The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
Role of Reduced Suppression of Glucose Production and Diminished Early Insulin Release in Impaired Glucose Tolerance
Open accessAbstract
BACKGROUND: Insulin resistance and impaired insulin secretion both occur in non-insulin-dependent diabetes (NIDDM), but their relative importance is unclear. Hyperglycemia itself has adverse effects on tissue insulin sensitivity and insulin secretion that make it difficult to distinguish between primary and secondary abnormalities. To avoid this problem we studied subjects with postprandial glucose intolerance but not sustained hyperglycemia. METHODS: We compared the rate of systemic appearance and disappearance of glucose, the output of endogenous hepatic glucose, splanchnic and muscle uptake of glucose, and plasma insulin and glucagon responses after the ingestion of 1 g of glucose per kilogram of body weight in 15 subjects with impaired glucose tolerance (8 of them nonobese and 7 obese) and in 16 normal subjects (9 nonobese and 7 obese) who were matched for age and weight. RESULTS: After glucose ingestion the mean (+/- SE) rate of total systemic appearance of glucose was significantly higher in both the nonobese subjects (455 +/- 12 mmol per five hours) and the obese subjects (486 +/- 17 mmol per five hours) with impaired glucose tolerance than in the respective normal subjects (411 +/- 11 and 436 +/- 7 mmol per five hours). This difference was fully accounted for by the reduced suppression of endogenous hepatic glucose in the subjects with impaired glucose tolerance (a reduction of about 28 percent, vs. 48 percent in the normal subjects; P less than 0.01). Despite late hyperinsulinemia, at 30 minutes the subjects with impaired glucose tolerance had smaller increases in plasma insulin and smaller reductions in plasma glucagon (both P less than 0.01). Molar ratios of plasma insulin to plasma glucagon levels correlated inversely (r = -0.62, P less than 0.001) with the rates of systemic glucose appearance; the latter correlated positively (r = 0.72, P less than 0.0001) with peak plasma glucose concentrations. CONCLUSIONS: Impaired glucose tolerance, the precursor of NIDDM, results primarily from reduced suppression of hepatic glucose output due to abnormal pancreatic islet-cell function. The late hyperinsulinemia may be the consequence of an inadequate early beta-cell response rather than of insulin resistance.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source doesn’t support the claim as written.
In the citing paper
“As indicated by several studies, insulin resistance leads to basal-fasting hyperinsulinemia, which may result in the insensitivity of beta-cell secretion. This insensitivity leads to a lower first-phase insulin secretion to the rising postprandial glucose but a subsequent exaggerated compensatory second-phase insulin secretion, which might result in hypoglycemia [2, 3].”
From Associated Factors with Biochemical Hypoglycemia during an Oral Glucose Tolerance Test in a Chinese Population (2017) · cites this paper as [3]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“When the first-phase insulin response decreases, firstly, blood glucose starts to rise after the meal, which leads to late but excessive secretion of the second-phase insulin secretion. Thus, late reactive hypoglycemia occurs.[3]”
From Postprandial Reactive Hypoglycemia (2019) · cites this paper as [3]
Experimental — accuracy not yet measuredIn the citing paper
“Indeed, with better matching of subjects for age, sex and obesity, there also does seem to be a decrease of the insulinogenic index in subjects with IGT [5, 87, 88].”
From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [5]
In the citing paper
“This reduction in the early insulin response results in a lack of adequate suppression of hepatic glucose production with subsequent post challenge hyperglycaemia and increased insulin concentrations late in the test [5, 126].”
From The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes (2003) · cites this paper as [5]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Coated Charcoal Immunoassay of Insulin
Herbert, V. D., Lau, K., Gottlieb, C. W., & Bleicher, S. J. (1965) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-25-10-1375 · Cited by 2,969
The Triumvirate: β-Cell, Muscle, Liver: A Collusion Responsible for NIDDM
DeFronzo, R. A. (1988) · Diabetes · doi:10.2337/diab.37.6.667 · Cited by 2,456
Plasma Insulin Responses to Oral and Intravenous Glucose: Studies in Normal and Diabetic Subjects*
Perley, M. J., & Kipnis, D. M. (1967) · Journal of Clinical Investigation · doi:10.1172/jci105685 · Cited by 917
Early Metabolic Defects in Persons at Increased Risk for Non-Insulin-Dependent Diabetes Mellitus
Eriksson, J., Franssila-Kallunki, A., Ekstrand, A., Saloranta, C., Widén, E., Schalin, C., & Groop, L. (1989) · New England Journal of Medicine · doi:10.1056/nejm198908103210601 · Cited by 807
Rossetti, L., Giaccari, A., & DeFronzo, R. A. (1990) · Diabetes Care · doi:10.2337/diacare.13.6.610 · Cited by 774
Kolterman, O., Gray, R. S., Griffin, J., BURSTEIN, P. J., Insel, J. R., Scarlett, J. A., & Olefsky, J. M. (1981) · Journal of Clinical Investigation · doi:10.1172/jci110350 · Cited by 628
Impaired Glucose Tolerance as a Disorder of Insulin Action
Lillioja, S., Mott, D. M., Howard, B. V., Bennett, P. H., Yki-Järvinen, H., Freymond, D., Nyomba, B. L., Zurlo, F., Swinburn, B., & Bogardus, C. (1988) · New England Journal of Medicine · doi:10.1056/nejm198805123181901 · Cited by 578
METHODS FOR THE INVESTIGATION OF PERIPHERAL BLOOD FLOW
Greenfield, A. D. M., Whitney, R. J., & Mowbray, J. F. (1963) · British Medical Bulletin · doi:10.1093/oxfordjournals.bmb.a070026 · Cited by 494
Andres, R., Cader, G., & Zierler, K. L. (1956) · Journal of Clinical Investigation · doi:10.1172/jci103324 · Cited by 389
Glucagon physiology and pathophysiology in the light of new advances
Unger, R. H. (1985) · Diabetologia · doi:10.1007/bf00281991 · Cited by 361
Research works printed but not linked: 6
- Gerich, 1988, Clin Endocrinol Metab, 2, 307
- Luzi, 1989, Am J Physiol, 257, E241
- 1980, WHO Tech Rep Ser, 646, 1
- Faloona GR, Unger RH. Glucagon. In: Jaffe BM, Behrman HR, eds. Methods of hormone radioimmunoassay. New York: Academic Press, 1974:317–30
- Hetenyi, 1974, Fed Proc, 33, 1841
- Chiasson, 1977, Fed Proc, 36, 229
Cited by
Sorted by citations
Items 101–200 of 593
Rask, E., Olsson, T., Söderberg, S., Holst, J. J., Tura, A., Pacini, G., & Åhrén, B. (2004) · Metabolism · doi:10.1016/j.metabol.2003.11.011 · Cited by 99
Åhrén, B., & Pacini, G. (2002) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00199.2002 · Cited by 98
Trimethylamine N-oxide impairs β-cell function and glucose tolerance
Kong, L., Zhao, Q., Jiang, X., Hu, J., Jiang, Q., Li, S., Peng, X., Wang, S., Chen, Y., Wan, Y., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-46829-0 · Cited by 103
Larsson, H. E., & Åhrén, B. (2000) · Diabetes Care · doi:10.2337/diacare.23.5.650 · Cited by 98
Ahr�n, B., & Larsson, H. (2001) · Diabetologia · doi:10.1007/s001250100003 · Cited by 95
Metabolic effects of glucagon in humans
Adeva-Andany, M. M., Funcasta-Calderón, R., Fernández-Fernández, C., Castro-Quintela, E., & Carneiro-Freire, N. (2019) · Journal of Clinical & Translational Endocrinology · doi:10.1016/j.jcte.2018.12.005 · Cited by 94
Hypoglycaemic effect of AICAriboside in mice
Vincent, M. F., Erion, M. D., Gruber, H. E., & den Berghe, G. V. (1996) · Diabetologia · doi:10.1007/bf02658500 · Cited by 93
Fukushima, A., Loh, K., Galić, S., Fam, B. C., Shields, B., Wiede, F., Tremblay, M. L., Watt, M. J., Andrikopoulos, S., & Tiganis, T. (2010) · Diabetes · doi:10.2337/db09-1365 · Cited by 94
Current Status of Islet Cell Replacement and Regeneration Therapy
Halban, P. A., German, M. S., Kahn, S. E., & Weir, G. C. (2010) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2009-1819 · Cited by 90
Association of fasting glucagon and proinsulin concentrations with insulin resistance
Ferrannini, E., Muscelli, E., Natali, A., Gabriel, R., Mitrakou, A., Flyvbjerg, A., Golay, A., Højlund, K., & The Relationship between Insulin Sensitivity and Cardiovascular Disease Risk (RISC) Project Investigators (2007) · Diabetologia · doi:10.1007/s00125-007-0806-x · Cited by 90
Self-citationNew insights into the role of connexins in pancreatic islet function and diabetes
Farnsworth, N. L., & Benninger, R. K. P. (2014) · FEBS Letters · doi:10.1016/j.febslet.2014.02.035 · Cited by 91
Meier, J. J., Deacon, C. F., Schmidt, W. E., Holst, J. J., & Nauck, M. A. (2007) · Diabetologia · doi:10.1007/s00125-007-0598-z · Cited by 92
Davies, M. J., Rayman, G., Gray, I. P., Day, J., & Hales, C. N. (1993) · Diabetic Medicine · doi:10.1111/j.1464-5491.1993.tb00071.x · Cited by 89
Non-insulin-dependent Diabetes Mellitus - A Collision between Thrifty Genes and an Affluent Society
Groop, L., & Tuomi, T. (1997) · Annals of Medicine · doi:10.3109/07853899708998742 · Cited by 88
Effects of glucocorticoids and exercise on pancreatic β‐cell function and diabetes development
Beaudry, J. L., & Riddell, M. C. (2012) · Diabetes/Metabolism Research Reviews · doi:10.1002/dmrr.2310 · Cited by 91
Clinical Pharmacology During Pregnancy
(2013) · Elsevier eBooks · doi:10.1016/c2010-0-67194-x · Cited by 84
Haffner, S. M., González-Bonilla, C. R., Mykkänen, L., & Stern, M. P. (1997) · Diabetologia · doi:10.1007/s001250050756 · Cited by 82
van Poelje, P. D., Potter, S. C., Chandramouli, V. C., Landau, B. R., Dang, Q., & Erion, M. D. (2006) · Diabetes · doi:10.2337/db05-1443 · Cited by 87
MicroRNA-214 Suppresses Gluconeogenesis by Targeting Activating Transcriptional Factor 4
Li, K., Zhang, J., Yu, J., Liu, B., Guo, Y., Deng, J., Chen, S., Wang, C., & Guo, F. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.m114.633990 · Cited by 81
Sugars and starch in the nutritional management of diabetes mellitus
Kelley, D. E. (2003) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/78.4.858s · Cited by 82
Self-citationBåvenholm, P., Pigon, J., Östenson, C., & Efendić, S. (2001) · Diabetes · doi:10.2337/diabetes.50.6.1449 · Cited by 81
The Emerging Role(s) for Kisspeptin in Metabolism in Mammals
Wolfe, A., & Hussain, M. A. (2018) · Frontiers in Endocrinology · doi:10.3389/fendo.2018.00184 · Cited by 83
Postprandial Dysmetabolism: the Missing Link Between Diabetes and Cardiovascular Events?
Bell, D. S. H., O’Keefe, J. H., & Jellinger, P. S. (2008) · Endocrine Practice · doi:10.4158/ep.14.1.112 · Cited by 77
Pathogenesis and management of postprandial hyperglycemia: role of incretin-based therapies
Gerich, J. E. (2013) · International Journal of General Medicine · doi:10.2147/ijgm.s51665 · Cited by 88
Self-citationRole of the SIK2–p35–PJA2 complex in pancreatic β-cell functional compensation
Sakamaki, J.-I., Fu, A., Reeks, C., Baird, S. D., Depatie, C., Azzabi, M. A., Bardeesy, N. M., Gingras, A., Yee, S., & Screaton, R. A. (2014) · Nature Cell Biology · doi:10.1038/ncb2919 · Cited by 78
Mechanisms of Impaired Fasting Glucose and Glucose Intolerance Induced by a ∼50% Pancreatectomy
Matveyenko, A. V., Veldhuis, J. D., & Butler, P. C. (2006) · Diabetes · doi:10.2337/db06-0345 · Cited by 77
ORAL THERAPIES FOR DIABETIC HYPERGLYCEMIA
Lebovitz, H. E. (2001) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/s0889-8529(05)70221-8 · Cited by 75
Tschritter, O., Stümvoll, M., Machicao, F. E., Holzwarth, M. G., Weisser, M., Maerker, E., Teigeler, A., Häring, H. U., & Fritsche, A. (2002) · Diabetes · doi:10.2337/diabetes.51.9.2854 · Cited by 76
Henkel, E., Menschikowski, M., Koehler, C., Leonhardt, W., & Hanefeld, M. (2005) · Metabolism · doi:10.1016/j.metabol.2005.03.024 · Cited by 74
Diet-Induced Weight Loss Is Associated with an Improvement in β-Cell Function in Older Men
Utzschneider, K. M., Carr, D. B., Barsness, S. M., Kahn, S. E., & Schwartz, R. S. (2004) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2003-031827 · Cited by 73
Kruszynska, Y. T., Harry, D. S., Bergman, R. N., & McIntyre, N. (1993) · Diabetologia · doi:10.1007/bf00400692 · Cited by 71
Luzi, L., Hering, B. J., SOCCI, C., Raptis, G., Battezzati, A., Terruzzi, I. M., Falqui, L., Brandhorst, H., Brandhorst, D., Regalia, E., et al. (1996) · Journal of Clinical Investigation · doi:10.1172/jci118710 · Cited by 71
Livesey, G., Wilson, P. D. G., Dainty, J. R., Brown, J. C., Faulks, R. M., Roe, M. A., Newman, T. A., Eagles, J., Mellon, F. A., & Greenwood, R. H. (1998) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1998.275.4.e717 · Cited by 71
Shrayyef, M. Z., & Gerich, J. E. (2009) · Springer eBooks · doi:10.1007/978-0-387-09841-8_2 · Cited by 74
Self-citationThe glucose triad and its role in comprehensive glycaemic control: current status, future management
Ceriello, A. (2010) · International Journal of Clinical Practice · doi:10.1111/j.1742-1241.2010.02517.x · Cited by 72
Perreault, L., & Færch, K. (2013) · Journal of Diabetes and its Complications · doi:10.1016/j.jdiacomp.2013.10.008 · Cited by 82
Kanauchi, M., Kimura, K., Kanauchi, K., & Saito, Y. (2005) · International Journal of Clinical Practice · doi:10.1111/j.1368-5031.2005.00422.x · Cited by 70
Marre, M., Gaal, L. V., Usadel, K., Ball, M., Whatmough, I., & Guitard, C. (2002) · Diabetes Obesity and Metabolism · doi:10.1046/j.1463-1326.2002.00196.x · Cited by 70
Anti-diabetic potential of selected Malaysian seaweeds
Chin, Y., Lim, P. E., Maggs, C. A., Phang, S. M., Sharifuddin, Y., & Green, B. D. (2014) · Journal of Applied Phycology · doi:10.1007/s10811-014-0462-8 · Cited by 70
Circulating microRNAs as biomarkers for metabolic disease
Párrizas, M., & Novials, A. (2016) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/j.beem.2016.08.001 · Cited by 67
Åhrén, B., & Pacini, G. (1997) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1997.273.4.e701 · Cited by 66
Effects of meal size and composition on incretin, α-cell, and β-cell responses
Rijkelijkhuizen, J. M., McQuarrie, K., Girman, C. J., Stein, P. P., Mari, A., Holst, J. J., Nijpels, G., & Dekker, J. M. (2009) · Metabolism · doi:10.1016/j.metabol.2009.07.039 · Cited by 67
Gårdebjer, E. M., Anderson, S. T., Pantaleon, M., Wlodek, M. E., & Moritz, K. M. (2015) · The FASEB Journal · doi:10.1096/fj.14-268979 · Cited by 65
Wang, L., Liu, Y., Lu, S. Y., Nguyen, K.-T. T., Schroer, S. A., Suzuki, A., Mak, T. W., Gaisano, H. Y., & Woo, M. (2010) · Diabetes · doi:10.2337/db09-1805 · Cited by 65
Suzuki, H., Fukushima, M., Usami, M., Ikeda, M., Taniguchi, A., Nakai, Y., Matsuura, T., Kuroe, A., Yasuda, K., Kurose, T., et al. (2003) · Diabetes Care · doi:10.2337/diacare.26.4.1211 · Cited by 65
Hamid, H. A., Yusoff, M. M., Liu, M., & Karim, M. R. (2015) · Journal of Functional Foods · doi:10.1016/j.jff.2015.04.011 · Cited by 65
Yoshinaga, H., & Kosáka, K. (1999) · Diabetes Research and Clinical Practice · doi:10.1016/s0168-8227(99)00019-4 · Cited by 64
Urabe, T., Watada, H., Okuma, Y., Tanaka, R., Ueno, Y., Miyamoto, N., Tanaka, Y., Hattori, N., & Kawamori, R. (2009) · Stroke · doi:10.1161/strokeaha.108.522557 · Cited by 64
Alaei-Shahmiri, F., Soares, M. J., Zhao, Y., & Sherriff, J. L. (2013) · European Journal of Nutrition · doi:10.1007/s00394-013-0534-6 · Cited by 63
Hales, C. N. (1994) · Diabetologia · doi:10.1007/bf00400840 · Cited by 63
Importance of changes in gastric emptying for postprandial plasma glucose fluxes in healthy humans
Woerle, H. J., Albrecht, M., Linke, R., Zschau, S., Neumann, C., Nicolaus, M., Gerich, J. E., Göke, B., & Schirra, J. R. J. (2007) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00514.2007 · Cited by 62
Self-citationKramer, C. K., Vuksan, V. V. V., Choi, H., Zinman, B., & Retnakaran, R. R. (2014) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2014.04.023 · Cited by 61
Elevated plasma glucose 2 h postchallenge predicts defects in beta-cell function
Byrne, M. M., Sturis, J., Sobel, R., & Polonsky, K. S. (1996) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1996.270.4.e572 · Cited by 61
Metabolic abnormalities in impaired glucose tolerance
Gerich, J. E. (1997) · Metabolism · doi:10.1016/s0026-0495(97)90316-4 · Cited by 63
Self-citationHjelmesaeth, J. S., Hagen, M., Hartmann, A., Midtvedt, K., Egeland, T., & Jenssen, T. G. (2002) · Clinical Transplantation · doi:10.1034/j.1399-0012.2002.02059.x · Cited by 63
Pancreatic α-Cell Dysfunction in Type 2 Diabetes: Old Kids on the Block
Moon, J. S., & Won, K. C. (2015) · Diabetes & Metabolism Journal · doi:10.4093/dmj.2015.39.1.1 · Cited by 61
Radziuk, J., & Pye, S. (2002) · Diabetologia · doi:10.1007/s00125-002-0841-6 · Cited by 64
Larsson, H. E., & Ahr�n, B. (1996) · Diabetologia · doi:10.1007/bf00400660 · Cited by 60
An examination of β‐cell function measures and their potential use for estimating β‐cell mass
Kahn, S. E., Carr, D. B., Faulenbach, M. V., & Utzschneider, K. M. (2008) · Diabetes Obesity and Metabolism · doi:10.1111/j.1463-1326.2008.00945.x · Cited by 59
Ranjit Unnikrishnan, I., Shaw, J. E., Chan, J. C. N., Wild, S. H., Peters, A. L., Orrange, S., Roden, M., & Mohan, V. (2025) · Nature Reviews Disease Primers · doi:10.1038/s41572-025-00635-0 · Cited by 69
Sundsten, T., Eberhardson, M., Göransson, M., & Bergsten, P. (2006) · Proteome Science · doi:10.1186/1477-5956-4-22 · Cited by 59
Nielsen, M. F., Basu, R., Wise, S., Caumo, A., Cobelli, C., & Rizza, R. A. (1998) · Diabetes · doi:10.2337/diabetes.47.11.1735 · Cited by 76
Li, K., Qiu, C., Sun, P. G., Liu, D.-C., Wu, T., Wang, K., Zhou, Y., Chang, X.-A., Yin, Y., Chen, F., et al. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.02.035 · Cited by 59
Derosa, G., Mugellini, A., Ciccarelli, L., Crescenzi, G., & Fogari, R. (2003) · Diabetes Research and Clinical Practice · doi:10.1016/s0168-8227(03)00057-3 · Cited by 57
Yao, X., Chen, L., & Nyomba, B. L. G. (2005) · Journal of Applied Physiology · doi:10.1152/japplphysiol.01115.2005 · Cited by 56
Theodorakis, M. J., Carlson, O. D., Muller, D. C., & Egan, J. M. (2004) · Diabetes Care · doi:10.2337/diacare.27.7.1692 · Cited by 56
Ahrén, B., Larsson, H. E., & Holst, J. J. (1997) · European Journal of Endocrinology · doi:10.1530/eje.0.1370127 · Cited by 54
Home, P. D., & Pacini, G. (2007) · Diabetes Obesity and Metabolism · doi:10.1111/j.1463-1326.2007.00761.x · Cited by 55
Altuntas, Y., Bilir, M., Ucak, S., & Gundogdu, S. (2005) · European Journal of Obstetrics & Gynecology and Reproductive Biology · doi:10.1016/j.ejogrb.2004.07.038 · Cited by 53
Walker, M., Mari, A., Jayapaul, M. K., Bennett, S. M. A., & Ferrannini, E. (2005) · Diabetologia · doi:10.1007/s00125-005-0004-7 · Cited by 53
Early therapy for type 2 diabetes in China
Yang, W., & Weng, J. (2014) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(14)70136-6 · Cited by 53
Hepatic ATGL knockdown uncouples glucose intolerance from liver TAG accumulation
Ong, K. T., Mashek, M. T., Bu, S. Y., & Mashek, D. G. (2012) · The FASEB Journal · doi:10.1096/fj.12-213454 · Cited by 53
Wang, L., Zhao, Y., Gui, B., Fu, R., Ma, F., Yu, J. M., Qü, P., Dong, L., & Chen, C. (2011) · Journal of Endocrinology · doi:10.1530/joe-11-0132 · Cited by 52
Hoenig, M. E., Alexander, S., Holson, J., & Ferguson, D. C. (2002) · Journal of Veterinary Internal Medicine · doi:10.1111/j.1939-1676.2002.tb02382.x · Cited by 52
Ullah, H., Uddin, I., Rahim, F., Khan, F., Sobia, Taha, M., Khan, M. U., Hayat, S., Ullah, M., Gul, Z., et al. (2021) · Journal of Molecular Structure · doi:10.1016/j.molstruc.2021.132058 · Cited by 50
Pancreatic islet dysfunction in type 2 diabetes: a rational target for incretin-based therapies
Meece, J. D. (2007) · Current Medical Research and Opinion · doi:10.1185/030079906x167336 · Cited by 49
Fritsche, Stefan, N., Hardt, Schützenauer, Häring, & Stümvoll, M. (2000) · European Journal of Clinical Investigation · doi:10.1046/j.1365-2362.2000.00649.x · Cited by 50
Point: A Glucose Tolerance Test Is Important for Clinical Practice
Tuomilehto, J. O. (2002) · Diabetes Care · doi:10.2337/diacare.25.10.1880 · Cited by 49
Beta-cell failure in the pathogenesis of type 2 diabetes mellitus
Steppel, J. H., & Horton, E. S. (2004) · Current Diabetes Reports · doi:10.1007/s11892-004-0019-3 · Cited by 47
Treviño, S., Sánchez‐Lara, E., Sarmiento-Ortega, V. E., Sánchez‐Lombardo, I., Flores-Hernández, J. Á., Pérez-Benı́tez, A., Brambila, E., & Vergara, E. G. (2015) · Journal of Inorganic Biochemistry · doi:10.1016/j.jinorgbio.2015.04.002 · Cited by 48
Pathophysiology of type 2 diabetes: targeting islet cell dysfunction.
Spellman, C. (2010) · PubMed · Cited by 48
EphA4 Receptor Forward Signaling Inhibits Glucagon Secretion From α-Cells
Hutchens, T., & Piston, D. W. (2015) · Diabetes · doi:10.2337/db15-0488 · Cited by 48
O’Brien, T. P., Jenkins, E. C., Estes, S. K., Castaneda, A. V., Ueta, K., Farmer, T. D., Puglisi, A. E., Swift, L. L., Printz, R. L., & Shiota, M. (2017) · Diabetes · doi:10.2337/db16-1410 · Cited by 50
Postprandial Reactive Hypoglycemia
Altuntaş, Y. (2019) · SiSli Etfal Hastanesi Tip Bulteni / The Medical Bulletin of Sisli Hospital · doi:10.14744/semb.2019.59455 · Cited by 47
“Thus, late reactive hypoglycemia occurs.[3] Elevated insulin levels also cause downregulation of the insulin postreceptor on the muscle and fat cells, thus decreasing insulin sensitivity.”
BackgroundInsulin resistance in diabetic nephropathy — cause or consequence?
Svensson, M. K. E., & Eriksson, J. W. (2006) · Diabetes/Metabolism Research and Reviews · doi:10.1002/dmrr.648 · Cited by 47
Exocytosis proteins as novel targets for diabetes prevention and/or remediation?
Aslamy, A., & Thurmond, D. C. (2017) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00002.2017 · Cited by 46
Polonsky, K. S., & Burant, C. (2016) · Elsevier eBooks · doi:10.1016/b978-0-323-29738-7.00031-9 · Cited by 53
Role of postprandial hyperglycemia in cardiovascular disease
Fava, S. (2008) · Expert Review of Cardiovascular Therapy · doi:10.1586/14779072.6.6.859 · Cited by 47
Larivière, F., Chiasson, J., Schiffrin, A., Taveroff, A., & Hoffer, L. J. (1994) · Metabolism · doi:10.1016/0026-0495(94)90077-9 · Cited by 47
First-phase insulin secretion: can its evaluation direct therapeutic approaches?
Di Giuseppe, G., Ciccarelli, G., Soldovieri, L., Capece, U., Cefalo, C. M. A., Moffa, S., Nista, E. C., Brunetti, M., Cinti, F., Gasbarrini, A., et al. (2023) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2023.02.001 · Cited by 46
Turner, N. C., & Clapham, J. C. (1998) · Birkhäuser Basel eBooks · doi:10.1007/978-3-0348-8845-5_2 · Cited by 46
Prevalence and Features of Impaired Glucose Tolerance in Young Underweight Japanese Women
Sato, M., Tamura, Y., Nakagata, T., Someya, Y., Kaga, H., Yamasaki, N., Kiya, M., Kadowaki, S., Sugimoto, D., Satoh, H., et al. (2021) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgab052 · Cited by 51
Overview of the Gliptin Class (Dipeptidyl Peptidase-4 Inhibitors) in Clinical Practice
Bohannon, N. J. V. (2009) · Postgraduate Medicine · doi:10.3810/pgm.2009.01.1953 · Cited by 45
Islet dysfunction in obese women with impaired glucose tolerance
Larsson, H., & Ahrén, B. (1996) · Metabolism · doi:10.1016/s0026-0495(96)90227-9 · Cited by 44
Impaired Crosstalk between Pulsatile Insulin and Glucagon Secretion in Prediabetic Individuals
Rohrer, S., Menge, B. A., Grüber, L., Deacon, C. F., Schmidt, W. E., Veldhuis, J. D., Holst, J. J., & Meier, J. J. (2012) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2011-3439 · Cited by 44
Nonesterified Fatty Acids and Hepatic Glucose Metabolism in the Conscious Dog
Moore, M. C., Satake, S., Lautz, M., Soleimanpour, S. A., Neal, D. W., Smith, M. S., & Cherrington, A. D. (2004) · Diabetes · doi:10.2337/diabetes.53.1.32 · Cited by 42
Controlling the glucose factory
Vidal‐Puig, A., & O’Rahilly, S. (2001) · Nature · doi:10.1038/35093198 · Cited by 42
Brain Control of Insulin and Glucagon Secretion
Osundiji, M. A., & Evans, M. L. (2012) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/j.ecl.2012.11.006 · Cited by 42
Seibæk, M., Sloth, C., Vallebo, L., Hansen, T. F., Urhammer, S. A., Burchardt, H., Torp-Pedersen, C., Pedersen, O. B., & Hildebrandt, P. R. (1997) · American Heart Journal · doi:10.1016/s0002-8703(97)70163-7 · Cited by 42
Fu, Q., Jiang, H., Qian, Y., Lv, H. X., Dai, H., Zhou, Y., Chen, Y., He, Y., Gao, R., Zheng, S., et al. (2022) · Diabetologia · doi:10.1007/s00125-022-05849-5 · Cited by 44
Metadata
- Authors
- Mitrakou, A., Kelley, D., Mokan, M., Veneman, T., Pangburn, T., Reilly, J., & Gerich, J.
- Affiliations
- University of Pittsburgh (US)
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 1992-01-02
- Volume
- 326
- Issue
- 1
- Pages
- 22-29
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2330273698
- Cited by
- 595
- References
- 47
- Citations by year
- 2026: 12 · 2025: 5 · 2024: 9 · 2023: 11 · 2022: 15 · 2021: 15 · 2020: 13 · 2019: 13 · 2018: 14 · 2017: 20 · 2016: 12 · 2015: 27 · 2014: 25 · 2013: 18 · 2012: 19
- FWCI
- 21.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (7r37dk020411-19)
- National Institute of Diabetes and Digestive and Kidney Diseases (5R37 DK20411)
- National Center for Research Resources (M01RR000056, 5 M01 RR00056)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- impaired glucose tolerance, type 2 diabetes, hepatic glucose production, insulin secretion, hyperinsulinemia, glucagon, insulin/glucagon ratio, muscle glucose uptake, obesity, beta-cell dysfunction, insulin resistance
- MeSH terms
- Insulin Secretion, Blood Glucose, Diabetes Mellitus, Type 2, Female, Glucagon, Glucose Tolerance Test, Humans, Insulin, Islets of Langerhans, Liver, Male, Middle Aged, Muscles, Prediabetic State
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
