Preserving insulin secretion in Type 2 diabetes mellitus

Expert Review of Endocrinology and Metabolism

Volumn 3, Issue 2, 2008, Pages 147-159

  Tibaldi, Joseph ^a  

^a FLUSHING HOSPITAL MEDICAL CENTER   (United States)

Author keywords

cell function; Bariatric surgery; Cytokine antagonists; Diabetes mellitus; dipeptidyl peptidase IV inhibitors; Incretin mimetics; Insulin; Insulin resistance; Insulin secretion; Potassium channel openers; Thiazolidinediones; Type 2 diabetes

Indexed keywords

6 CHLORO 3 (1 METHYLCYCLOPROPYLAMINO) 4H THIENO[3,2 E][1,2,4]THIADIAZINE 1,1 DIOXIDE; ADENOSINE TRIPHOSPHATE SENSITIVE POTASSIUM CHANNEL; ANGIOTENSIN RECEPTOR ANTAGONIST; ANTIDIABETIC AGENT; CYTOKINE RECEPTOR ANTAGONIST; DIAZOXIDE; DIPEPTIDYL CARBOXYPEPTIDASE INHIBITOR; DIPEPTIDYL PEPTIDASE IV INHIBITOR; EXENDIN 4; GLIBENCLAMIDE; GLIMEPIRIDE; GLITAZONE DERIVATIVE; GLUCAGON LIKE PEPTIDE 1; INCRETIN; INSULIN; INSULIN DERIVATIVE; LIRAGLUTIDE; METFORMIN; PIOGLITAZONE; PLACEBO; POTASSIUM CHANNEL STIMULATING AGENT; RECOMBINANT INTERLEUKIN 1 RECEPTOR BLOCKING AGENT; ROSIGLITAZONE; SITAGLIPTIN; TROGLITAZONE; UNCLASSIFIED DRUG; VILDAGLIPTIN;

BARIATRIC SURGERY; BEDTIME DOSAGE; BLOOD GLUCOSE MONITORING; CARDIOVASCULAR DISEASE; CELL ACTIVATION; CELL LOSS; CELL PROTECTION; CLINICAL TRIAL; CONTINUOUS INFUSION; DISEASE COURSE; DISEASE EXACERBATION; DRUG HALF LIFE; DRUG MECHANISM; DRUG RESPONSE; DRUG TREATMENT FAILURE; HUMAN; INSULIN RELEASE; INSULIN RESISTANCE; INSULIN SENSITIVITY; INSULIN TREATMENT; LIFESTYLE MODIFICATION; MONOTHERAPY; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; OBESITY; PANCREAS ISLET CELL FUNCTION; PATHOPHYSIOLOGY; PRIORITY JOURNAL; RENIN ANGIOTENSIN ALDOSTERONE SYSTEM; REVIEW; RISK FACTOR;

EID: 55649123198     PISSN: 17446651     EISSN: None     Source Type: Journal    
DOI: 10.1586/17446651.3.2.147     Document Type: Review

References (105)

1. King H, Aubert RE, Herman WH. Global burden of diabetes, 1995-2025: prevalence, numerical estimates, and projections. Diabetes Care 21, 1414-1431 (1998).
2. Bell GI, Polonsky KS. Diabetes mellitus and genetically programmed defects in β-cell function. Nature 414, 788-791 (2001).
3. Rolla A. The pathophysiological basis for intensive insulin replacement. Int. J. Obes. Relat. Metab. Disord. 28(Suppl. 2), S3-S7 (2004).
4. Boden G, Shulman GI. Free fatty acids in obesity and Type 2 diabetes: defining their role in the development of insulin resistance and β-cell dysfunction. Eur. J. Clin. Invest. 32, 14-33 (2002).
5. Kahn SE. The relative contributions of insulin resistance and β-cell dysfunction to the pathophysiology of Type 2 diabetes. Diabetologia 46, 3-19 (2003).
6. Holman RR. Assessing the potential for α-glucosidase inhibitors in prediabetic states. Diabetes Res. Clin. Pract. 40(Suppl.), S21-S25 (1998).
7. UK Prospective Diabetes Study Group. Effect of intensive blood-glucose control with metformin on complications in overweight patients with Type 2 diabetes. (UKPDS 34). Lancet 352, 854-865 (1998).
8. United Kingdom Prospective Diabetes Study (UKPDS) Group, Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with Type 2 diabetes (UKPDS 33). Lancet 352, 837-853 (1998).
9. Wajchenberg BL. β-cell failure in diabetes and preservation by clinical treatment. Endocr. Rev. 28, 187-218 (2007).
10. Katakura M, Komatsu M, Sato Y, Hashizume K, Aizawa T. Primacy of β-cell dysfunction in the development of hyperglycemia: a study in the Japanese general population. Metabolism 53, 949-953 (2004).
11. Jensen CC, Cnop M, Hull RL, Fujimoto WY, Kahn SE. β-cell function is a major contributor to oral glucose tolerance in high-risk relatives of four ethnic groups in the U.S. Diabetes 51, 2170-2178 (2002).
12. White MF. Insulin signaling in health and disease. Science 302, 1710-1711 (2003).
13. Saltiel AR, Kahn CR. Insulin signalling and the regulation of glucose and lipid metabolism. Nature 414, 799-806 (2001).
14. Pessin JE, Saltiel AR. Signaling pathways in insulin action: molecular targets of insulin resistance. J. Clin. Invest. 106, 165-169 (2000).
15. Weyer C, Bogardus C, Mott DM, Pratley RE. The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of Type 2 diabetes mellitus. J. Clin. Invest. 104, 787-794 (1999).
16. Levy J, Atkinson AB, Bell PM, McCance DR, Hadden DR. β-cell deterioration determines the onset and rate of progression of secondary dietary failure in Type 2 diabetes mellitus: the 10-year follow-up of the Belfast Diet Study. Diabet. Med. 15, 290-296 (1998).
17. Kloppel G, Lohr M, Habich K, Oberholzer M, Heitz PU. Islet pathology and the pathogenesis of Type 1 and Type 2 diabetes mellitus revisited. Surv. Synth. Pathol. Res. 4, 110-125 (1985).
18. Clark A, Wells CA, Buley ID et al. Islet amyloid, increased A-cells, reduced B-cells and exocrine fibrosis: quantitative changes in the pancreas in Type 2 diabetes. Diabetes Res. 9, 151-159 (1988).
19. Pick A, Clark J, Kubstrup C et al. Role of apoptosis in failure of β-cell mass compensation for insulin resistance and β-cell defects in the male Zucker diabetic fatty rat. Diabetes 47, 358-364 (1998).
20. Burks DJ, White MF. IRS proteins and β-cell function. Diabetes 50(Suppl. 1), S140-S145 (2001).
21. Rhodes CJ. Type 2 diabetes-a matter of β-cell life and death? Science 307, 380-384 (2005)
22. Vollenweider P, Menard B, Nicod P. Insulin resistance, defective insulin receptor substrate 2-associated phosphatidylinositol-3′ kinase activation, and impaired atypical protein kinase C (ζ/λ) activation in myotubes from obese patients with impaired glucose tolerance. Diabetes 51, 1052-1059 (2002).
23. Milburn JL Jr, Hirose H, Lee YH et al. Pancreatic β-cells in obesity. Evidence for induction of functional, morphologic, and metabolic abnormalities by increased long chain fatty acids. J. Biol. Chem. 270, 1295-1299 (1995).
24. Cockburn BN, Ostrega DM, Sturis J, Kubstrup C Polonsky KS, Bell GL Changes in pancreatic islet glucokinase and hexokinase activities with increasing age, obesity, and the onset of diabetes. Diabetes 46, 1434-1439 (1997).
25. Meece J. Pancreatic islet dysfunction in Type 2 diabetes: a rational target for incretin-based therapies. Curr. Med. Res. Opin. 23, 933-944 (2007).
26. Cavaghan MK, Ehrmann DA, Polonsky KS. Interactions between insulin resistance and insulin secretion in the development of glucose intolerance. J. Clin. Invest. 106, 329-333 (2000).
27. Weir GC, Bonner-Weir S. Five stages of evolving β-cell dysfunction during progression to diabetes. Diabetes 53(Suppl. 3), S16-S21 (2004).
28. Donath MY, Halban PA. Decreased β-cell mass in diabetes: significance, mechanisms and therapeutic implications. Diabetologia 47, 581-589 (2004).
29. Maedler K, Spinas GA, Lehmann R et al. Glucose induces β-cell apoptosis via upregulation of the Fas receptor in human islets. Diabetes 50, 1683-1690 (2001).
30. Robertson RP, Harmon J, Tran PO, Tanaka Y, Takahashi H. Glucose toxicity in β-cells: Type 2 diabetes, good radicals gone bad, and the glutathione connection. Diabetes 52, 581-587 (2003).
31. Kajimoto Y, Matsuoka T, Kaneto H et al. Induction of glycation suppresses glucokinase gene expression in HIT-T15 cells. Diabetologia 42, 1417-1424 (1999).
32. Kaneto H, Katakami N, Kawamori D et al. Involvement of oxidative stress in the pathogenesis of diabetes. Antiox. Redox Signal. 9, 355-366 (2007).
33. Hirsch IB, Brownlee M. Should minimal blood glucose variability become the gold standard of glycemic control? J. Diabetes Complication 19, 178-181 (2005).
34. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature 414, 813-820 (2001).
35. Shimabukuro M, Zhou YT, Levi M, Unger RH. Fatty acid-induced β cell apoptosis: a link between obesity and diabetes. Proc. Natl Acad. Sci. USA 95, 2498-2502 (1998).
36. Maedler K, Carr RD, Bosco D, Zuellig RA, Berney T, Donath MY. Sulfonylurea induced β-cell apoptosis in cultured human islets. J. Clin. Endocrinol. Metab. 90, 501-506 (2005).
37. Kolb H, Mandrup-Poulsen T. An immune origin of Type 2 diabetes? Diabetologia 48, 1038-1050 (2005).
38. Pacini G, Mari A. Methods for clinical assessment of insulin sensitivity and β-cell function. Best Pract. Res. Clin. Endocrinol. Metab. 17, 305-322 (2003).
39. Mykkanen L, Haffner SM, Hales CN, Ronnemaa T, Laakso M. The relation of proinsulin, insulin, and proinsulin-to-insulin ratio to insulin sensitivity and acute insulin response in normoglycemic subjects. Diabetes 46, 1990-1995 (1997).
40. Bell DS, Ovalle F. The role oF C-peptide levels in screening for latent autoimmune diabetes in adults. Am. J. Ther. 11, 308-311 (2004).
41. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Teacher DF, Turner RC. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 28, 412-419 (1985).
42. Wallace TM, Levy JC, Matthews DR. Use and abuse of HOMA modeling. Diabetes Care 27, 1487-1495 (2004).
43. Song Y, Manson JE, Tinker L et al. Insulin sensitivity and insulin secretion determined by the homeostasis model assessment (HOMA) and risk of diabetes mellitus in a multi-ethnic cohort of women: the Women's Health Initiative Observational Study. Diabetes Care 30, 1747-1752 (2007).
44. Sarafidis PA, Lasaridis AN, Nilsson PM et al. Validity and reproducibility of HOMA-IR, I/HOMA-IR, QUICKI and McAuley's indices in patients with hypertension and Type II diabetes. J. Hum. Hypertens. 21, 709-716 (2007).
45. Cavaghan MK, Ehrmann DA, Byrne MM, Polonsky KS. Treatment with the oral antidiabetic agent troglitazone improves β cell responses to glucose in subjects with impaired glucose tolerance. J. Clin. Invest. 100, 530-537 (1997).
46. Pontiroli AE, Pizzocri P, Caumo A, Perseghin G, Luzi L. Evaluation of insulin release and insulin sensitivity through oral glucose tolerance test: differences between NGT, IFG, IGT, and Type 2 diabetes mellitus. A cross-sectional and follow-up study. Acta Diabetol. 41, 70-76 (2004).
47. Stumvoll M, Mitrakou A, Pimenta W et al. Use of the oral glucose tolerance test to assess insulin release and insulin sensitivity. Diabetes Care 23, 295-301 (2000).
48. Tripathy D, Carlsson M, Almgren P et al. Insulin secretion and insulin sensitivity in relation to glucose tolerance: lessons from the Botnia Study. Diabetes 49, 975-980 (2000).
49. Guerrero-Romero F, Rodriguez-Moran M. Assessing progression to impaired glucose tolerance and Type 2 diabetes mellitus. Eur. J. Clin. Invest. 36, 796-802 (2006).
50. Shim WS, Kim SK, Kim HJ et al. Decrement of postprandial insulin secretion determines the progressive nature of Type-2 diabetes. Eur. J. Endocrinol. 155, 615-622 (2006).
51. American Association of Clinical Endocrinologists. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the management of diabetes mellitus. Endocr. Pract. 13(Suppl. 1), 4-68 (2007).
52. Tseng YH, Ueki K, Kriauciunas KM, Kahn CR. Differential roles of insulin receptor substrates in the anti-apoptotic function of insulin-like growth factor-1 and insulin. J. Biol. Chem. 277, 31601-31611 (2002).
53. Hennige AM, Ozcan U, Okada T et al. Alterations in growth and apoptosis of insulin receptor substrate-1 -deficient β-cells. Am. J. Physiol. Endocrinol. Metab. 289, E337-E346 (2005).
54. Dandona P, Chaudhuri A, Ghanim H, Mohanty P. Proinflammatory effects of glucose and anti-inflammatory effect of insulin: relevance to cardiovascular disease. Am. J. Cardiol. 99, 15B-26B (2007).
55. Dandona P, Chaudhuri A, Mohanty P, Ghanim H. Anti-inflammatory effects of insulin. Curr. Opin. Clin. Nutr. Metab. Care 10, 511-517 (2007).
56. Garvey WT, Olefsky JM, Griffin J, Hamman RF, Kolterman OG. The effect of insulin treatment on insulin secretion and insulin action in Type II diabetes mellitus. Diabetes 34, 222-234 (1985).
57. Gormley MJ, Hadden DR, Woods R, Sheridan B, Andrews WJ. One month's insulin treatment of Type II diabetes: the early and medium-term effects following insulin withdrawal. Metabolism 35, 1029-1036 (1986).
58. Ryan EA, Imes S, Wallace C. Short-term intensive insulin therapy in newly diagnosed Type 2 diabetes. Diabetes Care 27, 1028-1032 (2004).
59. Shichiri M, Kishikawa H, Ohkubo Y, Wake N. Long-term results of the Kumamoto Study on optimal diabetes control in Type 2 diabetic patients. Diabetes Care 23(Suppl. 2), B21-B29 (2000).
60. Alvarsson M, Sundkvist G, Lager I et al. Beneficial effects of insulin versus sulphonylurea on insulin secretion and metabolic control in recently diagnosed Type 2 diabetic patients. Diabetes Care 26, 2231-2237 (2003).
61. Li Y, Xu W, Liao Z et al. Induction of long-term glycemic control in newly diagnosed Type 2 diabetic patients is associated with improvement of β-cell function. Diabetes Care 27, 2597-2602 (2004).
62. Ilkova H, Glaser B, Tunckale A, Bagriacik N, Cerasi E. Induction of long-term glycemic control in newly diagnosed Type 2 diabetic patients by transient intensive insulin treatment. Diabetes Care 20, 1353-1356 (1997).
63. Ovalle F, Bell DS. Effect of rosiglitazone versus insulin on the pancreatic β-cell function of subjects with Type 2 diabetes. Diabetes Care 27, 2585-2589 (2004).
64. Diabetes Prevention Program Research Group. Reduction in the incidence of Type 2 diabetes with lifestyle intervention or metformin. N. Engl. J. Med. 346, 393-403 (2002).
65. Kitabchi AE, Temprosa M, Knowler WC et al. Role of insulin secretion and sensitivity in the evolution of Type 2 diabetes in the diabetes prevention program: effects of lifestyle intervention and metformin. Diabetes 54, 2404-2414 (2005).
66. Lebovitz HE, Dole JF, Patwardhan R, Rappaport EB, Freed MI. Rosiglitazone monotherapy is effective in patients with Type 2 diabetes. J. Clin. Endocrinol. Metab. 86, 280-288 (2001).
67. Einhorn D, Rendell M, Rosenzweig J, Egan JW, Mathisen AL, Schneider RL. Pioglitazone hydrochloride in combination with metformin in the treatment of Type 2 diabetes mellitus: a randomized, placebo-controlled study. The Pioglitazone 027 Study Group. Clin. Ther. 22, 1395-1409 (2000).
68. Rosenblatt S, Miskin B, Glazer NB, Prince MJ, Robertson KE. The impact of pioglitazone on glycemic control and atherogenic dyslipidemia in patients with Type 2 diabetes mellitus. Coron. Artery. Dis. 12, 413-423 (2001).
69. Durbin RJ. Thiazolidinedione therapy in the prevention/delay of Type 2 diabetes in patients with impaired glucose tolerance and insulin resistance. Diabetes Obes. Metab. 6, 280-285 (2004).
70. Rosen CJ. The rosiglitazone story - lessons from an FDA Advisory Committee meeting. N. Engl. J. Med. 357, 844-846 (2007).
71. Kahn SE, Haffner SM, Heise MA et al. Glycemic durability of rosiglitazone, metformin, or glyburide monotherapy. N. Engl. J. Med. 355, 2427-2443 (2006).
72. Li J, Tian H, Li Q et al. Improvement of insulin sensitivity and β-cell function by nateglinide and repaglinide in Type 2 diabetic patients: a randomized controlled double-blind and double-dummy multicentre clinical trial. Diabetes Obes. Metab. 9, 558-565 (2007).
73. Mari A, Gastaldelli A, Foley JE, Pratley RE, Ferrannini E. β-cell function in mild Type 2 diabetic patients: effects of 6-months glucose lowering with nateglinide. Diabetes Care 28, 1132-1138 (2005).
74. Takahashi A, Nagashima K, Hamasaki A et al. Sulfonylurea and glinide reduce insulin content, functional expression of K(ATP) channels, and accelerate apoptotic β-cell death in the chronic phase. Diabetes Res. Clin. Pract. 77, 343-350 (2007).
75. Chiasson JL, Brindisi MC, Rabasa-Lhoret R. The prevention of Type 2 diabetes: what is the evidence? Minerva Endocrinologica 30, 179-191 (2005).
76. Drucker DJ. Glucagon-like peptides: regulators of cell proliferation, differentiation, and apoptosis. Mol. Endocrinol. 17, 161-171 (2003).
77. Hui H, Nourparvar A, Zhao X, Perfetti R. Glucagon-like peptide-1 inhibits apoptosis of insulin-secreting cells via a cyclic 5′-adenosine monophosphate-dependent protein kinase A- and a phosphatidylinositol 3-kinase-dependent pathway. Endocrinology 144, 1444-1455 (2003).
78. Li Y, Hansotia T, Yusta B, Ris Halban PA, Drucker DJ. Glucagon-like peptide-1 receptor signaling modulates β cell apoptosis. J. Biol. Chem. 278, 471-478 (2003).
79. Fehse F, Trautmann M, Holst JJ et al. Exenatide augments first- and second-phase insulin secretion in response to intravenous glucose in subjects with Type 2 diabetes. J. Clin. Endocrinol. Metab. 90, 5991-5997 (2005).
80. Mari A, Degn K, Brock B, Rungby J, Ferrannini E, Schmitz O. Characterization of β-cell function improvement by liraglutide: modeling analysis of 24-h tests. Diabetes 55, A124 (2006).
81. Zinman B, Hoogwerf BJ, Duran GS et al. The effect of adding exenatide to a thiazolidinedione in suboptimally controlled Type 2 diabetes: a randomized trial. Ann. Intern. Med. 146, 477-485 (2007).
82. Buse JB, Klonoff DC, Nielsen LI et al. Metabolic effects of two years of exenatide treatment on diabetes, obesity, and hepatic biomarkers in patients with Type 2 diabetes: an interim analysis of data from the open-label, uncontrolled extension of three double-blind, placebo-controlled trials. Clin. Ther. 29, 139-153 (2007).
83. Sturis J, Gotfredsen CF, Romer J et al. GLP-1 derivative liraglutide in rats with β-cell deficiencies: influence of metabolic state on β-cell mass dynamics. Br. J. Pharmacol. 140, 123-132 (2003).
84. Rolin B, Larsen MO, Gotfredsen CF et al. The long-acting GLP-1 derivative NN2211 ameliorates glycemia and increases β-cell mass in diabetic mice. Am. J. Physiol. Endocrinol. Metab. 283, E745-E752 (2002).
85. Bregenholt S, Moldrup A, Blume N et al. The long-acting glucagon-like peptide-1 analogue, liraglutide, inhibits β-cell apoptosis in vitro. Biochem. Biophys. Res. Commun. 330, 577-584 (2005).
86. Degn KB, Juhl CB, Sturis J et al. One week's treatment with the long-acting glucagon-like peptide 1 derivative liraglutide (NN2211) markedly improves 24-h glycemia and α-and β-cell function and reduces endogenous glucose release in patients with Type 2 diabetes. Diabetes 53, 1187-1194 (2004).
87. Chang AM, Jakobsen G, Sturis J et al. The GLP-1 derivative NN2211 restores β-cell sensitivity to glucose in Type 2 diabetic patients after a single dose. Diabetes 52, 1786-1791 (2003).
88. Mari A, Sallas WM, He YL et al. Vildagliptin, a dipeptidyl peptidase-IV inhibitor, improves model-assessed β-cell function in patients with Type 2 diabetes. J. Clin. Endocrinol. Metab. 90, 4888-4894 (2005).
89. Aschner P, Kipnes MS, Lunceford JK, Sanchez M, Mickel C, Williams-Herman DE. Effect of the dipeptidyl peptidase-4 inhibitor sitagliptin as monotherapy on glycemic control in patients with Type 2 diabetes. Diabetes Care 29, 2632-2637 (2006).
90. Williams-Herman D, Xu L. Initial combination therapy with sitagliptin, a selective DPP-4 inhibitor, and metformin leads to marked improvement in β-cell function in patients with Type 2 diabetes. Diabetes 56, A142 (2007).
91. Utzschneider KM, Tong J, Udayasankar J. The dipeptidyl peptidase-4 (DPP-4) vildaglitin improves insulin sensitivity and B-cell function in subjects with impaired fasting glucose. Diabetes 56, A137 (2007).
92. Andraws R, Brown DL. Effect of inhibition of the renin-angiotensin system on development of Type 2 diabetes mellitus (meta-analysis of randomized trials). Am. J. Cardiol. 99, 1006-1012 (2007).
93. Jandeleit-Dahm KA, Tikellis C, Reid CM, Johnston CI, Cooper ME. Why blockade of the renin-angiotensin system reduces the incidence of new-onset diabetes. J. Hypertens. 23, 463-473 (2005).
94. Scheen AJ. Prevention of Type 2 diabetes mellitus through inhibition of the renin-angiotensin system. Drugs 64, 2537-2565 (2004).
95. Leung PS. Mechanisms of protective effects induced by blockade of the renin-angiotensin system: novel role of the pancreatic islet angiotensin-generating system in Type 2 diabetes. Diabet. Med. 24, 110-116 (2007).
96. Larsen CM, Faulenbach M, Vaag A et al. Interleukin-1-receptor antagonist in Type 2 diabetes mellitus. N. Engl. J. Med. 356, 1517-1526 (2007).
97. Meneghini LF. Impact of bariatric surgery on Type 2 diabetes. Cell. Biochem. Biophys. 48, 97-102 (2007).
98. Dixon JB, O'Brien PE. Health outcomes of severely obese Type 2 diabetic subjects 1 year after laparoscopic adjustable gastric banding. Diabetes Care 25, 358-363 (2002).
99. Polyzogopoulou EV, Kalfarentzos F, Vagenakis AG, Alexandrides TK. Restoration of euglycemia and normal acute insulin response to glucose in obese subjects with Type 2 diabetes following bariatric surgery. Diabetes 52, 1098-1103 (2003).
100. Hickey MS, Pories WJ, MacDonald KG Jr et al. A new paradigm for Type 2 diabetes mellitus: could it be a disease of the foregut? Ann. Surg. 227, 637-643 (1998).
101. Miholic J, Orskov C, Holst JJ, Kotzerke J, Meyer HJ. Emptying of the gastric substitute, glucagon-like peptide-1 (GLP-1), and reactive hypoglycemia after total gastrectomy. Dig. Dis. Sci. 36, 1361-1370 (1991).
102. Gebhard B, Holst JJ, Biegelmayer C, Miholic J. Postprandial GLP-1, norepinephrine, and reactive hypoglycemia in dumping syndrome. Dig. Dis. Sci. 46, 1915-1923 (2001).
103. Bjork E, Berne C, Kampe O, Wibell L, Oskarsson P, Karlsson FA. Diazoxide treatment at onset preserves residual insulin secretion in adults with autoimmune diabetes. Diabetes 45, 1427-1430 (1996).
104. Ortqvist E, Bjork E, Waliensteen M et al. Temporary preservation of β-cell function by diazoxide treatment in childhood Type 1 diabetes. Diabetes Care 27, 2191-2197 (2004).
105. Nathan DM, Buse JB, Davidson MB et al. Management of hyperglycemia in Type 2 diabetes: a consensus algorithm for the initiation and adjustment of therapy. A consensus statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care 29, 1963-1972 (2006).