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Localization of Rate-Limiting Defect for Glucose Disposal in Skeletal Muscle of Insulin-Resistant Type I Diabetic Patients
Abstract
We searched for metabolic crossover points in muscle glucose metabolite profiles during maintenance of matched glucose fluxes across forearm muscle in insulin-resistant type I (insulin-dependent) diabetic patients and nondiabetic subjects. To classify subjects as insulin sensitive or insulin resistant, whole-body and forearm glucose disposal, oxidative and nonoxidative glucose disposal (indirect calorimetry), and glycogen synthesis (muscle glycogen content in needle biopsies) were measured under euglycemic conditions at two insulin concentrations. Wholebody and forearm muscle glucose disposal were significantly reduced in diabetic patients compared with control subjects. The reduction in total glucose disposal was due to similar relative reductions in oxidative and nonoxidative glucose disposal, pointing toward rate limitation early in glucose metabolism. The defect in nonoxidative glucose disposal was at least partly due to a defect in muscle glycogen synthesis, because muscle glycogen content failed to increase in response to an increase in the plasma insulin concentration in the diabetic patients. The mostinsulin-resistant type 1 diabetic patients were restudied under conditions where, by glucose mass action, whole-body glucose disposal was forced to be similar to that in the control subjects. Matching glucose fluxes in the two groups resulted in similar rates of forearm and whole-body oxidative and nonoxidative glucose disposal and muscle glycogen synthesis, but it did not result in accumulation of free intracellular glucose, glucose-6-phosphate, glucose-1-phosphate, fructose-6-phosphate, or lactate in muscle. These data imply that the rate-limiting defect for glucose disposal in skeletal muscle of type I diabetic patients is at the level of glucose transport.
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“Further support for these findings comes from studies in which glucose disposal rates were matched by increasing the glucose or insulin infusion rates ([27](#r27), [66](#r66)).”
From Metabolic flexibility and insulin resistance (2008) · cites this paper as [66]
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Thorell, A., Nygren, J., & Ljungqvist, O. H. (1999) · Current Opinion in Clinical Nutrition & Metabolic Care · doi:10.1097/00075197-199901000-00012 · Cited by 552
Alterations in carbohydrate metabolism during stress: A review of the literature
Mizock, B. A. (1995) · The American Journal of Medicine · doi:10.1016/s0002-9343(99)80083-7 · Cited by 534
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Galgani, J. E., Moro, C., & Ravussin, E. (2008) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.90558.2008 · Cited by 532
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BackgroundSimpson, I. A., Chundu, K. R., Davies‐Hill, T., Honer, W. G., & Davies, P. (1994) · Annals of Neurology · doi:10.1002/ana.410350507 · Cited by 490
Kim, Y.-B., Nikoulina, S. E., Ciaraldi, T. P., Henry, R. R., & Kahn, B. B. (1999) · Journal of Clinical Investigation · doi:10.1172/jci6928 · Cited by 487
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BackgroundBlood flow and muscle metabolism: a focus on insulin action
Clark, M. G., Wallis, M. G., Barrett, E. J., Keske, M. A., Richards, S. M., Clerk, L. H., & Rattigan, S. (2003) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00408.2002 · Cited by 359
Rothman, D. L., Magnusson, I., Cline, G., Gerard, D., Kahn, C. R., Shulman, R. G., & Shulman, G. I. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.4.983 · Cited by 325
Rothman, D. L., Shulman, R. G., & Shulman, G. I. (1992) · Journal of Clinical Investigation · doi:10.1172/jci115686 · Cited by 327
Chemistry and Biochemistry of Type 2 Diabetes
Ross, S. A., Gulve, E. A., & Wang, M. (2004) · Chemical Reviews · doi:10.1021/cr0204653 · Cited by 326
Glucose-free fatty acid cycle operates in human heart and skeletal muscle in vivo.
Nuutila, P., Koivisto, V. A., Knuuti, J. M., Ruotsalainen, U., Teräs, M., Haaparanta‐Solin, M., Bergman, J. R., Solin, O. H., Voipio-Pulkki, L. M., & Wegelius, U. (1992) · Journal of Clinical Investigation · doi:10.1172/jci115780 · Cited by 309
“Although the decrease in skeletal muscle glucose uptake is quantitatively more important for the decrease in whole body glucose disposal in insulinresistant diabetic patients (13, 14) as well as in normal subjects exposed to high free fatty acid concentrations (Fig.”
BackgroundMethodSelf-citation̈kimattila, S. M., ̈ki, A. V., Groop, P., Cockcroft, J., Utriainen, T., Fagerudd, J. A., & ̈rvinen, H. Y.-J. (1996) · Circulation · doi:10.1161/01.cir.94.6.1276 · Cited by 286
Molecular Mechanism of Insulin Resistance in Obesity and Type 2 Diabetes
Choi, K., & Kim, Y. (2010) · The Korean Journal of Internal Medicine · doi:10.3904/kjim.2010.25.2.119 · Cited by 281
“Resistance to the actions of insulin in skeletal muscle is a major pathogenic factor in type 2 or type 1 diabetes mellitus [2,3]; it also contributes to the morbidity of obesity, and complicates poorly controlled type 1 (autoimmune) diabetes [2].”
BackgroundInsulin-induced vasodilatation: physiology or pharmacology?
Yki‐Järvinen, H., & Utriainen, T. (1998) · Diabetologia · doi:10.1007/s001250050919 · Cited by 261
Self-citationEbeling, P. R., Bourey, R. E., Koranyi, L. I., Tuominen, J. A., Groop, L., Henriksson, J., Mueckler, M. M., Sovijärvi, A. R. A., & Koivisto, V. A. (1993) · Journal of Clinical Investigation · doi:10.1172/jci116747 · Cited by 239
Self-citationBaron, A., Laakso, M., Brechtel, G., & Edelman, S. V. (1991) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-73-3-637 · Cited by 210
Kelley, D. E., & Mandarino, L. J. (1990) · Journal of Clinical Investigation · doi:10.1172/jci114935 · Cited by 210
Baron, A., Tarshoby, M., Brechtel, G., Lazaridis, E. N., Cronin, J., Johnson, A., & Steinberg, H. O. (2000) · Diabetes · doi:10.2337/diabetes.49.5.768 · Cited by 174
“Although reports are conflicting (27,28), we have previously suggested that decreased insulin sensitivity in these groups may be contributed to by perfusion defects rather than solely by defects in glucose extraction (24,26).”
BackgroundRen, J., Marshall, B. A., Mueckler, M. M., McCaleb, M. L., Amatruda, J. M., & Shulman, G. I. (1995) · Journal of Clinical Investigation · doi:10.1172/jci117673 · Cited by 171
Self-citationGLUT 4 and insulin receptor binding and kinase activity in trained human muscle.
Dela, F., Handberg, A., Mikines, K. J., Vinten, J., & Galbo, H. (1993) · The Journal of Physiology · doi:10.1113/jphysiol.1993.sp019833 · Cited by 170
Kahn, B. B., Rossetti, L., Lodish, H. F., & Charron, M. J. (1991) · Journal of Clinical Investigation · doi:10.1172/jci115254 · Cited by 166
Utriainen, T., Malmstr�m, R., ̈kimattila, S. M., & Yki-J�rvinen, H. (1995) · Diabetologia · doi:10.1007/bf00400724 · Cited by 158
“Thus, the failure to observe a significant increase in blood flow in some [8, 9, 11-14 ] but not in other studies [16, 17] at an insulin concentration of approximately 100 mU/1 could at least partly be explained by methodological factors as well as by interindividual variation.”
BackgroundMethodResultInfluentialSelf-citationIn vivo regulation of muscle glycogen synthase and the control of glycogen synthesis.
Shulman, R. G., Bloch, G., & Rothman, D. L. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.19.8535 · Cited by 152
Yki‐Järvinen, H., Mäkimattila, S., Utriainen, T., & Rutanen, E. ‐. (1995) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.80.11.7593430 · Cited by 150
Self-citationThe Insulin-Sensitive Glucose Transporter
Bimbaum, M. J. (1992) · International review of cytology · doi:10.1016/s0074-7696(08)62678-9 · Cited by 133
Hofmann, C. A., Lorenz, K., & Colca, J. R. (1991) · Endocrinology · doi:10.1210/endo-129-4-1915 · Cited by 134
Galgani, J. E., Heilbronn, L. K., Azuma, K., Kelley, D. E., Albu, J. B., Pi-Sunyer, X., Smith, S. R., Ravussin, E., & and the Look AHEAD Adipose Research Group (2008) · Diabetes · doi:10.2337/db08-0043 · Cited by 133
“Few studies have compared in vivo fuel oxidation under similar glucose disposal rates in diabetic and nondiabetic subjects (5,17,18).”
BackgroundKahn, B. B., & Pedersen, O. B. (1993) · Endocrinology · doi:10.1210/endo.132.1.8419118 · Cited by 121
Insulin-induced hexokinase II expression is reduced in obesity and NIDDM.
Pendergrass, M., Koval, J., Vogt, C., Yki-Jarvinen, H., Iozzo, P., Pipek, R., Ardehali, H., Printz, R., Granner, D., DeFronzo, R. A., et al. (1998) · Diabetes · doi:10.2337/diabetes.47.3.387 · Cited by 119
Role of insulin resistance in the pathogenesis of NIDDM
Yki-J�rvinen, H. (1995) · Diabetologia · doi:10.1007/bf00400597 · Cited by 116
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BackgroundMethodSelf-citationDivergent regulation of Akt1 and Akt2 isoforms in insulin target tissues of obese Zucker rats.
Kim, Y. B., Peroni, O. D., Franke, T. F., & Kahn, B. B. (2000) · Diabetes · doi:10.2337/diabetes.49.5.847 · Cited by 111
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BackgroundAcute and chronic effects of hyperglycaemia on glucose metabolism
Yki-J�rvinen, H. (1990) · Diabetologia · doi:10.1007/bf00400200 · Cited by 108
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BackgroundInfluentialSelf-citationYki‐Järvinen, H., Puhakainen, I., & Koivisto, V. A. (1991) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-72-6-1268 · Cited by 100
Self-citationVestergaard, H., Lund, S., Larsen, F. S., Bjerrum, O. J., & Pedersen, O. (1993) · Journal of Clinical Investigation · doi:10.1172/jci116466 · Cited by 98
Vestergaard, H., Bjørbæk, C., Hansen, T. F., Larsen, F. S., Granner, D. K., & Pedersen, O. B. (1995) · Journal of Clinical Investigation · doi:10.1172/jci118329 · Cited by 92
Virkamäki, A., Daniels, M. C., Hämäläinen, S., Utriainen, T., McClain, D. A., & Yki‐Järvinen, H. (1997) · Endocrinology · doi:10.1210/endo.138.6.5172 · Cited by 96
Self-citationHow to measure insulin action in vivo
Scheen, A. J., Paquot, N., Castillo, M. J., & Lefèbvre, P. J. (1994) · Diabetes/Metabolism Reviews · doi:10.1002/dmr.5610100206 · Cited by 90
Tozzo, E., Gnudi, L., & Kahn, B. B. (1997) · Endocrinology · doi:10.1210/endo.138.4.5043 · Cited by 99
Insulin Resistance in Type 1 Diabetes: Pathophysiological, Clinical, and Therapeutic Relevance
Apostolopoulou, M., Lambadiari, V., Roden, M., & Dimitriadis, G. D. (2025) · Endocrine Reviews · doi:10.1210/endrev/bnae032 · Cited by 90
Evidence that glucose transport is rate-limiting for in vivo glucose uptake
Fink, R. I., Wallace, P., Brechtel, G., & Olefsky, J. M. (1992) · Metabolism · doi:10.1016/0026-0495(92)90174-9 · Cited by 80
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Thorell, A., Nygren, J., Hirshman, M. F., Hayashi, T., Nair, K. S., Horton, E. S., Goodyear, L. J., & Ljungqvist, O. H. (1999) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1999.276.4.e754 · Cited by 78
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BackgroundPuhakainen, I., Ahola, I., & Yki‐Järvinen, H. (1995) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/61.1.121 · Cited by 76
Self-citationVaag, A. A., Damsbo, P., Nielsen, O. H., & Beck‐Nielsen, H. (1992) · Diabetologia · doi:10.1007/bf00400856 · Cited by 67
1 Cellular insulin action and insulin resistance
Garvey, W. T., & Birnbaum, M. J. (1993) · Baillière s Clinical Endocrinology and Metabolism · doi:10.1016/s0950-351x(05)80237-x · Cited by 67
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Metzler, B., Schocke, M. F. H., Steinboeck, P., Wolf, C., Judmaier, W., Lechleitner, M., Lukas, P. H., & Pachinger, O. M. (2002) · Journal of Cardiovascular Magnetic Resonance · doi:10.1081/jcmr-120016387 · Cited by 67
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BackgroundMechanisms of hepatic and peripheral insulin resistance during acute infections in humans.
Virkamäki, A., Puhakainen, I., Koivisto, V. A., Vuorinen-Markkola, H., & Yki-Järvinen, H. (1992) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.74.3.1740504 · Cited by 65
Self-citationGregory, J. M., Smith, T. J., Slaughter, J. C., Mason, H. R., Hughey, C. C., Smith, M. S., Kandasamy, B., Greeley, S. A. W., Philipson, L. H., Naylor, R. N., et al. (2019) · Diabetes · doi:10.2337/db19-0324 · Cited by 64
Koranyi, L. I., Bourey, R. E., Vuorinen-Markkola, H., Koivisto, V. A., Mueckler, M. M., Permutt, M. A., & Yki-J�rvinen, H. (1991) · Diabetologia · doi:10.1007/bf00401526 · Cited by 59
“Under many conditions, glucose transport appears to be rate-limiting for its metabolism in skeletal muscle [2, 6].”
BackgroundMethodSelf-citationKahn, B. B., Rosen, A. S., Bak, J. F., Andersen, P. H., Damsbo, P., Lund, S. A., & Pedersen, O. B. (1992) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.74.5.1569156 · Cited by 64
Myocardial Blood Flow and Glucose Metabolism in Diabetes Mellitus
Meyer, C., & Schwaiger, M. (1997) · The American Journal of Cardiology · doi:10.1016/s0002-9149(97)00463-3 · Cited by 60
Influence of Exercise on Protein and Amino Acid Metabolism
Rennie, M. J. (1996) · Comprehensive physiology · doi:10.1002/cphy.cp120122 · Cited by 62
Normal splanchnic but impaired peripheral insulin-stimulated glucose uptake in cirrhosis
Shmueli, E., Walker, M., Alberti, G., & Record, C. O. (1993) · Hepatology · doi:10.1002/hep.1840180115 · Cited by 55
Utriainen, T., Mäkimattila, S., Virkamäki, A., Bergholm, R., & Yki‐Järvinen, H. (1996) · Diabetologia · doi:10.1007/s001250050601 · Cited by 55
“At high insulin concentrations, defects in blood flow have been found in subjects with marginally elevated blood pressure [43], and in patients with IDDM [47] and NIDDM [48], although these findings have not been uniform in either hypertensive subjects [49, 50] or in patients with NIDDM [51, 52].”
BackgroundInfluentialSelf-citationPedersen, S. B., Børglum, J. D., Schmitz, O., Bak, J. F., Sørensen, N. S., & Richelsen, B. (1993) · Metabolism · doi:10.1016/0026-0495(93)90013-e · Cited by 54
3 Action of insulin on glucose metabolism in vivo
Yki‐Järvinen, H. (1993) · Baillière s Clinical Endocrinology and Metabolism · doi:10.1016/s0950-351x(05)80239-3 · Cited by 52
Self-citationGreenfield, J. R., Samaras, K., & Chisholm, D. J. (2002) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.87.3.8324 · Cited by 53
Regulation of glucose transport by pioglitazone in cultured muscle cells
El‐Kebbi, I. M., Roser, S., & POLLET, R. J. (1994) · Metabolism · doi:10.1016/0026-0495(94)90173-2 · Cited by 51
Polonsky, K. S., & Burant, C. (2016) · Elsevier eBooks · doi:10.1016/b978-0-323-29738-7.00031-9 · Cited by 53
Yki-Järvinen, H., Vogt, C., Iozzo, P., Pipek, R., Daniels, M. C., Virkamäki, A., Mäkimattila, S., Mandarino, L. J., DeFronzo, R. A., McClain, D. A., et al. (1997) · Diabetologia · doi:10.1007/s001250050645 · Cited by 46
Self-citationNapoli, R., Hirshman, M. F., & Horton, E. S. (1995) · Journal of Clinical Investigation · doi:10.1172/jci118053 · Cited by 47
Turner, N. C., & Clapham, J. C. (1998) · Birkhäuser Basel eBooks · doi:10.1007/978-3-0348-8845-5_2 · Cited by 46
Insulin resistance in type I diabetes mellitus: a major role for reduced glucose extraction
Mäkimattila, S., Virkamäki, A., Malmström, R., Utriainen, T., & Yki‐Järvinen, H. (1996) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.81.2.8636292 · Cited by 48
Self-citationShulman, R. G., & Rothman, D. L. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.15.7491 · Cited by 44
Gregory, J. M., Kraft, G., Scott, M. F., Neal, D. W., Farmer, B., Smith, M. S., Hastings, J. R., Allen, E. J., Donahue, E. P., Rivera, N., et al. (2015) · Diabetes · doi:10.2337/db15-0071 · Cited by 43
“This suggests that Pe insulin delivery would be even more problematic in T1DM patients who had antecedent hypoglycemia.”
BackgroundInfluentialSasson, S., Kaiser, Ν., Dan‐Goor, M., Oron, R., Koren, S., Wertheimer, E., Unluhizarci, K., & Cerasi, E. (1997) · Diabetologia · doi:10.1007/s001250050639 · Cited by 41
“[29] reported that the content of glucose-6-P was 2.”
BackgroundVenkatesan, N., Lim, J., Bouch, C., Marciano, D. K., & Davidson, M. B. (1996) · Metabolism · doi:10.1016/s0026-0495(96)90205-x · Cited by 39
Ortmeyer, H. K., Bodkin, N. L., & HANSEN, B. C. (1994) · Diabetologia · doi:10.1007/s001250050082 · Cited by 37
“Finally, Yki-Jarvinen et al. [ 28 ] suggested that the rate-limiting step for glucose disposal in insulin-dependent diabetic humans was transport, partially based on the finding that muscle (vastus lateralis) glucose 6-phosphate was not different in these subjects between low and high insulin concentrations.”
BackgroundGnudi, L., Shepherd, P. R., & Kahn, B. B. (1996) · Proceedings of The Nutrition Society · doi:10.1079/pns19960020 · Cited by 37
Ebeling, P. R., & Koivisto, V. A. (1994) · Diabetologia · doi:10.1007/s001250050094 · Cited by 33
“In the current study, the baseline glycogen synthase fractional activity was higher and the rise during insulin stimulus was less than we have previously reported in sedentary subjects [16, 30].”
ResultSelf-citationMyocardial insulin resistance in patients with syndrome X.
Bøtker, H. E., Møller, N., Schmitz, O., Bagger, J. P., & Nielsen, T. T. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119722 · Cited by 33
“Such mechanisms may involve a defect located at the membrane transport level, as demonstrated in skeletal muscle from patients with diabetes mellitus (5).”
BackgroundIGF-I increases forearm blood flow without increasing forearm glucose uptake
Pendergrass, M., Fazioni, E., Collins, D., & DeFronzo, R. A. (1998) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1998.275.2.e345 · Cited by 33
Robitaille, M., Dubé, M.-C., Weisnagel, S. J., Prud’homme, D., Massicotte, D., Péronnet, F., & Lavoie, C. (2007) · Journal of Applied Physiology · doi:10.1152/japplphysiol.01462.2006 · Cited by 31
“Nuutila et al. (16) and Yki-Jarvinen et al. ( 31 ) also showed that insulin-stimulated muscle plasma glucose uptake was 25‐45% lower in Type 1 diabetic patients than in control subjects.”
Background13 C/ 31 P NMR studies of glucose transport in human skeletal muscle
Roussel, R., Carlier, P. G., Robert, J., Velho, G., & Bloch, G. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.3.1313 · Cited by 30
Increased circulating levels of musclin in newly diagnosed type 2 diabetic patients
Chen, W.-J., Liu, Y., Sui, Y.-B., Zhang, B., Zhang, X., & Yin, X. (2017) · Diabetes and Vascular Disease Research · doi:10.1177/1479164116675493 · Cited by 30
Buse, J. B., Polonsky, K. S., & Burant, C. (2011) · Elsevier eBooks · doi:10.1016/b978-1-4377-0324-5.00031-6 · Cited by 28
Expression of Glucokinase in Skeletal Muscle: A New Approach to Counteract Diabetic Hyperglycemia
Otaegui, P. J., Ferré, T., Pujol, A., Riu, E., Jiménez, R. P., & Bosch, F. (2000) · Human Gene Therapy · doi:10.1089/10430340050083270 · Cited by 28
Yki‐Järvinen, H., Vuorinen-Markkola, H., Koranyi, L. I., Bourey, R. E., Tordjman, K. M., Mueckler, M. M., Permutt, A., & Koivisto, V. A. (1992) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.75.3.1517369 · Cited by 26
Self-citationVestergaard, H., Andersen, P. H., Lund, S. A., Vedel, P. N., & Pedersen, O. B. (1994) · Diabetologia · doi:10.1007/bf00428782 · Cited by 26
Metabolic Transporters in the Peripheral Nerve—What, Where, and Why?
Rawat, A. K., & Morrison, B. M. (2021) · Neurotherapeutics · doi:10.1007/s13311-021-01150-2 · Cited by 26
Inflexibility of energy substrate oxidation in type 1 diabetic patients
Wohl, P., Wohl, P., Girman, P., & Pelikánová, T. (2004) · Metabolism · doi:10.1016/j.metabol.2003.12.013 · Cited by 24
New players in high fat diet-induced obesity: LETM1 and CTMP
Park, J., Li, Y., Kim, S., Yang, K.-J., Kong, G., Shrestha, R., Tran, Q., Park, K. A., Jeon, J., Hur, G. M., et al. (2013) · Metabolism · doi:10.1016/j.metabol.2013.10.012 · Cited by 23
“Resistance to insulin action in skeletal muscle is a major pathogenic factor in type II diabetesmellitus [7,8].”
BackgroundFasching, P., Ratheiser, K., Damjancic, P., Schneider, B., Nowotny, P., Vierhapper, H., & Waldh�usl, W. K. (1993) · Diabetologia · doi:10.1007/bf00400239 · Cited by 23
Holmäng, A. B., Mimura, K., & Lönnroth, P. (2002) · Journal of Applied Physiology · doi:10.1152/japplphysiol.01194.2000 · Cited by 22
“Most of these studies have focused on muscle glucose metabolism during resting conditions (15, 36).”
BackgroundEffects of physiological hyperinsulinemia on the intracellular metabolic partition of plasma glucose
Bonadonna, R. C., Prato, S. D., Bonora, E., Gulli, G., Solini, A., & DeFronzo, R. A. (1993) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1993.265.6.e943 · Cited by 22
Napoli, R., Davalli, A. M., Hirshman, M. F., Weitgasser, R., Weir, G. C., & Horton, E. S. (1996) · Journal of Clinical Investigation · doi:10.1172/jci118559 · Cited by 20
Davidson, M. B., Bouch, C., Venkatesan, N., & Karjala, R. G. (1994) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1994.267.6.e808 · Cited by 21
Marzban, L., Bhanot, S., & McNeill, J. H. (2001) · Molecular and Cellular Biochemistry · doi:10.1023/a:1017943200785 · Cited by 19
“Resistance to insulin action at the level of liver results in an increase in hepatic glucose production, while in the skeletal muscle it causes a decrease in glucose uptake [3], the rate-limiting step for glucose utilization [5, 6].”
BackgroundInfluentialRegulation of Muscle Glucose Uptake In Vivo
Mandarino, L. J., Bonadonna, R. C., McGuinness, O. P., Halseth, A. E., & Wasserman, D. H. (2001) · Comprehensive physiology · doi:10.1002/cphy.cp070227 · Cited by 19
“Quantitation of extracellular and intracellular glucose concentrations can only be estimated at present from the measurement of total glucose in a biopsy specimen (165, 341).”
InfluentialSepsis inhibits insulin-stimulated glucose transport in isolated rat adipocytes
Igarashi, M., Yamatani, K., Fukase, N., et al. (1992) · Diabetes Research and Clinical Practice · doi:10.1016/0168-8227(92)90027-o · Cited by 18
Energy expenditure and substrate metabolism after oral fructose in patients with cirrhosis.
Kruszynska, Y., Meyer-Alber, A., Wollen, N., & McIntyre, N. (1993) · Journal of Hepatology · doi:10.1016/s0168-8278(05)80578-1 · Cited by 14
Parsapour, K., Pullela, R., Raff, G. W., & Pretzlaff, R. K. (2008) · Pediatric Critical Care Medicine · doi:10.1097/01.pcc.0000298767.20400.66 · Cited by 14
Otaegui, P. J., Ferré, T., Riu, E., & Bosch, F. (2003) · The FASEB Journal · doi:10.1096/fj.03-0081fje · Cited by 13
Changes in Muscle Glucose Metabolism in Type 1 Diabetes
Koivisto, V. A., & Yki‐Järvinen, H. (1990) · Annals of Medicine · doi:10.3109/07853899009147270 · Cited by 12
Self-citationMcGuinness, O. P., & Mari, A. (1997) · Metabolism · doi:10.1016/s0026-0495(97)90202-x · Cited by 11
Christopher, M., Rantzau, C., McConell, G. K., Kemp, B. E., & ALFORD, F. P. (2005) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00687.2004 · Cited by 10
“resting, poorly controlled diabetic state involve both compensatory (48, 55) and glucose toxic (38, 39) effects.”
BackgroundEvidence for 100% 13C NMR visibility of glucose in human skeletal muscle
Roussel, R., Carlier, P. G., Wary, C., Velho, G., & Bloch, G. (1997) · Magnetic Resonance in Medicine · doi:10.1002/mrm.1910370604 · Cited by 9
Alterations in Fuel Metabolism in Critical Illness
Mizoch, B. A. (1997) · Humana Press eBooks · doi:10.1007/978-1-4757-2584-1_10 · Cited by 9
Insulin-resistant glucose metabolism in patients with microvascular angina—syndrome X
Vestergaard, H., Skøtt, P., Steffensen, R., Wroblewski, H., Pedersen, O. B., & Kastrup, J. (1995) · Metabolism · doi:10.1016/0026-0495(95)90240-6 · Cited by 7
Insulin action and skeletal muscle blood flow in patients with Type 1 diabetes and microalbuminuria
Wiggam, M. I., Hunter, S. J., Ennis, C. N., Sheridan, B., Atkinson, A. B., & Bell, P. M. (2001) · Diabetes Research and Clinical Practice · doi:10.1016/s0168-8227(01)00244-3 · Cited by 8
“[24] H.”
Background
Metadata
- Authors
- Yki-Järvinen, H., Sahlin, K., Ren, J. M., & Koivisto, V. A.
- Affiliations
- Second Department of Medicine, University of Helsinki Finland Department of Clinical Physiology, Huddinge Hospital Stockholm, Sweden
- University of Helsinki (FI)
- ORCID
- Koivisto, Veikko A
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1990-02-01
- Volume
- 39
- Issue
- 2
- Pages
- 157-167
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2075855413
- Cited by
- 131
- References
- 0
- Citations by year
- 2025: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 3 · 2015: 4 · 2013: 3 · 2012: 1
- FWCI
- 4.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- type 1 diabetes, insulin resistance, glucose transport, nonoxidative glucose disposal, muscle glycogen synthesis, glucose-6-phosphate, glucose-1-phosphate, fructose-6-phosphate, lactate
- MeSH terms
- Adult, Biological Transport, Diabetes Mellitus, Type 1, Glucose, Glycogen, Glycogen Synthase, Humans, Insulin, Insulin Resistance, Metabolic Clearance Rate, Muscles, Oxidation-Reduction
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