Glucose Intolerance Medication

  • Author: Samuel T Olatunbosun, MD, FACP; Chief Editor: George T Griffing, MD   more...
 
Updated: Feb 2, 2012
 

Medication Summary

Oral antidiabetic agents can be classified into functional categories, as follows[38, 55, 56, 57, 58, 59, 60, 61, 62, 63] :

  • Secretagogues (eg, sulfonylureas, meglitinides), which stimulate insulin release
  • Insulin sensitizers (eg, biguanides, thiazolidinediones), which reduce insulin resistance
  • Medications that slow the digestive/absorptive process (eg, alpha-glucosidase inhibitors)
  • DPP-4 inhibitors (eg, sitagliptin), which inhibit DPP-4, the enzyme that inactivates incretin hormones GLP-1 and GIP.[36, 37]
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Sulfonylureas

Class Summary

Sulfonylureas stimulate insulin release from pancreatic beta cells. These agents include chlorpropamide and tolbutamide (first-generation), as well as glipizide, glyburide, and glimepiride (second-generation), are secretagogues (ie, medications that stimulate insulin secretion).

Glipizide (Glucotrol)

 

Glipizide is a second-generation sulfonylurea that stimulates the release of insulin from pancreatic beta cells.

Glyburide

 

Glyburide is a second-generation sulfonylurea and is more potent and exhibits fewer drug interactions than first-generation agents.

Glimepiride (Amaryl)

 

Glimepiride is a third-generation sulfonylurea that may cause more physiologic insulin release than some of the older agents.

Chlorpropamide

 

Chlorpropamide is a first-generation sulfonylurea that stimulates the release of insulin from pancreatic beta cells. It is the longest-acting sulfonylurea, present in blood longer than 24 hour in many patients, and longer in patients with renal insufficiency.

Tolbutamide (Orinase)

 

First-generation sulfonylurea that stimulates the release of insulin from pancreatic beta cells.

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Meglitinides

Class Summary

These agents stimulate insulin secretion from pancreatic cells, lowering blood glucose levels.

Repaglinide (Prandin)

 

Repaglinide is a meglitinide analogue, a secretagogue that acts on the pancreas to stimulate the release of insulin.

Nateglinide (Starlix)

 

Nateglinide is an analogue of D-phenylalanine. It mimics endogenous insulin patterns, restores early insulin secretion, and controls mealtime glucose surges.

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Biguanides

Class Summary

These agents improve peripheral glucose uptake and utilization.

Metformin (Glucophage)

 

Metformin reduces insulin resistance (ie, metformin is an insulin sensitizer). Hepatic glucose output is decreased; peripheral insulin-stimulated uptake is increased.

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Thiazolidinediones

Class Summary

These agents stimulate peripheral use of glucose as stimulated by insulin. Rosiglitazone and pioglitazone are commonly used.

Following the online publication of a meta-analysis, the Food and Drug Administration on May 21, 2007, issued an alert to patients and health care professionals stating that rosiglitazone can potentially cause an increased risk of myocardial infarction and heart-related deaths. Rosiglitazone is an antidiabetic agent (thiazolidinedione derivative) that improves glycemic control by improving insulin sensitivity.

The drug is highly selective and is a potent agonist for peroxisome proliferator-activated receptor gamma (PPAR gamma). Activation of PPAR-gamma receptors regulates insulin-responsive gene transcription involved in glucose production, transport, and utilization, thereby reducing blood glucose concentrations and reducing hyperinsulinemia. Potent PPAR-gamma agonists have been shown to increase the incidence of edema. A large scale phase III trial (RECORD) is underway that is specifically designed to study cardiovascular outcomes of rosiglitazone.

As of September 2010, the FDA is requiring a restricted access program to be developed for rosiglitazone under a risk evaluation and mitigation strategy (REMS). Patients currently taking rosiglitazone and benefiting from the drug will be able to continue if they choose to do so. Rosiglitazone will only be available to new patients if they are unable to achieve glucose control on other medications and are unable to take pioglitazone, the only other thiazolidinedione.

For more information, see FDA’s Safety Alert on Avandia. The meta-analysis published online, entitled "Effect of Rosiglitazone on the Risk of Myocardial Infarction and Death from Cardiovascular Causes" can be viewed at The New England Journal of Medicine. Additionally, responses to the controversy can be viewed at the Heartwire news (theheart.org from WebMD), including the following articles: Rosiglitazone increases MI and CV death in meta-analysis and The rosiglitazone aftermath: legitimate concerns or hype?.

Rosiglitazone (Avandia)

 

Available only through a restricted access program. Rosiglitazone sensitizes target cells' response to insulin and has an effect on the stimulation of glucose uptake in skeletal muscle and adipose tissue.

Pioglitazone (Actos)

 

Pioglitazone improves target cell response to insulin and increases insulin-dependent glucose use in skeletal muscle and adipose tissue.

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Alpha-glucosidase inhibitors

Class Summary

These agents include acarbose and miglitol, medications that slow the digestive and absorptive process, preventing postprandial glucose surges.

Acarbose (Precose)

 

Acarbose slows digestive and absorptive processes. It delays hydrolysis of ingested complex carbohydrates and disaccharides and absorption of glucose. Acarbose inhibits the metabolism of sucrose to glucose and fructose.

Miglitol (Glyset)

 

Miglitol delays glucose absorption in the small intestine and lowers postprandial hyperglycemia.

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Rapid-acting insulins

Class Summary

Rapid-acting insulins have a short duration of action and are appropriate before meals or when blood glucose levels exceed target levels and correction doses are needed. These agents are associated with less hypoglycemia than regular insulin.

Insulin aspart (NovoLog)

 

Insulin aspart has a short onset of action of 5-15 minutes and a short duration of action of 3-5 hours. The peak effect occurs within 30-90 minutes. Insulin aspart is FDA approved for use in insulin pumps.

Insulin glulisine (Apidra)

 

Insulin glulisine has a rapid onset of action of 5-15 minutes and a short duration of action of 3-5 hours. The peak effect occurs within 30-90 minutes. Insulin glulisine is FDA approved for use in insulin pumps.

Insulin lispro (Humalog)

 

Insulin lispro has a rapid onset of action of 5-15 minutes and a short duration of action of 4 hours.

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Short-acting insulins

Class Summary

Short-acting insulins are commonly used when a slower onset of action or greater duration of action is desired.

Regular insulin (Humulin R, Novolin R)

 

Regular insulin has a rapid onset of action of 0.5-1 hours and duration of action of 4-6 hours. The peak effects are seen within 2-4 hours. Preparations that contain a mixture of 70% neutral protamine Hagedorn (NPH) and 30% regular human insulin (ie, Novolin 70/30, Humulin 70/30) are also available.

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Intermediate-acting insulins

Class Summary

Intermediate-acting insulins have a slow onset of action and a longer duration of action. These agents are commonly combined with faster-acting insulins to maximize the benefits of a single injection.

Insulin NPH (Humulin N, Novolin N)

 

Insulin NPH has an onset of action of 3-4 hours and duration of action of 16-24 hours. The peak effect of insulin NPH occurs within 8-14 hours.

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Long-acting insulins

Class Summary

These insulins provide a longer duration of action, and, when combined with rapid- or short-acting insulins, they provide better glucose control.

Insulin detemir (Levemir)

 

Insulin detemir is indicated for once- or twice-daily dosing for patients with type 1 or 2 diabetes mellitus. The duration of action is up to 24 hours, resulting from slow systemic absorption of detemir from the injection site.

Insulin Glargine (Lantus)

 

Insulin glargine has an onset of action of 4-8 hours and duration of action of 24 hours. Peak effects occur within 16-18 hours.

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Premixed Insulins

Class Summary

Premixed insulins are used in the treatment of type 1 or 2 diabetes mellitus. These combinations combine rapid- and long-acting insulins.

Insulin aspart protamine/insulin aspart (NovoLog 50/50, NovoLog 70/30)

 

The insulin aspart protamine/insulin aspart combination includes a rapid-onset insulin, insulin aspart, and intermediate-acting insulin, insulin aspart protamine. Insulin aspart is absorbed more rapidly than regular human insulin, and insulin aspart protamine has a prolonged absorption profile after injection.

Insulin lispro protamine/insulin lispro (Humalog 50/50, Humalog 75/25)

 

The insulin lispro protamine/insulin lispro combination includes a rapid-onset insulin, insulin lispro, and insulin lispro protamine, which has a prolonged duration of action.

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Incretin mimetics

Class Summary

This new class broadens the armamentarium of antidiabetic medications. Exenatide and liraglutide are DPP-4–resistant glucagonlike peptide-1 (GLP-1) receptor agonists or analogues. As incretin mimetics, they enhance insulin secretion, suppress glucagon secretion, and slow gastric emptying. Exenatide has been approved by the FDA as adjunctive therapy in patients who have not achieved adequate control with metformin or sulfonylurea; exenatide has been available since June 2005, and a new, long-acting, once-weekly subcutaneous injection (Bydureon) was approved by the FDA in January 2012. Liraglutide was approved by the FDA in January 2010.

In the DURATION-5 (Diabetes therapy Utilization: Researching changes in A1C, weight and other factors Through Intervention with exenatide ONce weekly) study, the exenatide once-weekly formulation was found to provide significantly greater improvement in glycemic control than the twice-daily preparation. Additionally, less nausea was observed with the once-weekly exenatide formulation compared with the twice-daily preparation.[73]

Exenatide injectable solution (Byetta)

 

Exenatide is a 39-amino acid incretin mimetic peptide derived from Gila monster hormone exendin-4. It is structurally similar to glucagonlike peptide-1 (GLP-1). It enhances glucose-mediated insulin secretion in the beta cell, decreases the pathologic hypersecretion of glucagon in the alpha cell, slows gastric emptying, and induces satiety. It also improves postprandial hyperglycemia without a significant risk of hypoglycemia, producing moderate weight loss. Improvement in islet cell function has been demonstrated by increased proinsulin-to-insulin ratio.

Liraglutide (Victoza)

 

Liraglutide is an incretin mimetic agent that elicits glucagonlike peptide-1 (GLP-1) receptor agonist activity. It activates GLP-1 receptor by stimulating G-protein in pancreatic beta cells. It also increases intracellular cyclic AMP, leading to insulin release in the presence of elevated glucose concentrations.

Liraglutide is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. It has not been studied in combination with insulin.

Exenatide injectable suspension (Bydureon)

 

This formulation of exenatide allows once-weekly dosing by SC administration. Clinical trials observed a statistically significant improvement in HBA1c levels and fasting plasma glucose levels with the long-acting exenatide once-weekly SC injection compared with the twice-daily SC injection.

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Amylin analogue

Class Summary

Pramlintide is an amylinomimetic agent that modulates gastric emptying, prevents postprandial increases in plasma glucagon, and promotes satiety, leading to decreased caloric intake and potential weight loss.[40, 41, 42, 43, 44, 45]

Although naturally occurring human amylin is unsuitable for clinical use because of several physicochemical properties (eg, poor solubility; self-aggregation; formation of b-pleated sheets, amyloid fibrils, amyloid plaques), the selective substitution of the amino acid proline for Ala25, Ser28, and Ser29 addresses the suboptimal physicochemical properties of human amylin while preserving the important metabolic actions. Pramlintide acetate injection, which contains this amylin analogue, is a sterile, clear, colorless, aqueous solution that also contains mannitol for isotonicity and the preservative m-cresol.

Pramlintide (Symlin)

 

Pramlintide is a synthetic analogue of human amylin, a naturally occurring hormone made in pancreas beta cells. Pramlintide slows gastric emptying, suppresses postprandial glucagon secretion, and regulates food intake through centrally mediated appetite modulation. It is indicated to treat type 1 or type 2 diabetes in combination with insulin.

Pramlintide is administered before meals in patients who have not achieved desired glucose control despite optimal insulin therapy. The drug helps to achieve lower blood glucose levels after meals, less fluctuation of blood glucose levels during the day, and improvement of long-term control of glucose levels (ie, HbA1c levels) compared with insulin alone. Reductions in insulin use and body weight are also observed.

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Dipeptidyl Peptidase-4 Inhibitor

Class Summary

The DPP-4 inhibitors are oral agents that inactivate the major enzyme responsible for degrading incretin hormones in vivo.

Sitagliptin (Januvia)

 

Sitagliptin blocks the enzyme DPP-4, which is known to degrade incretin hormones. Sitagliptin increases concentrations of active intact incretin hormones (GLP-1 and GIP). The hormones stimulate insulin release in response to increased blood glucose levels following meals. This action enhances glycemic control. Sitagliptin is indicated for diabetes type 2 as monotherapy or in combination with metformin or with a peroxisome proliferator-activated receptor gamma agonist (eg, thiazolidinediones).

Saxagliptin (Onglyza)

 

Saxagliptin blocks the enzyme DPP-4, which is known to degrade incretin hormones. It increases concentrations of active intact incretin hormones (GLP-1 and GIP). The hormones stimulate insulin release in response to increased blood glucose levels following meals. This action enhances glycemic control. Saxagliptin is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.

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Contributor Information and Disclosures
Author

Samuel T Olatunbosun, MD, FACP  Endocrinology Department, Wilford Hall Medical Center, 59th Medical Wing, Lackland Air Force Base

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

Disclosure: Nothing to disclose.

Coauthor(s)

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, Endocrine Society, and Royal College of Physicians

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

Specialty Editor Board

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.

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

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.

Chief Editor

George T Griffing, MD  Professor 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, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

References
  1. [Guideline] American Diabetes Association. Standards of medical care in diabetes--2011. Diabetes Care. Jan 2011;34 Suppl 1:S11-61. [Medline]. [Full Text].

  2. Buchanan TA, Xiang AH. Gestational diabetes mellitus. J Clin Invest. Mar 2005;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). May 2008;16(5):1025-32. [Medline].

  6. DeFronzo RA. Pathogenesis of type 2 diabetes mellitus. Med Clin North Am. Jul 2004;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. Sep 8 1997;157(16):1802-17. [Medline].

  8. Sjöström L. Analysis of the XENDOS study (Xenical in the Prevention of Diabetes in Obese Subjects). Endocr Pract. Jan-Feb 2006;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. Mar 3 2010;[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. Jun 2010;36(3):192-7. [Medline].

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

  12. Joy SV, Rodgers PT, Scates AC. Incretin mimetics as emerging treatments for type 2 diabetes. Ann Pharmacother. Jan 2005;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. Feb 21-27 2005;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. Dec 2006;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. Jun 2006;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. Apr 1998;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. Jan 1993;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. Jan-Feb 2006;12 Suppl 1:47-51. [Medline].

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

  21. Reaven GM. Insulin resistance and its consequences: non-insulin-dependent diabetes mellitus and coronary heart disease. In: 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. Jul 2004;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. Jun 2010;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. Feb 11 2010;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. Apr 2010;118(4):234-6. [Medline].

  26. Alberti KG. Impaired glucose tolerance: what are the clinical implications?. Diabetes Res Clin Pract. Jul 1998;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. Aug 2004;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. Jun 2004;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. Aug 1998;41(2):147-8. [Medline].

  30. 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. May 2008;51(5):853-61. [Medline].

  31. 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. Mar 2007;30(3):753-9. [Medline].

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

  33. 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. May-Jun 2003;9(3):237-52. [Medline].

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

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

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

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

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

  39. 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. Feb 2011;34(2):412-7. [Medline]. [Full Text].

  40. 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. Mar 2005;28(3):632-7. [Medline].

  41. 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. Nov 2003;5(6):408-14. [Medline].

  42. 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. Nov 2004;21(11):1204-12. [Medline].

  43. 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. Nov 2007;30(11):2794-9. [Medline].

  44. 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. Apr 15 2005;62(8):816-22. [Medline].

  45. 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. Jan 2008;24(1):79-85. [Medline].

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

  47. 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. Jan-Feb 2006;12 Suppl 1:25-30. [Medline].

  48. [Best Evidence] 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. Feb 10 2007;334(7588):299. [Medline]. [Full Text].

  49. 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. Nov 1994;17(11):1311-9. [Medline].

  50. [Best Evidence] 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. Mar 1 2005;142(5):323-32. [Medline]. [Full Text].

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

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

  53. 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. Feb 2011;164(2):231-8. [Medline]. [Full Text].

  54. 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. Mar 2008;87(3):655-61. [Medline].

  55. 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. Sep 25 2004;148(39):1912-7. [Medline].

  56. 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. Sep 12 1998;352(9131):854-65. [Medline].

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

  58. 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. Sep 12 1998;352(9131):837-53. [Medline].

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

  60. 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. Jun 1999;16(6):477-81. [Medline].

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

  62. 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. Dec 2006;291(6):E1144-50. [Medline].

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

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

  65. 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. Mar 1999;16(3):212-8. [Medline].

  66. 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. Dec 2004;53(12):3091-6. [Medline].

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

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

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

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

  71. 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. Jun 2004;64(3):213-9. [Medline].

  72. 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. Sep 30 1993;329(14):977-86. [Medline].

  73. 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. May 2011;96(5):1301-10. [Medline].

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