10.2337/db18-0288 · Cited by 12
Redox Modulation of Insulin Signaling and Endothelial Function
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“…activation of AMPK by the insulin-sensitizing drugs troglitazone and metformin markedly inhibits inducible nitric oxide (NO) synthase (iNOS), a proinflammatory mediator in multiple chronic inflammatory states, including obesity-linked diabetes (13, 47–49, 58, 64) and atherosclerosis (14, 25).”
Self-citationMahajan, H., Richards, S. M., Rattigan, S., & Clark, M. G. (2003) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0705548 · Cited by 10
“NO does not appear to be involved in insulin action in vitro (Kapur et al., 1997; Higaki et al., 2001) but, because of haemodynamic effects involving vasodilation, NO may be involved in insulin action in vivo to increase muscle glucose uptake.”
BackgroundOral nitrate therapy does not affect glucose metabolism in healthy men
Henstridge, D. C., Duffy, S. J., Formosa, M. F., Ahimastos, A. A., Thompson, B. R., & Kingwell, B. A. (2009) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/j.1440-1681.2009.05195.x · Cited by 10
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The effect of nitric oxide on glucose metabolism
Ragoobirsingh, D., McGrowder, D. A., Dasgupta, T. P., & Brown, P. D. (2004) · Molecular and Cellular Biochemistry · doi:10.1023/b:mcbi.0000041846.99698.5d · Cited by 8
“In one of the first studies conducted in this area by Kapur and colleagues [ 21 ], demonstrated that low dosages of GEA 5024 (100 µmol/L) and SNP (1 mmol/L) failed to reduce insulin binding to its receptors on L6 muscle cells, and did not affect the affinity of the receptor for insulin.”
BackgroundMethodInfluentialWasada, T., Watanabe, C., Nakagami, T., et al. (1999) · Metabolism · doi:10.1016/s0026-0495(99)90099-9 · Cited by 8
Nitric oxide myotoxicity is age related
Richmonds, C. R., & Kaminski, H. J. (2000) · Mechanisms of Ageing and Development · doi:10.1016/s0047-6374(99)00106-2 · Cited by 7
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Dietary supplementation with L-leucine reduces nitric oxide synthesis by endothelial cells of rats
Tekwe, C. D., Luan, Y., Meininger, C. J., Bazer, F. W., & Wu, G. (2023) · Experimental Biology and Medicine · doi:10.1177/15353702231199078 · Cited by 5
“44 A decrease in NO availability in the cardiovascular system contributes to reductions in blood flow, 19 glucose uptake and oxidation by skeletal muscle, 45 fatty acid oxidation by skeletal muscle and liver, 31,32,46 and whole-body insulin sensitivity.”
BackgroundThe expression of neuronal nitric oxide synthase and dystrophin in rat regenerating muscles
Hoshino, S., Ohkoshi, N., Ishii, A., et al. (2002) · Journal of Muscle Research and Cell Motility · doi:10.1023/a:1020268700730 · Cited by 5
“Furthermore, NOS expression in NADPH–diaphorase histochemistry was shown to be localized in vascular endothelium and muscle fibers, and the staining was more prominent in type 2B fibers than in types 1 and 2A (Kapur et al., 1997).”
BackgroundZhang, J., Kawashima, S., Yokoyama, M., et al. (2007) · Nitric Oxide · doi:10.1016/j.niox.2007.06.001 · Cited by 5
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The effects of Nω-propyl-l-arginine on reperfusion injury of skeletal muscle
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The Impact of Oxidative Stress on Postmortem Meat Quality
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MOLECULAR MECHANISMS OF INSULIN RESISTANCE IN OBESITY
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Self-citationSchwab, M., Bloch, J., Duplain, H., Sartori, C. S., & Scherrer, U. (2008) · PubMed · Cited by 2
Obesity and the Risk for Diabetes
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Satyanarayana, S., Kilari, E. K., & Sekhar, J. R. (2006) · Therapy · doi:10.1586/14750708.3.5.613 · Cited by 2
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“Indeed, endothelial NO production is anti- atherogenic and modulates not only arterial pressure (Forte et al., 1997) but also insulin sensitivity by promoting delivery of substrate and insulin to skeletal muscle (Kapur et al., 1997; Roy et al., 1998).”
BackgroundPotential Applications of Nitric Oxide Donors in Type 2 Diabetes
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Endotoxin induced muscle wasting in avian and murine skeletal muscle
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Obesity and the Risk for Type 2 Diabetes
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Satyanarayana, S., Kumar, K. E., & Sekhar, J. R. (2006) · Therapy · doi:10.2217/14750708.3.5.613
Metadata
- Authors
- Kapur, S., Bédard, S., Marcotte, B., Côté, C. H., & Marette, A.
- Affiliations
- Université Laval (CA)
- Department of Physiology and Lipid Research Unit, Laval University Hospital Research Center Quebec, G1V 4G2, Canada
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1997-11-01
- Volume
- 46
- Issue
- 11
- Pages
- 1691-1700
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2104847030
- Cited by
- 225
- References
- 0
- Citations by year
- 2026: 2 · 2024: 1 · 2023: 3 · 2022: 2 · 2020: 2 · 2019: 4 · 2018: 4 · 2017: 5 · 2016: 5 · 2015: 8 · 2014: 5 · 2013: 5 · 2012: 11
- FWCI
- 5.70
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- nitric oxide synthase, nitric oxide, skeletal muscle, insulin action, insulin-stimulated glucose transport, fast-twitch muscle, slow-twitch muscle, extensor digitorum longus, soleus muscle, neuronal nitric oxide synthase, endothelial nitric oxide synthase, inducible nitric oxide synthase, endotoxin, amino acid uptake, cGMP-independent signaling, autocrine signaling
- MeSH terms
- Amino Acids, Animals, Cell Line, Dibutyryl Cyclic GMP, Endothelium, Vascular, Glucose, Insulin, Isoenzymes, Kinetics, Dihydrolipoamide Dehydrogenase, Myosins, Nitric Oxide, Organ Specificity, Triazoles, Rats, Sprague-Dawley, Muscle, Skeletal, Muscle Fibers, Fast-Twitch, Muscle Fibers, Slow-Twitch, Nitric Oxide Synthase, Rats
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