Skip to main content
Erschienen in: Current Diabetes Reports 6/2015

01.06.2015 | Pathogenesis of Type 2 Diabetes and Insulin Resistance (RM Watanabe, Section Editor)

The Forgotten Role of Glucose Effectiveness in the Regulation of Glucose Tolerance

verfasst von: Simmi Dube, Isabel Errazuriz-Cruzat, Ananda Basu, Rita Basu

Erschienen in: Current Diabetes Reports | Ausgabe 6/2015

Einloggen, um Zugang zu erhalten

Abstract

Glucose effectiveness (S G) is the ability of glucose per se to stimulate its own uptake and to suppress its own production under basal/constant insulin concentrations. In an individual, glucose tolerance is a function of insulin secretion, insulin action and S G. Under conditions of declining insulin secretion and action (e.g. type 2 diabetes), the degree of S G assumes increasing significance in determining the level of glucose tolerance both in fasted and postprandial states. Although the importance of S G has been recognized for years, mechanisms that contribute to S G are poorly understood. Research data on modulation of S G and its impact in glucose intolerance is limited. In this review, we will focus on the role of S G in the regulation of glucose tolerance, its evaluation, and potential advantages of therapies that can enhance glucose-induced stimulation of glucose uptake and suppression of its own production in conditions of impaired insulin secretion and action.
Literatur
1.
Zurück zum Zitat Hoffman RP, Armstrong PT. Glucose effectiveness, peripheral and hepatic insulin sensitivity, in obese and lean prepuberal children. Int J Obes Relat Metab Disord. 1996;20:521–5.PubMed Hoffman RP, Armstrong PT. Glucose effectiveness, peripheral and hepatic insulin sensitivity, in obese and lean prepuberal children. Int J Obes Relat Metab Disord. 1996;20:521–5.PubMed
2.
Zurück zum Zitat Firth RG, Bell PM, Marsh HM, et al. Postprandial hyperglycemia in patients with non-insulin-dependent diabetes mellitus. J Clin Invest. 1986;77:1525–32.CrossRefPubMedCentralPubMed Firth RG, Bell PM, Marsh HM, et al. Postprandial hyperglycemia in patients with non-insulin-dependent diabetes mellitus. J Clin Invest. 1986;77:1525–32.CrossRefPubMedCentralPubMed
3.
Zurück zum Zitat Mitrakou A, Kelley D, Veneman T, et al. Contribution of abnormal muscle and liver glucose metabolism to postprandial hyperglycemia in NIDDM. Diabetes. 1990;39:1381–90.CrossRefPubMed Mitrakou A, Kelley D, Veneman T, et al. Contribution of abnormal muscle and liver glucose metabolism to postprandial hyperglycemia in NIDDM. Diabetes. 1990;39:1381–90.CrossRefPubMed
4.
Zurück zum Zitat Ferrannini E, Simonson DC, Katz LD, et al. The disposal of an oral glucose load in patients with non-insulin-dependent diabetes. Metabolism. 1988;37:79–85.CrossRefPubMed Ferrannini E, Simonson DC, Katz LD, et al. The disposal of an oral glucose load in patients with non-insulin-dependent diabetes. Metabolism. 1988;37:79–85.CrossRefPubMed
5.
Zurück zum Zitat DeFronzo RA, Ferrannini E, Hendler R, et al. Regulation of splanchnic and peripheral glucose uptake by insulin and hyperglycemia in man. Diabetes. 1983;32:35–45.CrossRefPubMed DeFronzo RA, Ferrannini E, Hendler R, et al. Regulation of splanchnic and peripheral glucose uptake by insulin and hyperglycemia in man. Diabetes. 1983;32:35–45.CrossRefPubMed
7.
Zurück zum Zitat Yki-Jarvinen H, Young AA, Lamkin C, et al. Kinetics of glucose disposal in whole body and across the forearm in man. J Clin Invest. 1987;79:1713–9.CrossRefPubMedCentralPubMed Yki-Jarvinen H, Young AA, Lamkin C, et al. Kinetics of glucose disposal in whole body and across the forearm in man. J Clin Invest. 1987;79:1713–9.CrossRefPubMedCentralPubMed
8.
Zurück zum Zitat Rossetti L, Giaccari A, Barzilai N, et al. Mechanism by which hyperglycemia inhibits hepatic glucose production in conscious rats. J Clin Invest. 1993;92:1126–34.CrossRefPubMedCentralPubMed Rossetti L, Giaccari A, Barzilai N, et al. Mechanism by which hyperglycemia inhibits hepatic glucose production in conscious rats. J Clin Invest. 1993;92:1126–34.CrossRefPubMedCentralPubMed
9.
Zurück zum Zitat Rizza RA, Mandarino LJ, Gerich JE. Dose-response characteristics for effects of insulin on production and utilization of glucose in man. Am J Physiol. 1981;240:E630–9.PubMed Rizza RA, Mandarino LJ, Gerich JE. Dose-response characteristics for effects of insulin on production and utilization of glucose in man. Am J Physiol. 1981;240:E630–9.PubMed
10.
Zurück zum Zitat Kolterman OG, Gray RS, Griffin J, et al. Receptor and postreceptor defects contribute to the insulin resistance in non-insulin-dependent diabetes mellitus. J Clin Invest. 1981;68:957–69.CrossRefPubMedCentralPubMed Kolterman OG, Gray RS, Griffin J, et al. Receptor and postreceptor defects contribute to the insulin resistance in non-insulin-dependent diabetes mellitus. J Clin Invest. 1981;68:957–69.CrossRefPubMedCentralPubMed
11.
Zurück zum Zitat Liljenquist J, Meuller G, Cherrington A, et al. Hyperglycemia per se can inhibit glucose production in man. J Clin Endocrinol Metab. 1979;48:171–5.CrossRefPubMed Liljenquist J, Meuller G, Cherrington A, et al. Hyperglycemia per se can inhibit glucose production in man. J Clin Endocrinol Metab. 1979;48:171–5.CrossRefPubMed
12.
Zurück zum Zitat Bergman RN, Bucolo RJ. Interaction of insulin and glucose in the control of hepatic glucose balance. Am J Physiol. 1974;227:1314–22.PubMed Bergman RN, Bucolo RJ. Interaction of insulin and glucose in the control of hepatic glucose balance. Am J Physiol. 1974;227:1314–22.PubMed
13.
Zurück zum Zitat Shulman G, Liljenquist J, Williams P, et al. Glucose disposal during insulinopenia in somatostatin-treated dogs: the roles of glucose and glucagon. J Clin Invest. 1978;62:487–91.CrossRefPubMedCentralPubMed Shulman G, Liljenquist J, Williams P, et al. Glucose disposal during insulinopenia in somatostatin-treated dogs: the roles of glucose and glucagon. J Clin Invest. 1978;62:487–91.CrossRefPubMedCentralPubMed
14.
Zurück zum Zitat Sacca L, Cicala M, Trimarco B, et al. Differential effects of insulin on splanchnic and peripheral glucose disposal after an intravenous glucose load in man. J Clin Invest. 1982;70:117–26.CrossRefPubMedCentralPubMed Sacca L, Cicala M, Trimarco B, et al. Differential effects of insulin on splanchnic and peripheral glucose disposal after an intravenous glucose load in man. J Clin Invest. 1982;70:117–26.CrossRefPubMedCentralPubMed
15.
Zurück zum Zitat Cherrington A, Williams P, Harris M. Relationship between the plasma glucose level and glucose uptake in the conscious dog. Metabolism. 1978;27:787–91.CrossRefPubMed Cherrington A, Williams P, Harris M. Relationship between the plasma glucose level and glucose uptake in the conscious dog. Metabolism. 1978;27:787–91.CrossRefPubMed
16.
Zurück zum Zitat Verdonk C, Rizza R, Gerich J. Effects of plasma glucose concentration on glucose utilization and glucose clearance in normal man. Diabetes. 1981;30:535–7.CrossRefPubMed Verdonk C, Rizza R, Gerich J. Effects of plasma glucose concentration on glucose utilization and glucose clearance in normal man. Diabetes. 1981;30:535–7.CrossRefPubMed
17.
Zurück zum Zitat Best J, Taborsky G, Halter J, et al. Glucose disposal is not proportional to plasma glucose level in man. Diabetes. 1981;30:847–50.CrossRefPubMed Best J, Taborsky G, Halter J, et al. Glucose disposal is not proportional to plasma glucose level in man. Diabetes. 1981;30:847–50.CrossRefPubMed
18.
Zurück zum Zitat Lewis S, Schultz T, Westbie D, et al. Insulin glucose dynamics during flow through perfusion of the isolated rat hind limb. Horm Metab Res. 1977;9:190–5.CrossRefPubMed Lewis S, Schultz T, Westbie D, et al. Insulin glucose dynamics during flow through perfusion of the isolated rat hind limb. Horm Metab Res. 1977;9:190–5.CrossRefPubMed
19.
Zurück zum Zitat Bell PM, Firth RG, Rizza RA. Assessment of insulin action in insulin-dependent diabetes mellitus using [61 4C]glucose, [33H]glucose, and [23H]glucose. J Clin Invest. 1986;78:1479–86.CrossRefPubMedCentralPubMed Bell PM, Firth RG, Rizza RA. Assessment of insulin action in insulin-dependent diabetes mellitus using [61 4C]glucose, [33H]glucose, and [23H]glucose. J Clin Invest. 1986;78:1479–86.CrossRefPubMedCentralPubMed
20.
Zurück zum Zitat Vranic M, Fono P, Kovacevic N, et al. Glucose kinetics and fatty acids in dogs on matched insulin infusion after glucose load. Metabolism. 1971;20:954–67.CrossRefPubMed Vranic M, Fono P, Kovacevic N, et al. Glucose kinetics and fatty acids in dogs on matched insulin infusion after glucose load. Metabolism. 1971;20:954–67.CrossRefPubMed
21.
Zurück zum Zitat Ishiwata K, Hetenyi Jr G, Vranic M. Effect of D-glucose or D-ribose on the turnover of glucose in pancreatectomized dogs maintained on a matched intraportal infusion of insulin. Diabetes. 1969;18(12):820–7.CrossRefPubMed Ishiwata K, Hetenyi Jr G, Vranic M. Effect of D-glucose or D-ribose on the turnover of glucose in pancreatectomized dogs maintained on a matched intraportal infusion of insulin. Diabetes. 1969;18(12):820–7.CrossRefPubMed
22.
Zurück zum Zitat Sacca L, Hendler R, Sherwin RS. Hyperglycemia inhibits glucose production in man independent of changes in glucoregulatory hormones. J Clin Endocrinol Metab. 1978;47:1160–3.CrossRefPubMed Sacca L, Hendler R, Sherwin RS. Hyperglycemia inhibits glucose production in man independent of changes in glucoregulatory hormones. J Clin Endocrinol Metab. 1978;47:1160–3.CrossRefPubMed
23.
Zurück zum Zitat Del Prato S, Matsuda M, Simonson DC, et al. Studies on the mass action effect of glucose in NIDDM and IDDM: evidence for glucose resistance. Diabetologia. 1997;40:687–97.CrossRefPubMed Del Prato S, Matsuda M, Simonson DC, et al. Studies on the mass action effect of glucose in NIDDM and IDDM: evidence for glucose resistance. Diabetologia. 1997;40:687–97.CrossRefPubMed
24.
Zurück zum Zitat Petersen KF, Laurent D, Rothman DL, et al. Mechanism by which glucose and insulin inhibit net hepatic glycogenolysis in humans. J Clin Invest. 1998;101:1203–9.CrossRefPubMedCentralPubMed Petersen KF, Laurent D, Rothman DL, et al. Mechanism by which glucose and insulin inhibit net hepatic glycogenolysis in humans. J Clin Invest. 1998;101:1203–9.CrossRefPubMedCentralPubMed
25.
Zurück zum Zitat Bucolo RJ, Bergman RN, Marsh DJ, et al. Dynamics of glucose auto-regulation in the isolated, blood-perfused canine liver. Am J Physiol. 1974;221:209–17. Bucolo RJ, Bergman RN, Marsh DJ, et al. Dynamics of glucose auto-regulation in the isolated, blood-perfused canine liver. Am J Physiol. 1974;221:209–17.
26.
Zurück zum Zitat Best J, Kahn SE, Ader M, et al. Role of glucose effectiveness in the determination of glucose tolerance. Diabetes Care. 1996;19:1018–30.CrossRefPubMed Best J, Kahn SE, Ader M, et al. Role of glucose effectiveness in the determination of glucose tolerance. Diabetes Care. 1996;19:1018–30.CrossRefPubMed
27.
Zurück zum Zitat Galante P, Mosthaf L, Kellerer M, et al. Acute hyperglycemia provides an insulin-independent inducer for GLUT4 translocation in C2C12 myotubes and rat skeletal muscle. Diabetes. 1995;44:646–51.CrossRefPubMed Galante P, Mosthaf L, Kellerer M, et al. Acute hyperglycemia provides an insulin-independent inducer for GLUT4 translocation in C2C12 myotubes and rat skeletal muscle. Diabetes. 1995;44:646–51.CrossRefPubMed
28.
Zurück zum Zitat Nolte LA, Rincon J, Wahlstrom EO, et al. Hyperglycemia activates glucose transport in rat skeletal muscle via a Ca2+-dependent mechanism. Diabetes. 1995;44:1345–8.CrossRefPubMed Nolte LA, Rincon J, Wahlstrom EO, et al. Hyperglycemia activates glucose transport in rat skeletal muscle via a Ca2+-dependent mechanism. Diabetes. 1995;44:1345–8.CrossRefPubMed
29.•
Zurück zum Zitat Schwartz MW, Seeley RJ, Tschöp MH, et al. Cooperation between brain and islet in glucose homeostasis and diabetes. Nature. 2013;503(7474):59–66. This review article discusses the role of brain-centric glucoregulatory systems in lowering blood glucose levels via insulin-independent and -dependent mechanisms.CrossRefPubMedCentralPubMed Schwartz MW, Seeley RJ, Tschöp MH, et al. Cooperation between brain and islet in glucose homeostasis and diabetes. Nature. 2013;503(7474):59–66. This review article discusses the role of brain-centric glucoregulatory systems in lowering blood glucose levels via insulin-independent and -dependent mechanisms.CrossRefPubMedCentralPubMed
30.
Zurück zum Zitat Vicini P, Caumo A, Cobelli C. Glucose effectiveness and insulin sensitivity from the minimal models: consequences of undermodeling assessed by Monte Carlo simulation. IEEE Trans Biomed Eng. 1999;46(2):130–7.CrossRefPubMed Vicini P, Caumo A, Cobelli C. Glucose effectiveness and insulin sensitivity from the minimal models: consequences of undermodeling assessed by Monte Carlo simulation. IEEE Trans Biomed Eng. 1999;46(2):130–7.CrossRefPubMed
31.
Zurück zum Zitat Pacini G, Tonolo G, Sambataro M, et al. Insulin sensitivity and glucose effectiveness: minimal model analysis of regular and insulin-modified FSIGT. Am J Physiol. 1998;274(4 Pt 1):E592–9.PubMed Pacini G, Tonolo G, Sambataro M, et al. Insulin sensitivity and glucose effectiveness: minimal model analysis of regular and insulin-modified FSIGT. Am J Physiol. 1998;274(4 Pt 1):E592–9.PubMed
32.
Zurück zum Zitat Bordenave S, Brandou F, Manetta J, et al. Effects of acute exercise on insulin sensitivity, glucose effectiveness and disposition index in type 2 diabetic patients. Diabetes Metab. 2008;34(3):250–7.CrossRefPubMed Bordenave S, Brandou F, Manetta J, et al. Effects of acute exercise on insulin sensitivity, glucose effectiveness and disposition index in type 2 diabetic patients. Diabetes Metab. 2008;34(3):250–7.CrossRefPubMed
33.
Zurück zum Zitat Ni TC, Ader M, Bergman RN. Reassessment of glucose effectiveness and insulin sensitivity from minimal model analysis: a theoretical evaluation of the single-compartment glucose distribution assumption. Diabetes. 1997;46(11):1813–21.CrossRefPubMed Ni TC, Ader M, Bergman RN. Reassessment of glucose effectiveness and insulin sensitivity from minimal model analysis: a theoretical evaluation of the single-compartment glucose distribution assumption. Diabetes. 1997;46(11):1813–21.CrossRefPubMed
34.
Zurück zum Zitat Caumo A, Vicini P, Zachwieja JJ, et al. Undermodeling affects minimal model indexes: insights from a two-compartment model. Am J Physiol. 1999;276(6 Pt 1):E1171–93.PubMed Caumo A, Vicini P, Zachwieja JJ, et al. Undermodeling affects minimal model indexes: insights from a two-compartment model. Am J Physiol. 1999;276(6 Pt 1):E1171–93.PubMed
35.
Zurück zum Zitat Martin BC, Warram JH, Krolewski AS, et al. Role of glucose and insulin resistance in development of type 2 diabetes mellitus: results of a 25-year follow-up study. Lancet. 1992;340:925–9.CrossRefPubMed Martin BC, Warram JH, Krolewski AS, et al. Role of glucose and insulin resistance in development of type 2 diabetes mellitus: results of a 25-year follow-up study. Lancet. 1992;340:925–9.CrossRefPubMed
36.
Zurück zum Zitat Lorenzo C, Wagenknecht LE, Rewers MJ, et al. Disposition index, glucose effectiveness, and conversion to type 2 diabetes: the Insulin Resistance Atherosclerosis Study (IRAS). Diabetes Care. 2010;33(9):2098–103.CrossRefPubMedCentralPubMed Lorenzo C, Wagenknecht LE, Rewers MJ, et al. Disposition index, glucose effectiveness, and conversion to type 2 diabetes: the Insulin Resistance Atherosclerosis Study (IRAS). Diabetes Care. 2010;33(9):2098–103.CrossRefPubMedCentralPubMed
37.
Zurück zum Zitat Henriksen JE, Alford F, Handberg A, et al. Increased glucose effectiveness in normoglycemic but insulin-resistant relatives of patients with non-insulin-dependent diabetes mellitus. J Clin Invest. 1994;94:1196–204.CrossRefPubMedCentralPubMed Henriksen JE, Alford F, Handberg A, et al. Increased glucose effectiveness in normoglycemic but insulin-resistant relatives of patients with non-insulin-dependent diabetes mellitus. J Clin Invest. 1994;94:1196–204.CrossRefPubMedCentralPubMed
38.
Zurück zum Zitat Bergman RN. Lilly lecture 1989. Toward physiological understanding of glucose tolerance. Minimal-model approach. Diabetes. 1989;38:1512–27.CrossRefPubMed Bergman RN. Lilly lecture 1989. Toward physiological understanding of glucose tolerance. Minimal-model approach. Diabetes. 1989;38:1512–27.CrossRefPubMed
39.
Zurück zum Zitat Doi K, Taniguchi A, Nakai Y, et al. Decreased glucose effectiveness but not insulin resistance in glucose-tolerant offspring of Japanese non-insulin-dependent diabetic patients: a minimal-model analysis. Metabolism. 1997;46(8):880–3.CrossRefPubMed Doi K, Taniguchi A, Nakai Y, et al. Decreased glucose effectiveness but not insulin resistance in glucose-tolerant offspring of Japanese non-insulin-dependent diabetic patients: a minimal-model analysis. Metabolism. 1997;46(8):880–3.CrossRefPubMed
40.
Zurück zum Zitat Osei K, Cottrell DA, Orabella MM. Insulin sensitivity, glucose effectiveness, and body fat distribution pattern in nondiabetic offspring of patients with NIDDM. Diabetes Care. 1991;14:890–6.CrossRefPubMed Osei K, Cottrell DA, Orabella MM. Insulin sensitivity, glucose effectiveness, and body fat distribution pattern in nondiabetic offspring of patients with NIDDM. Diabetes Care. 1991;14:890–6.CrossRefPubMed
41.
Zurück zum Zitat Nielsen MF, Nyholm B, Caumo A, et al. Prandial glucose effectiveness and fasting gluconeogenesis in insulin-resistant first-degree relatives of patients with type 2 diabetes. Diabetes. 2000;49(12):2135–41.CrossRefPubMed Nielsen MF, Nyholm B, Caumo A, et al. Prandial glucose effectiveness and fasting gluconeogenesis in insulin-resistant first-degree relatives of patients with type 2 diabetes. Diabetes. 2000;49(12):2135–41.CrossRefPubMed
42.
Zurück zum Zitat Alzaid AA, Dinneen SF, Turk DJ, et al. Assessment of insulin action and glucose effectiveness in diabetic and nondiabetic humans. J Clin Invest. 1994;94:2341–8.CrossRefPubMedCentralPubMed Alzaid AA, Dinneen SF, Turk DJ, et al. Assessment of insulin action and glucose effectiveness in diabetic and nondiabetic humans. J Clin Invest. 1994;94:2341–8.CrossRefPubMedCentralPubMed
43.
Zurück zum Zitat Basu A, Caumo A, Bettini F, et al. Impaired basal glucose effectiveness in NIDDM: contribution of defects in glucose disappearance and production, measured using an optimized minimal model independent protocol. Diabetes. 1997;46:421–32.CrossRefPubMed Basu A, Caumo A, Bettini F, et al. Impaired basal glucose effectiveness in NIDDM: contribution of defects in glucose disappearance and production, measured using an optimized minimal model independent protocol. Diabetes. 1997;46:421–32.CrossRefPubMed
44.
Zurück zum Zitat Nielsen MF, Basu R, Wise S, et al. Normal glucose induced suppression of glucose production but impaired stimulation of glucose disposal in type 2 diabetes: evidence for a concentration-dependent defect in uptake. Diabetes. 1998;47:1735–47.CrossRefPubMed Nielsen MF, Basu R, Wise S, et al. Normal glucose induced suppression of glucose production but impaired stimulation of glucose disposal in type 2 diabetes: evidence for a concentration-dependent defect in uptake. Diabetes. 1998;47:1735–47.CrossRefPubMed
45.
Zurück zum Zitat Basu A, Dalla Man C, Basu R, et al. Effects of type 2 diabetes on insulin secretion, insulin action, glucose effectiveness, and postprandial glucose metabolism. Diabetes Care. 2009;32(5):866–72.CrossRefPubMedCentralPubMed Basu A, Dalla Man C, Basu R, et al. Effects of type 2 diabetes on insulin secretion, insulin action, glucose effectiveness, and postprandial glucose metabolism. Diabetes Care. 2009;32(5):866–72.CrossRefPubMedCentralPubMed
46.
Zurück zum Zitat Taniguchi A, Nakai Y, Fukushima M, et al. Pathogenic factors responsible for glucose intolerance in patients with NIDDM. Diabetes. 1992;41:1540–6.CrossRefPubMed Taniguchi A, Nakai Y, Fukushima M, et al. Pathogenic factors responsible for glucose intolerance in patients with NIDDM. Diabetes. 1992;41:1540–6.CrossRefPubMed
47.
Zurück zum Zitat Wajchenberg BL, Santomauro ATMG, Porrelli RN. Effect of a sulfonylurea (gliclazide) treatment on insulin sensitivity and glucose-mediated glucose disposal in patients with non-insulin-dependent diabetes mellitus (NIDDM). Diabetes Res Clin Pract. 1993;20:147–54.CrossRefPubMed Wajchenberg BL, Santomauro ATMG, Porrelli RN. Effect of a sulfonylurea (gliclazide) treatment on insulin sensitivity and glucose-mediated glucose disposal in patients with non-insulin-dependent diabetes mellitus (NIDDM). Diabetes Res Clin Pract. 1993;20:147–54.CrossRefPubMed
48.
Zurück zum Zitat Welch S, Gebhart SSP, Bergman RN, et al. Minimal model analysis of intravenous glucose tolerance test-derived insulin sensitivity in diabetic subjects. J Clin Endocrinol Metab. 1990;71:1508–18.CrossRefPubMed Welch S, Gebhart SSP, Bergman RN, et al. Minimal model analysis of intravenous glucose tolerance test-derived insulin sensitivity in diabetic subjects. J Clin Endocrinol Metab. 1990;71:1508–18.CrossRefPubMed
49.
Zurück zum Zitat Avogaro A, Vicini P, Valerio A, et al. The hot but not the cold minimal model allows precise assessment of insulin sensitivity in NIDDM subjects. Am J Physiol. 1996;270:E532–40.PubMed Avogaro A, Vicini P, Valerio A, et al. The hot but not the cold minimal model allows precise assessment of insulin sensitivity in NIDDM subjects. Am J Physiol. 1996;270:E532–40.PubMed
50.
Zurück zum Zitat Quon MJ, Cochran C, Taylor SI, et al. Non-insulin-mediated glucose disappearance in subjects with IDDM. Diabetes. 1994;43:890–6.CrossRefPubMed Quon MJ, Cochran C, Taylor SI, et al. Non-insulin-mediated glucose disappearance in subjects with IDDM. Diabetes. 1994;43:890–6.CrossRefPubMed
51.
Zurück zum Zitat Finegood DT, Tzur D. Reduced glucose effectiveness associated with reduced insulin release: an artifact of the minimal-model method. Am J Physiol. 1996;271(3 Pt 1):E485–95.PubMed Finegood DT, Tzur D. Reduced glucose effectiveness associated with reduced insulin release: an artifact of the minimal-model method. Am J Physiol. 1996;271(3 Pt 1):E485–95.PubMed
52.
Zurück zum Zitat Cobelli C, Vicini P, Caumo A. If the minimal model is too minimal, who suffers more: SG or SI ? Diabetologia. 1997;40:362–3.PubMed Cobelli C, Vicini P, Caumo A. If the minimal model is too minimal, who suffers more: SG or SI ? Diabetologia. 1997;40:362–3.PubMed
53.
54.
Zurück zum Zitat Sandoval D, Cota D, Seeley RJ. The integrative role of CNS fuel-sensing mechanisms in energy balance and glucose regulation. Annu Rev Physiol. 2008;70:513–35.CrossRefPubMed Sandoval D, Cota D, Seeley RJ. The integrative role of CNS fuel-sensing mechanisms in energy balance and glucose regulation. Annu Rev Physiol. 2008;70:513–35.CrossRefPubMed
55.
Zurück zum Zitat Elmquist JK, Coppari R, Balthasar N, et al. Identifying hypothalamic pathways controlling food intake, body weight, and glucose homeostasis. J Comp Neurol. 2005;493:63–71.CrossRefPubMed Elmquist JK, Coppari R, Balthasar N, et al. Identifying hypothalamic pathways controlling food intake, body weight, and glucose homeostasis. J Comp Neurol. 2005;493:63–71.CrossRefPubMed
56.
Zurück zum Zitat Obici S, Zhang BB, Karkanias G, et al. Hypothalamic insulin signaling is required for inhibition of glucose production. Nat Med. 2008;8:1376–82.CrossRef Obici S, Zhang BB, Karkanias G, et al. Hypothalamic insulin signaling is required for inhibition of glucose production. Nat Med. 2008;8:1376–82.CrossRef
57.
Zurück zum Zitat Lam TK, Gutierrez-Juarez R, Pocai A, et al. Regulation of blood glucose by hypothalamic pyruvate metabolism. Science. 2005;309:943–7.CrossRefPubMed Lam TK, Gutierrez-Juarez R, Pocai A, et al. Regulation of blood glucose by hypothalamic pyruvate metabolism. Science. 2005;309:943–7.CrossRefPubMed
58.
Zurück zum Zitat Coppari R, Ichinose M, Lee CE, et al. The hypothalamic arcuate nucleus: a key site for mediating leptin’s effects on glucose homeostasis and locomotor activity. Cell Metab. 2005;1:63–72.CrossRefPubMed Coppari R, Ichinose M, Lee CE, et al. The hypothalamic arcuate nucleus: a key site for mediating leptin’s effects on glucose homeostasis and locomotor activity. Cell Metab. 2005;1:63–72.CrossRefPubMed
59.
Zurück zum Zitat Morton GJ, Gelling RW, Niswender KD, et al. Leptin regulates insulin sensitivity via phosphatidylinositol-3-OH kinase signaling in mediobasal hypothalamic neurons. Cell Metab. 2005;2:411–20.CrossRefPubMed Morton GJ, Gelling RW, Niswender KD, et al. Leptin regulates insulin sensitivity via phosphatidylinositol-3-OH kinase signaling in mediobasal hypothalamic neurons. Cell Metab. 2005;2:411–20.CrossRefPubMed
60.
Zurück zum Zitat D’Alessio DA, Kahn SE, Leusner CR, et al. Glucagon-like peptide 1 enhances glucose tolerance both by stimulation of insulin release and by increasing insulin-independent glucose disposal. J Clin Invest. 1994;93:2263–6.CrossRefPubMedCentralPubMed D’Alessio DA, Kahn SE, Leusner CR, et al. Glucagon-like peptide 1 enhances glucose tolerance both by stimulation of insulin release and by increasing insulin-independent glucose disposal. J Clin Invest. 1994;93:2263–6.CrossRefPubMedCentralPubMed
61.
Zurück zum Zitat Sandoval DA, Bagnol D, Woods SC, et al. Arcuate glucagon-like peptide 1 receptors regulate glucose homeostasis but not food intake. Diabetes. 2008;57:2046–54.CrossRefPubMedCentralPubMed Sandoval DA, Bagnol D, Woods SC, et al. Arcuate glucagon-like peptide 1 receptors regulate glucose homeostasis but not food intake. Diabetes. 2008;57:2046–54.CrossRefPubMedCentralPubMed
62.
Zurück zum Zitat Hardie DG, Carling D, Carlson M. The AMP-activated/SNF1 protein kinase subfamily: metabolic sensors of the eukaryotic cell? Annu Rev Biochem. 1998;67:821–55.CrossRefPubMed Hardie DG, Carling D, Carlson M. The AMP-activated/SNF1 protein kinase subfamily: metabolic sensors of the eukaryotic cell? Annu Rev Biochem. 1998;67:821–55.CrossRefPubMed
63.
Zurück zum Zitat Musi N, Hirshman MF, Nygren J, et al. Metformin increases AMPactivated protein kinase activity in skeletal muscle of subjects with type 2 diabetes. Diabetes. 2002;51:2074–81.CrossRefPubMed Musi N, Hirshman MF, Nygren J, et al. Metformin increases AMPactivated protein kinase activity in skeletal muscle of subjects with type 2 diabetes. Diabetes. 2002;51:2074–81.CrossRefPubMed
64.
Zurück zum Zitat Kahn BB, Alquier T, Carling D, et al. AMP-activated protein kinase: ancient energy gauge provides clues to modern understanding of metabolism. Cell Metab. 2005;1:15–25.CrossRefPubMed Kahn BB, Alquier T, Carling D, et al. AMP-activated protein kinase: ancient energy gauge provides clues to modern understanding of metabolism. Cell Metab. 2005;1:15–25.CrossRefPubMed
65.••
Zurück zum Zitat Pau CT, Keefe C, Duran J, et al. Metformin improves glucose effectiveness, not insulin sensitivity: predicting treatment response in women with polycystic ovary syndrome in an open-label, interventional study. J Clin Endocrinol Metab. 2014;99(5):1870–8. This study provides evidence that a possible mechanism of action of metformin is via improvement of glucose effectiveness.CrossRefPubMedCentralPubMed Pau CT, Keefe C, Duran J, et al. Metformin improves glucose effectiveness, not insulin sensitivity: predicting treatment response in women with polycystic ovary syndrome in an open-label, interventional study. J Clin Endocrinol Metab. 2014;99(5):1870–8. This study provides evidence that a possible mechanism of action of metformin is via improvement of glucose effectiveness.CrossRefPubMedCentralPubMed
66.
Zurück zum Zitat Brun JF, Guintrand-Hugret R, Boegner C, et al. Influence of short-term submaximal exercise on parameters of glucose assimilation analyzed with the minimal model. Metabolism. 1995;44:833–40.CrossRefPubMed Brun JF, Guintrand-Hugret R, Boegner C, et al. Influence of short-term submaximal exercise on parameters of glucose assimilation analyzed with the minimal model. Metabolism. 1995;44:833–40.CrossRefPubMed
67.
Zurück zum Zitat Hayashi Y, Nagasaka S, Takahashi N, et al. A single bout of exercise at higher intensity enhances glucose effectiveness in sedentary men. J Clin Endocrinol Metab. 2005;90:4035–40.CrossRefPubMed Hayashi Y, Nagasaka S, Takahashi N, et al. A single bout of exercise at higher intensity enhances glucose effectiveness in sedentary men. J Clin Endocrinol Metab. 2005;90:4035–40.CrossRefPubMed
68.
Zurück zum Zitat Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346:393–403.CrossRefPubMed Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346:393–403.CrossRefPubMed
69.
Zurück zum Zitat Tuomilehto J, Lindstrom J, Eriksson JG, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med. 2001;344:1343–50.CrossRefPubMed Tuomilehto J, Lindstrom J, Eriksson JG, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med. 2001;344:1343–50.CrossRefPubMed
70.
Zurück zum Zitat Zierath JR. Invited review: exercise training-induced changes in insulin signaling in skeletal muscle. J Appl Physiol. 2002;93:773–81.CrossRefPubMed Zierath JR. Invited review: exercise training-induced changes in insulin signaling in skeletal muscle. J Appl Physiol. 2002;93:773–81.CrossRefPubMed
71.
Zurück zum Zitat Manetta J, Brun JF, Mercier J, et al. The effects of exercise training intensification on glucose disposal in elite cyclists. Int J Sports Med. 2000;21:338–43.CrossRefPubMed Manetta J, Brun JF, Mercier J, et al. The effects of exercise training intensification on glucose disposal in elite cyclists. Int J Sports Med. 2000;21:338–43.CrossRefPubMed
72.
Zurück zum Zitat Manetta J, Brun JF, Callis A, et al. Insulin and non-insulin-dependent glucose disposal in middle-aged and young athletes versus sedentary men. Metabolism. 2001;50:349–54.CrossRefPubMed Manetta J, Brun JF, Callis A, et al. Insulin and non-insulin-dependent glucose disposal in middle-aged and young athletes versus sedentary men. Metabolism. 2001;50:349–54.CrossRefPubMed
73.
Zurück zum Zitat Higaki Y, Kagawa T, Fujitani Y, et al. Effects of a single bout of exercise on glucose effectiveness. J Appl Physiol. 1996;80:754–9.PubMed Higaki Y, Kagawa T, Fujitani Y, et al. Effects of a single bout of exercise on glucose effectiveness. J Appl Physiol. 1996;80:754–9.PubMed
74.
Zurück zum Zitat Araujo-Vilar D, Osifo E, Kirk M, et al. Influence of moderate physical exercise on insulin-mediated and non-insulin-mediated glucose uptake in healthy subjects. Metabolism. 1997;46:203–9.CrossRefPubMed Araujo-Vilar D, Osifo E, Kirk M, et al. Influence of moderate physical exercise on insulin-mediated and non-insulin-mediated glucose uptake in healthy subjects. Metabolism. 1997;46:203–9.CrossRefPubMed
75.
Zurück zum Zitat Boule NG, Weisnagel SJ, Lakka TA, et al. Effects of exercise training on glucose homeostasis: the HERITAGE Family Study. Diabetes Care. 2005;28:108–14.CrossRefPubMed Boule NG, Weisnagel SJ, Lakka TA, et al. Effects of exercise training on glucose homeostasis: the HERITAGE Family Study. Diabetes Care. 2005;28:108–14.CrossRefPubMed
76.
Zurück zum Zitat Fujitani J, Higaki Y, Kagawa T, et al. Intravenous glucose tolerance test-derived glucose effectiveness in strength-trained humans. Metabolism. 1998;47:874–7.CrossRefPubMed Fujitani J, Higaki Y, Kagawa T, et al. Intravenous glucose tolerance test-derived glucose effectiveness in strength-trained humans. Metabolism. 1998;47:874–7.CrossRefPubMed
77.
Zurück zum Zitat Nishida Y, Higaki Y, Tokuyama K, et al. Effect of mild exercise training on glucose effectiveness in healthy men. Diabetes Care. 2001;24:1008–13.CrossRefPubMed Nishida Y, Higaki Y, Tokuyama K, et al. Effect of mild exercise training on glucose effectiveness in healthy men. Diabetes Care. 2001;24:1008–13.CrossRefPubMed
78.
Zurück zum Zitat Kennedy JW, Hirshman MF, Gervino EV, et al. Acute exercise induces GLUT4 translocation in skeletal muscle of normal human subjects and subjects with type 2 diabetes. Diabetes. 1999;48:1192–7.CrossRefPubMed Kennedy JW, Hirshman MF, Gervino EV, et al. Acute exercise induces GLUT4 translocation in skeletal muscle of normal human subjects and subjects with type 2 diabetes. Diabetes. 1999;48:1192–7.CrossRefPubMed
79.
Zurück zum Zitat Hayashi T, Hirshman MF, Kuth EJ, et al. Evidence for 5′-AMP-activated protein kinase mediation of the effect of muscle contraction on glucose transport. Diabetes. 1998;47:1369–73.PubMed Hayashi T, Hirshman MF, Kuth EJ, et al. Evidence for 5′-AMP-activated protein kinase mediation of the effect of muscle contraction on glucose transport. Diabetes. 1998;47:1369–73.PubMed
Metadaten
Titel
The Forgotten Role of Glucose Effectiveness in the Regulation of Glucose Tolerance
verfasst von
Simmi Dube
Isabel Errazuriz-Cruzat
Ananda Basu
Rita Basu
Publikationsdatum
01.06.2015
Verlag
Springer US
Erschienen in
Current Diabetes Reports / Ausgabe 6/2015
Print ISSN: 1534-4827
Elektronische ISSN: 1539-0829
DOI
https://doi.org/10.1007/s11892-015-0605-6

Weitere Artikel der Ausgabe 6/2015

Current Diabetes Reports 6/2015 Zur Ausgabe

Health Care Delivery Systems and Implementation in Diabetes (EB Morton-Eggleston, Section Editor)

Diabetes Self-Management Interventions for Adults with Type 2 Diabetes Living in Rural Areas: A Systematic Literature Review

Diabetes, Other Diseases, and New Complications: Emerging Associations (JJ Nolan, Section Editor)

Nonalcoholic Fatty Liver Disease and Type 2 Diabetes: Common Pathophysiologic Mechanisms

Pathogenesis of Type 2 Diabetes and Insulin Resistance (RM Watanabe, Section Editor)

Does Nutrient Sensing Determine How We “See” Food?

Pharmacologic Treatment of Type 2 Diabetes (HE Lebovitz and G Bahtiyar, Section Editors)

Pathways in the Diagnosis and Management of Diabetic Polyneuropathy

Pathogenesis of Type 2 Diabetes and Insulin Resistance (RM Watanabe, Section Editor)

Ambient Air Pollution: An Emerging Risk Factor for Diabetes Mellitus

Pathogenesis of Type 2 Diabetes and Insulin Resistance (RM Watanabe, Section Editor)

β Cell Dysfunction Versus Insulin Resistance in the Pathogenesis of Type 2 Diabetes in East Asians

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.