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Glucose Intolerance Treatment & Management

  • Author: Samuel T Olatunbosun, MD, FACP, FACE; Chief Editor: George T Griffing, MD  more...
 
Updated: Sep 14, 2015
 

Approach Considerations

Routine evaluation in an ambulatory setting is feasible for most patients. Patients with acute decompensation due to glucose intolerance or any related disorders may require inpatient care.[39] A major goal in the management of glucose intolerance is glycemic control.

Of note is the novel treatment with DPP-4–resistant GLP-1 receptor agonists, such as exenatide and liraglutide, which are incretin mimetics, as well as with the DPP-4 inhibitors sitagliptin and vildagliptin.[40, 41, 42] Exenatide may be effective in preventing steroid-induced glucose intolerance through suppression.[43]

Both strategies have been successful in clinical studies. Liraglutide was approved by the FDA in January 2010 for monotherapy, as a second-line treatment and in combination with oral agents. The mechanisms of action of incretin mimetics include stimulation of insulin secretion in response to nutrient intake, inhibition of glucagon secretion, delay of gastric emptying, and induction of early satiety. Other benefits include preservation of beta cell mass and improvement of secretory function. The advantages of the DPP-IV inhibitors include oral availability, good tolerability, and weight neutrality.

Amylin has several glucoregulatory effects that complement those of insulin in postprandial glucose regulation; thus, mealtime amylin administration may be adjunctive to mealtime insulin replacement and may facilitate improvement of postprandial and overall glycemic control in patients with type 1 or type 2 diabetes. Naturally occurring human amylin is unsuitable for clinical use because of several physicochemical properties, however; pramlintide acetate contains an amylin analogue without those limitations.[44, 45, 46, 47, 48, 49]

All patients with type 1 diabetes are insulin-dependent. Treatment of severe hyperglycemia during acute decompensation in a patient with type 2 diabetes may reverse the state of glucose toxicity, further improving secretory function of beta cells in the pancreas. Type 2 diabetes can be treated effectively with oral hypoglycemic drugs, with or without the addition of insulin. The natural history of type 2 diabetes is that of progressive beta-cell deterioration, secondary failure of oral agents, and the subsequent need for insulin therapy.

Gestational diabetes mellitus is treated with insulin and/or with lifestyle change. Oral agents are contraindicated in pregnancy.

With regard to the management of impaired glucose tolerance, the current approach is aggressive lifestyle modification. The results of the Diabetes Prevention Program showed that metformin therapy and intensive lifestyle intervention reduced the risk of developing type 1 and type 2 diabetes by 31% and 58% respectively, compared with placebo, in individuals with impaired glucose tolerance.[50] The Study to Prevent Non-Insulin–Dependent Diabetes Mellitus Trial demonstrated a 25% relative risk reduction in the development of diabetes, and an associated reduction in hypertension (34%) and cardiovascular events (49%).[51]

Orlistat may be beneficial in the context of obesity.[52]

For more information, see Diabetes Mellitus, Type 1 and Diabetes Mellitus, Type 2.

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Lifestyle Modification

Intensive lifestyle modification has been shown to effectively delay or prevent diabetes in a cost-effective manner.[53, 52, 54] Nonpharmacologic therapy and lifestyle modification include the following:

  • Diet 
  • Exercise
  • Counseling related to smoking cessation and alcohol intake
  • Reversing drug-related, iatrogenic causation of glucose intolerance
  • Substituting or adding agents that do not adversely affect glucose tolerance; reducing dosage of offending drugs
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Pharmacologic Therapy

Pharmacologic therapy may be required in the following situations:[55]

  • Fasting glucose more than 126 mg/dL, postprandial glucose more than 160 mg/dL, or glycosylated hemoglobin (HbA1c) more than 7%
  • Hyperglycemia (a significant risk factor in development of vascular complications)

In addition to lifestyle counseling, metformin therapy for prevention of type 2 diabetes may be considered in those with IGT, IFG, or HBA1C 5.7–6.4%, especially for those with BMI greater than 35 kg/m2, age younger than 60 years, and in women with prior GDM, according to the ADA.[1]

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Bariatric Surgery

Bariatric surgery should be considered in a patient with type 2 diabetes who has a BMI of more than 35 kg/m2, especially if glycemic control with lifestyle and pharmacotherapy is difficult.[1]  Surgically induced weight loss may result in improvements in insulin sensitivity and beta cell function, as well as changes in gut hormones.[56, 57] Better diabetic control or complete resolution of the disease (64-93%) is the end result.

A bariatric procedure is not currently recommended in the management of IGT or IFG; however, glucose intolerance resolved in 99-100% of cases of patients who underwent bariatric surgery for a comorbid state that required such an intervention (eg, class 3 obesity).

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Nutritional Therapy

Medical nutritional therapy should be guided by the American Dietetic Association recommendations and individualized by weight and height, level of physical activity, and requirements for calories and nutrients.[58]

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Physical Activity

A high level of physical activity is desirable, as appropriate to the patient's ability and general health. Most patients benefit from carefully planned exercise programs tailored to individual needs.

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Long-term Monitoring

Long-term monitoring of affected patients includes ensuring medication compliance, identifying adverse effects, blood glucose and HbA1c monitoring, dietary consultations and measures, and exercise management.

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Long-Term Monitoring

Long-term support and medical monitoring are still important after a bariatric procedure. Various complications, including postprandial hyperinsulinemic hypoglycemia, have been reported following gastric bypass surgery.

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Contributor Information and Disclosures
Author

Samuel T Olatunbosun, MD, FACP, FACE Endocrinology Service, SAMMC/59th Medical Wing and Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine

Samuel T Olatunbosun, MD, FACP, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, American Diabetes Association, Endocrine Society, American College of Physicians-American Society of Internal Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Acknowledgements

Samuel Dagogo-Jack, MD, MBBS, MSc, FRCP Professor of Medicine, Program Director, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center

Samuel Dagogo-Jack, MD, MBBS, MSc, FRCP is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Royal College of Physicians, and The Endocrine Society

Disclosure: Eli Lilly None Speaking and teaching; GlaxoSmithKline None Speaking and teaching; Merck None Speaking and teaching

David S Schade, MD Chief, Division of Endocrinology and Metabolism, Professor, Department of Internal Medicine, University of New Mexico School of Medicine and Health Sciences Center

David S Schade, MD is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, New Mexico Medical Society, New York Academy of Sciences, and Society for Experimental Biology and Medicine

Disclosure: Nothing to disclose.

Don S Schalch, MD Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics

Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. American Diabetes Association. Standards of medical care in diabetes--2015: summary of revisions. Diabetes Care. 2015 Jan. 38 Suppl:S4. [Medline].

  2. Buchanan TA, Xiang AH. Gestational diabetes mellitus. J Clin Invest. 2005 Mar. 115(3):485-91. [Medline]. [Full Text].

  3. Cooper DH, Krainik AJ, Lubner SJ, et al, eds. The Washington Manual of Medical Therapeutics. Philadelphia, Pa: Lippincott Williams & Wilkins; 2007.

  4. Fauci AS, Braunwald E, Kasper DL, et al, eds. Harrison's Principles of Internal Medicine. 17th ed. New York, NY: McGraw-Hill; 2008.

  5. Corpeleijn E, Mensink M, Kooi ME, Roekaerts PM, Saris WH, Blaak EE. Impaired skeletal muscle substrate oxidation in glucose-intolerant men improves after weight loss. Obesity (Silver Spring). 2008 May. 16(5):1025-32. [Medline].

  6. DeFronzo RA. Pathogenesis of type 2 diabetes mellitus. Med Clin North Am. 2004 Jul. 88(4):787-835, ix. [Medline].

  7. Dagogo-Jack S, Santiago JV. Pathophysiology of type 2 diabetes and modes of action of therapeutic interventions. Arch Intern Med. 1997 Sep 8. 157(16):1802-17. [Medline].

  8. Sjöström L. Analysis of the XENDOS study (Xenical in the Prevention of Diabetes in Obese Subjects). Endocr Pract. 2006 Jan-Feb. 12 Suppl 1:31-3. [Medline].

  9. Li CL, Chen SY, Lan C, Pan WH, Chou HC, Bai YB, et al. The effects of physical activity, body mass index (BMI) and waist circumference (WC) on glucose intolerance in older people: A nationwide study from Taiwan. Arch Gerontol Geriatr. 2010 Mar 3. [Medline].

  10. Ko GT, So WY, Tong P, Ma RC, Kong AP, Ozaki R, et al. Hypoadiponectinaemia enhances waist circumference as a predictor of glucose intolerance and clustering of risk factors in Chinese men. Diabetes Metab. 2010 Jun. 36(3):192-7. [Medline].

  11. Vella A, Camilleri M, Rizza RA. The gastrointestinal tract and glucose tolerance. Curr Opin Clin Nutr Metab Care. 2004 Jul. 7(4):479-84. [Medline].

  12. Joy SV, Rodgers PT, Scates AC. Incretin mimetics as emerging treatments for type 2 diabetes. Ann Pharmacother. 2005 Jan. 39(1):110-8. [Medline].

  13. Ahrén B. [New strategy in type 2 diabetes tested in clinical trials. Glucagon-like peptide 1 (GLP-1) affects basic caused of the disease]. Lakartidningen. 2005 Feb 21-27. 102(8):545-9. [Medline].

  14. Bock G, Dalla Man C, Campioni M, Chittilapilly E, Basu R, Toffolo G, et al. Pathogenesis of pre-diabetes: mechanisms of fasting and postprandial hyperglycemia in people with impaired fasting glucose and/or impaired glucose tolerance. Diabetes. 2006 Dec. 55(12):3536-49. [Medline]. [Full Text].

  15. Cowie CC, Rust KF, Byrd-Holt DD, et al. Prevalence of diabetes and impaired fasting glucose in adults in the U.S. population: National Health And Nutrition Examination Survey 1999-2002. Diabetes Care. 2006 Jun. 29(6):1263-8. [Medline]. [Full Text].

  16. Harris MI, Flegal KM, Cowie CC, Eberhardt MS, Goldstein DE, Little RR, et al. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988-1994. Diabetes Care. 1998 Apr. 21(4):518-24. [Medline]. [Full Text].

  17. King H, Rewers M. Global estimates for prevalence of diabetes mellitus and impaired glucose tolerance in adults. WHO Ad Hoc Diabetes Reporting Group. Diabetes Care. 1993 Jan. 16(1):157-77. [Medline].

  18. Diabetes mellitus. Report of a WHO Study Group. World Health Organ Tech Rep Ser. 1985. 727:1-113. [Medline].

  19. Gerich JE. Postprandial hyperglycemia and cardiovascular disease. Endocr Pract. 2006 Jan-Feb. 12 Suppl 1:47-51. [Medline].

  20. Nissen SE, Wolski K. Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes. N Engl J Med. 2007 Jun 14. 356(24):2457-71. [Medline]. [Full Text].

  21. Reaven GM. Insulin resistance and its consequences: non-insulin-dependent diabetes mellitus and coronary heart disease. Leroith D, ed. Diabetes Mellitus: A Fundamental and Clinical Text. Philadelphia, Pa: Lippincott-Raven; 1996. 509-19.

  22. Tai ES, Goh SY, Lee JJ, Wong MS, Heng D, Hughes K, et al. Lowering the criterion for impaired fasting glucose: impact on disease prevalence and associated risk of diabetes and ischemic heart disease. Diabetes Care. 2004 Jul. 27(7):1728-34. [Medline]. [Full Text].

  23. Tam WH, Ma RC, Yang X, Li AM, Ko GT, Kong AP, et al. Glucose intolerance and cardiometabolic risk in adolescents exposed to maternal gestational diabetes: a 15-year follow-up study. Diabetes Care. 2010 Jun. 33(6):1382-4. [Medline]. [Full Text].

  24. Franks PW, Hanson RL, Knowler WC, Sievers ML, Bennett PH, Looker HC. Childhood obesity, other cardiovascular risk factors, and premature death. N Engl J Med. 2010 Feb 11. 362(6):485-93. [Medline].

  25. Kakad R, Anwar A, Dyer P, Webber J, Dale J. Fasting plasma glucose is not sufficient to detect ongoing glucose intolerance after pregnancy complicated by gestational diabetes. Exp Clin Endocrinol Diabetes. 2010 Apr. 118(4):234-6. [Medline].

  26. Alberti KG. Impaired glucose tolerance: what are the clinical implications?. Diabetes Res Clin Pract. 1998 Jul. 40 Suppl:S3-8. [Medline].

  27. Blake DR, Meigs JB, Muller DC, Najjar SS, Andres R, Nathan DM. Impaired glucose tolerance, but not impaired fasting glucose, is associated with increased levels of coronary heart disease risk factors: results from the Baltimore Longitudinal Study on Aging. Diabetes. 2004 Aug. 53(8):2095-100. [Medline].

  28. Festa A, D'Agostino R Jr, Hanley AJ, Karter AJ, Saad MF, Haffner SM. Differences in insulin resistance in nondiabetic subjects with isolated impaired glucose tolerance or isolated impaired fasting glucose. Diabetes. 2004 Jun. 53(6):1549-55. [Medline].

  29. Olatunbosun ST. Diagnosis and follow-up of subjects with impaired glucose tolerance: how reliable is OGTT? Report from a Nigerian survey. Diabetes Res Clin Pract. 1998 Aug. 41(2):147-8. [Medline].

  30. Singleton JR, Smith AG, Russell JW, Feldman EL. Microvascular complications of impaired glucose tolerance. Diabetes. 2003 Dec. 52 (12):2867-73. [Medline].

  31. Grundy SM. Pre-diabetes, metabolic syndrome, and cardiovascular risk. J Am Coll Cardiol. 2012 Feb 14. 59 (7):635-43. [Medline].

  32. Faerch K, Vaag A, Holst JJ, Glümer C, Pedersen O, Borch-Johnsen K. Impaired fasting glycaemia vs impaired glucose tolerance: similar impairment of pancreatic alpha and beta cell function but differential roles of incretin hormones and insulin action. Diabetologia. 2008 May. 51(5):853-61. [Medline].

  33. Nathan DM, Davidson MB, DeFronzo RA, Heine RJ, Henry RR, Pratley R, et al. Impaired fasting glucose and impaired glucose tolerance: implications for care. Diabetes Care. 2007 Mar. 30(3):753-9. [Medline].

  34. HAPO Study Cooperative Research Group, Metzger BE, Lowe LP, Dyer AR, Trimble ER, Chaovarindr U, et al. Hyperglycemia and adverse pregnancy outcomes. N Engl J Med. 2008 May 8. 358 (19):1991-2002. [Medline].

  35. Committee on Practice Bulletins--Obstetrics. Practice Bulletin No. 137: Gestational diabetes mellitus. Obstet Gynecol. 2013 Aug. 122 (2 Pt 1):406-16. [Medline].

  36. Bersoux S, Cook CB, Wu Q, et al. Hemoglobin a1c testing alone does not sufficiently identify patients with prediabetes. Am J Clin Pathol. 2011 May. 135(5):674-7. [Medline].

  37. Einhorn D, Reaven GM, Cobin RH, Ford E, Ganda OP, Handelsman Y, et al. American College of Endocrinology position statement on the insulin resistance syndrome. Endocr Pract. 2003 May-Jun. 9(3):237-52. [Medline].

  38. Flier JS. Syndromes of insulin resistance. Becker KL, ed. Principles and Practice of Endocrinology and Metabolism. 2nd ed. Philadelphia, Pa: Lippincott; 1249-59.

  39. American Diabetes Association. Standards of medical care in diabetes--2008. Diabetes Care. 2008 Jan. 31 Suppl 1:S12-54. [Medline].

  40. Pham DQ, Nogid A, Plakogiannis R. Sitagliptin: a novel agent for the management of type 2 diabetes mellitus. Am J Health Syst Pharm. 2008 Mar 15. 65(6):521-31. [Medline].

  41. Mest HJ, Mentlein R. Dipeptidyl peptidase inhibitors as new drugs for the treatment of type 2 diabetes. Diabetologia. 2005 Apr. 48(4):616-20. [Medline].

  42. Ahrén B, Schmitz O. GLP-1 receptor agonists and DPP-4 inhibitors in the treatment of type 2 diabetes. Horm Metab Res. 2004 Nov-Dec. 36(11-12):867-76. [Medline].

  43. van Raalte DH, van Genugten RE, Linssen MM, Ouwens DM, Diamant M. Glucagon-like peptide-1 receptor agonist treatment prevents glucocorticoid-induced glucose intolerance and islet-cell dysfunction in humans. Diabetes Care. 2011 Feb. 34(2):412-7. [Medline]. [Full Text].

  44. Ceriello A, Piconi L, Quagliaro L, et al. Effects of pramlintide on postprandial glucose excursions and measures of oxidative stress in patients with type 1 diabetes. Diabetes Care. 2005 Mar. 28(3):632-7. [Medline].

  45. Hollander P, Ratner R, Fineman M, Strobel S, Shen L, Maggs D, et al. Addition of pramlintide to insulin therapy lowers HbA1c in conjunction with weight loss in patients with type 2 diabetes approaching glycaemic targets. Diabetes Obes Metab. 2003 Nov. 5(6):408-14. [Medline].

  46. Ratner RE, Dickey R, Fineman M, Maggs DG, Shen L, Strobel SA, et al. Amylin replacement with pramlintide as an adjunct to insulin therapy improves long-term glycaemic and weight control in Type 1 diabetes mellitus: a 1-year, randomized controlled trial. Diabet Med. 2004 Nov. 21(11):1204-12. [Medline].

  47. Riddle M, Frias J, Zhang B, Maier H, Brown C, Lutz K, et al. Pramlintide improved glycemic control and reduced weight in patients with type 2 diabetes using basal insulin. Diabetes Care. 2007 Nov. 30(11):2794-9. [Medline].

  48. Weyer C, Fineman MS, Strobel S, Shen L, Data J, Kolterman OG, et al. Properties of pramlintide and insulin upon mixing. Am J Health Syst Pharm. 2005 Apr 15. 62(8):816-22. [Medline].

  49. Wysham C, Lush C, Zhang B, Maier H, Wilhelm K. Effect of pramlintide as an adjunct to basal insulin on markers of cardiovascular risk in patients with type 2 diabetes. Curr Med Res Opin. 2008 Jan. 24(1):79-85. [Medline].

  50. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. 1997 Jul. 20(7):1183-97. [Medline].

  51. Chiasson JL. Acarbose for the prevention of diabetes, hypertension, and cardiovascular disease in subjects with impaired glucose tolerance: the Study to Prevent Non-Insulin-Dependent Diabetes Mellitus (STOP-NIDDM) Trial. Endocr Pract. 2006 Jan-Feb. 12 Suppl 1:25-30. [Medline].

  52. Gillies CL, Abrams KR, Lambert PC, Cooper NJ, Sutton AJ, Hsu RT, et al. Pharmacological and lifestyle interventions to prevent or delay type 2 diabetes in people with impaired glucose tolerance: systematic review and meta-analysis. BMJ. 2007 Feb 10. 334(7588):299. [Medline]. [Full Text].

  53. Bourn DM, Mann JI, McSkimming BJ, Waldron MA, Wishart JD. Impaired glucose tolerance and NIDDM: does a lifestyle intervention program have an effect?. Diabetes Care. 1994 Nov. 17(11):1311-9. [Medline].

  54. Herman WH, Hoerger TJ, Brandle M, Hicks K, Sorensen S, Zhang P, et al. The cost-effectiveness of lifestyle modification or metformin in preventing type 2 diabetes in adults with impaired glucose tolerance. Ann Intern Med. 2005 Mar 1. 142(5):323-32. [Medline]. [Full Text].

  55. DeFronzo RA. Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med. 1999 Aug 17. 131(4):281-303. [Medline].

  56. Meneghini LF. Impact of bariatric surgery on type 2 diabetes. Cell Biochem Biophys. 2007. 48(2-3):97-102. [Medline].

  57. Hofsø D, Jenssen T, Bollerslev J, Ueland T, Godang K, Stumvoll M, et al. Beta cell function after weight loss: a clinical trial comparing gastric bypass surgery and intensive lifestyle intervention. Eur J Endocrinol. 2011 Feb. 164(2):231-8. [Medline]. [Full Text].

  58. Du H, van der A DL, van Bakel MM, et al. Glycemic index and glycemic load in relation to food and nutrient intake and metabolic risk factors in a Dutch population. Am J Clin Nutr. 2008 Mar. 87(3):655-61. [Medline].

  59. Diamant M, Bunck MC, Heine RJ. [Analogs of glucagon-like peptide-1 (GLP-1): an old concept as a new treatment of patients with diabetes mellitus type 2]. Ned Tijdschr Geneeskd. 2004 Sep 25. 148(39):1912-7. [Medline].

  60. UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study (UKPDS) Group. Lancet. 1998 Sep 12. 352(9131):854-65. [Medline].

  61. Henry RR. Thiazolidinediones. Endocrinol Metab Clin North Am. 1997 Sep. 26(3):553-73. [Medline].

  62. UK 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). UK Prospective Diabetes Study (UKPDS) Group. Lancet. 1998 Sep 12. 352(9131):837-53. [Medline].

  63. Krentz AJ, Bailey CJ. Oral antidiabetic agents: current role in type 2 diabetes mellitus. Drugs. 2005. 65(3):385-411. [Medline].

  64. Li CL, Pan CY, Lu JM, Zhu Y, Wang JH, Deng XX, et al. Effect of metformin on patients with impaired glucose tolerance. Diabet Med. 1999 Jun. 16(6):477-81. [Medline].

  65. McIntosh CH, Demuth HU, Pospisilik JA, Pederson R. Dipeptidyl peptidase IV inhibitors: how do they work as new antidiabetic agents?. Regul Pept. 2005 Jun 15. 128(2):159-65. [Medline].

  66. Muscelli E, Mari A, Natali A, Astiarraga BD, Camastra S, Frascerra S, et al. Impact of incretin hormones on beta-cell function in subjects with normal or impaired glucose tolerance. Am J Physiol Endocrinol Metab. 2006 Dec. 291(6):E1144-50. [Medline].

  67. Nauck MA, Meier JJ. Glucagon-like peptide 1 and its derivatives in the treatment of diabetes. Regul Pept. 2005 Jun 15. 128(2):135-48. [Medline].

  68. Blevins T, Pullman J, Malloy J, Yan P, Taylor K, Schulteis C, et al. DURATION-5: exenatide once weekly resulted in greater improvements in glycemic control compared with exenatide twice daily in patients with type 2 diabetes. J Clin Endocrinol Metab. 2011 May. 96(5):1301-10. [Medline].

  69. Standards of medical care in diabetes--2013. Diabetes Care. 2013 Jan. 36 Suppl 1:S11-66. [Medline]. [Full Text].

  70. Ahrén B, Pacini G. Islet adaptation to insulin resistance: mechanisms and implications for intervention. Diabetes Obes Metab. 2005 Jan. 7(1):2-8. [Medline].

  71. Hanefeld M, Temelkova-Kurktschiev T, Schaper F, Henkel E, Siegert G, Koehler C. Impaired fasting glucose is not a risk factor for atherosclerosis. Diabet Med. 1999 Mar. 16(3):212-8. [Medline].

  72. Koska J, DelParigi A, de Courten B, Weyer C, Tataranni PA. Pancreatic polypeptide is involved in the regulation of body weight in pima Indian male subjects. Diabetes. 2004 Dec. 53(12):3091-6. [Medline].

  73. National Diabetes Data Group. Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. National Diabetes Data Group. Diabetes. 1979 Dec. 28(12):1039-57. [Medline].

  74. Newcomer JW. Second-generation (atypical) antipsychotics and metabolic effects: a comprehensive literature review. CNS Drugs. 2005. 19 Suppl 1:1-93. [Medline].

  75. Ratner RE. An update on the Diabetes Prevention Program. Endocr Pract. 2006 Jan-Feb. 12 Suppl 1:20-4. [Medline]. [Full Text].

  76. Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes. 1988 Dec. 37(12):1595-607. [Medline].

  77. Suzuki H, Fukushima M, Usami M, et al. IGT with fasting hyperglycemia is more strongly associated with microalbuminuria than IGT without fasting hyperglycemia. Diabetes Res Clin Pract. 2004 Jun. 64(3):213-9. [Medline].

  78. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group. N Engl J Med. 1993 Sep 30. 329(14):977-86. [Medline].

 
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Etiologic types and stages of the major disorders of glucose tolerance.
 
 
 
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