Skip to main content

Acarbose (Monograph)

Drug class: alpha-Glucosidase Inhibitors
VA class: HS502
Chemical name: O-4,6-dideoxy-4-[[[1S-(1α,4α,5β,6α)]-4,5,6-trihydroxy-3-(hydroxymethyl)-2-cyclohexen-1-yl]amino]-α-d -glucopyranosyl-(1→4)-O-α-d-glucopyranosyl-(1→4)-d-glucose
Molecular formula: C25H43NO18
CAS number: 56180-94-0

Medically reviewed by Drugs.com on Jun 11, 2024. Written by ASHP.

Introduction

Antidiabetic agent; an α-glucosidase inhibitor.1 6 30 52

Uses for Acarbose

Type 2 Diabetes Mellitus

Used as monotherapy as an adjunct to diet and exercise for the management of type 2 diabetes mellitus in patients whose hyperglycemia cannot be controlled by diet and exercise alone.1 6 14 47

Also used as adjunct to diet and exercise in combination with metformin, a sulfonylurea, or insulin for management of type 2 diabetes mellitus in patients whose hyperglycemia cannot be controlled with monotherapy with these agents, diet, and exercise.1 3 6 14 23 26 44 47

Current guidelines for the treatment of type 2 diabetes mellitus generally recommend metformin as first-line therapy in addition to lifestyle modifications in patients with recent-onset type 2 diabetes mellitus or mild hyperglycemia because of its well-established safety and efficacy (i.e., beneficial effects on glycosylated hemoglobin [hemoglobin A1c; HbA1c], weight, and cardiovascular mortality).698 704 705

In patients with metformin contraindications or intolerance (e.g., risk of lactic acidosis, GI intolerance) or in selected other patients, some experts suggest that initial therapy with a drug from another class of antidiabetic agents (e.g., a glucagon-like peptide-1 [GLP-1] receptor agonist, sodium-glucose cotransporter 2 [SGLT2] inhibitor, dipeptidyl peptidase-4 [DPP-4] inhibitor, sulfonylurea, thiazolidinedione, basal insulin) may be acceptable based on patient factors.698 704

May need to initiate therapy with 2 agents (e.g., metformin plus another drug) in patients with high initial HbA1c (>7.5% or ≥1.5% above target).698 704 In such patients with metformin intolerance, some experts suggest initiation of therapy with 2 drugs from other antidiabetic drug classes with complementary mechanisms of action.698 704

An α-glucosidase inhibitor (acarbose, miglitol) generally not recommended as second-line therapy after failure of metformin monotherapy because of comparatively lesser efficacy, frequent adverse GI effects, and greater cost, but may be appropriate therapy in selected patients.110 698

Consider early initiation of combination therapy for the treatment of type 2 diabetes mellitus to extend the time to treatment failure and more rapidly attain glycemic goals.704

For patients with inadequate glycemic control on metformin monotherapy, consider patient comorbidities (e.g., atherosclerotic cardiovascular disease [ASCVD], established kidney disease, heart failure), hypoglycemia risk, impact on weight, cost, risk of adverse effects, and patient preferences when selecting additional antidiabetic agents for combination therapy.698 699 704 705 706

Consider early introduction of insulin for severe hyperglycemia (e.g., blood glucose ≥300 mg/dL or HbA1c >9–10%), especially if accompanied by catabolic manifestations (e.g., weight loss, hypertriglyceridemia, ketosis) or symptoms of hyperglycemia.698 704

Acarbose Dosage and Administration

General

Administration

Oral Administration

Administer orally at the beginning (with the first bite) of each main meal.1 23

To minimize adverse GI effects, closely follow diabetic diet as prescribed.1 (See Adherence to Prescribed Diet under Cautions.)

Dosage

Adults

Type 2 Diabetes Mellitus
Oral

Initially, 25 mg at the beginning of each main meal (with first bite) 3 times daily.1 23 In patients with adverse GI effects,2 12 23 34 initiate at 25 mg once daily and increase dosage gradually as necessary to 25 mg 3 times daily.1

Once dosage of 25 mg 3 times daily has been reached, increase dosage at intervals of 4–8 weeks as tolerated to achieve the desired 1-hour postprandial glucose concentration (i.e., <180 mg/dL) or until maximum dosage (according to weight) is reached.1 23 34 41 52 62 (See Prescribing Limits under Dosage and Administration.) Maintenance dosage ranges from 50–100 mg 3 times daily.1 6 47

Dosages higher than 100 mg 3 times daily are not recommended since such dosages have been associated with an increased risk of elevated serum aminotransferase concentrations.1 10 18 19 20 22 23 25 27 30 37 43 52 If no further therapeutic benefit occurs at the maximum recommended dosage, consider lowering the dosage.1

Prescribing Limits

Adults

Type 2 Diabetes Mellitus
Oral

Patients ≤60 kg: maximum 50 mg 3 times daily.1 23 34 41 52

Patients >60 kg: maximum 100 mg 3 times daily.1

Detailed Acarbose dosage information

Cautions for Acarbose

Contraindications

Warnings/Precautions

General Precautions

Metabolic Effects

Should not cause hypoglycemia when administered alone in the fasted or postprandial state.1 However, hypoglycemia (rarely hypoglycemic shock) may occur when used concomitantly with a sulfonylurea antidiabetic agent and/or insulin.1 If hypoglycemia occurs, adjust dosage of these agents appropriately.1 Use oral glucose (dextrose) for the treatment of mild to moderate hypoglycemia instead of sucrose (table sugar);1 the absorption of oral glucose is not inhibited by acarbose.1 Severe hypoglycemia may require the use of either IV glucose or parenteral glucagon.1

Insulin may be required for correction of temporary hyperglycemia that is not controlled by dietary regulation or oral antidiabetic agents during periods of severe stress (e.g., acute infection, trauma, surgery, fever).1 57 59

Hepatic Effects

Elevations in serum aminotransferase (i.e., ALT, AST) concentrations and, in rare instances, hyperbilirubinemia may occur, particularly with dosages exceeding 150 mg daily (50 mg 3 times daily).1 23 Jaundice and fatal hepatitis reported during postmarketing experience.1

Determine serum aminotransferase concentrations every 3 months during the first year of therapy and periodically thereafter.1 If elevations in serum aminotransferase concentrations occur, reduce dosage.1 May be necessary to withdraw the drug, particularly if elevated serum aminotransferase concentrations persist.1

Adherence to Prescribed Diet

If prescribed diet not followed closely, adverse GI effects may be intensified.1 If symptoms are strongly distressing despite adherence to prescribed diabetic diet, temporarily or permanently reduce acarbose dosage.1

Specific Populations

Pregnancy

Category B.1

Lactation

Distributed into milk in rats.1 Not known whether distributed into human milk.1 Use not recommended in nursing women.1

Pediatric Use

Safety and efficacy in children <18 years of age not established.1 23

Geriatric Use

Safety and efficacy in those ≥65 years of age similar to that in younger adults.1 (See Special Populations under Pharmacokinetics: Absorption.)

Hepatic Impairment

Contraindicated in patients with cirrhosis.1 23 52 Not studied in other conditions associated with hepatic impairment.1 23 52

Renal Impairment

Not recommended for use in diabetic patients with appreciable renal impairment (Scr >2 mg/dL).1 23

Common Adverse Effects

Flatulence, diarrhea, abdominal discomfort/pain.1

Digestive Enzyme Supplements

Possible reduction in the glycemic effects of acarbose.1 Avoid concomitant use.1

Intestinal Adsorbents

Possible reduction in the glycemic effects of acarbose.1 Avoid concomitant use.1

Specific Drugs and Laboratory Tests

Drug or Test

Interaction

Comments

1,5-Anhydroglucitol assay

Unreliable results in patients taking acarbose1

Manufacturer recommends use of alternative method to monitor glycemic control 1

Amylase (digestive enzyme preparation)

Possible reduction in glycemic effects of acarbose1

Avoid concomitant use1

Calcium-channel blocking agents

Potential to exacerbate hyperglycemia, resulting in loss of glycemic control1

No effect of acarbose on the pharmacokinetic or pharmacodynamics of nifedipine1

Monitor for loss of glycemic control1

When calcium-channel blocking agents are withdrawn in patients receiving concurrent sulfonylureas or insulin, monitor for evidence of hypoglycemia1

Charcoal (intestinal adsorbent)

Possible reduction in glycemic effects of acarbose1

Avoid concomitant use1

Corticosteroids

Potential to exacerbate hyperglycemia, resulting in loss of glycemic control1

Monitor for loss of glycemic control1

When corticosteroids are withdrawn in patients receiving concurrent sulfonylureas or insulin, monitor for evidence of hypoglycemia1

Contraceptives, oral

Potential exacerbation of hyperglycemia/loss of glycemic control1

Monitor for loss of glycemic control1

When oral contraceptives are withdrawn in patients receiving concurrent sulfonylureas or insulin, observe for evidence of hypoglycemia1

Digoxin

Decreased blood concentrations of digoxin1

May require increased digoxin dosage1

Diuretics (e.g., thiazides)

Potential exacerbation of hyperglycemia, resulting in loss of glycemic control1

Monitor for loss of glycemic control1

When diuretics are withdrawn in patients receiving concurrent sulfonylureas or insulin, observe for evidence of hypoglycemia1

Estrogens

Potential to exacerbate hyperglycemia, resulting in loss of glycemic control1

Monitor for loss of glycemic control1

When estrogens are withdrawn in patients receiving concurrent sulfonylureas or insulin, observe for evidence of hypoglycemia1

Glyburide

No effect on absorption or disposition of concomitant glyburide1

Pharmacokinetic interaction with glyburide unlikely1

Insulin

Increased risk of hypoglycemia, rarely hypoglycemic shock, with concomitant insulin1

If hypoglycemia occurs, reduce insulin dosage1

Isoniazid

Potential to exacerbate hyperglycemia, resulting in loss of glycemic control1

Monitor for loss of glycemic control1

When isoniazid is withdrawn in patients receiving concurrent sulfonylureas or insulin, monitor for evidence of hypoglycemia1

Metformin

Possible decreased peak plasma concentration of metformin1

Pharmacokinetic interaction not considered clinically important1

Nicotinic acid

Potential to exacerbate diabetes mellitus, resulting in loss of glycemic control1

Monitor for loss of glycemic control1

When nicotinic acid is withdrawn in patients receiving concurrent sulfonylureas or insulin, observe for evidence of hypoglycemia1

Pancreatin (digestive enzyme preparation; no longer commercially available in the US)

Possible reduction in glycemic effects of acarbose1

Avoid concomitant use1

Phenothiazines

Potential to exacerbate hyperglycemia, resulting in loss of glycemic control1

Monitor for loss of glycemic control1

When phenothiazines are withdrawn in patients receiving concurrent sulfonylureas or insulin, monitor for evidence of hypoglycemia1

Phenytoin

Potential to exacerbate hyperglycemia, resulting in loss of glycemic control1

Monitor for loss of glycemic control1

When phenytoin is withdrawn in patients receiving concurrent sulfonylureas or insulin, monitor for evidence of hypoglycemia1

Pramlintide

Delayed gastric emptying caused by α-glucosidase inhibitors may alter effects of pramlintide on GI absorption of nutrients112

Avoid concomitant pramlintide; safety/efficacy of combination therapy not established112

Propranolol

Pharmacokinetic or pharmacodynamic interaction unlikely1

Ranitidine

Pharmacokinetic or pharmacodynamic interaction unlikely1

Rosiglitazone

Reduced extent of absorption and prolonged half-life of rosiglitazone113

Potential for altered glycemic control is uncertain114

Pharmacokinetic interaction not considered clinically important113

Sulfonylureas

Increased risk of hypoglycemia, hypoglycemic shock with sulfonylureas1

If hypoglycemia occurs, reduce sulfonylurea dosage1

Sympathomimetic agents

Potential to exacerbate hyperglycemia, resulting in loss of glycemic control1

Monitor for loss of glycemic control1

When sympathomimetic agents are withdrawn in patients receiving concurrent sulfonylureas or insulin, monitor for evidence of hypoglycemia.1

Thyroid agents

Potential to exacerbate hyperglycemia, resulting in loss of glycemic control1

Monitor for loss of glycemic control1

When thyroid agents are withdrawn in patients receiving concurrent sulfonylureas or insulin, monitor for evidence of hypoglycemia1

Acarbose Pharmacokinetics

Absorption

Bioavailability

Low systemic bioavailability of parent compound; <2% of dose is absorbed as active drug (parent compound and active metabolite).1 Peak plasma concentrations of active drug attained at approximately 1 hour.1 Approximately 34% of dose absorbed as numerous metabolites.1

Onset

Satisfactory control of blood glucose concentrations achieved within a few days after dosage adjustment; however18 23 maximum response may be delayed for up to 2 weeks.18 23

Special Populations

In geriatric patients, mean AUC and peak blood concentrations of the drug were higher compared with younger adults;1 differences not statistically significant.1

In individuals with severe renal impairment (CLcr <25 mL/minute), peak plasma drug concentrations and AUC increased compared with those values in individuals with normal renal function.1

Distribution

Extent

Distributed into milk in rats.1

Elimination

Metabolism

Metabolized exclusively in GI tract, principally by intestinal bacteria but also by digestive enzymes to numerous metabolites, one of which is active.1

Elimination Route

Excreted principally in feces (51% of dose) as unabsorbed drug and in urine as metabolites (34% of dose).1 No accumulation with recommended dosing frequency.1

Half-life

Approximately 2 hours.1

Stability

Storage

Oral

Tablets

≤25°C.1 Protect from moisture.1

Actions

Advice to Patients

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

Acarbose

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Tablets

25 mg*

Acarbose Tablets

50 mg*

Acarbose Tablets

100 mg*

Acarbose Tablets

AHFS DI Essentials™. © Copyright 2025, Selected Revisions June 21, 2021. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

References

1. Mylan. Acarbose tablets prescribing information. Morgantown, WV; 2015 Apr.

2. Clissold SP, Edwards C. Acarbose: a preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential. Drugs. 1988; 35:214-43. https://pubmed.ncbi.nlm.nih.gov/3286212

3. Anon. Acarbose–an α-glucosidase inhibitor. Int Pharm J. 1994; 8:11-12.

6. Santeusanio F, Compagnucci P. A risk-benefit appraisal of acarbose in the management of non-insulin-dependent diabetes mellitus. Drug Saf. 1994; 11:432-44. https://pubmed.ncbi.nlm.nih.gov/7727053

7. Jenkins DJA, Taylor RH, Goff DV et al. Scope and specificity of acarbose in slowing carbohydrate absorption in man. Diabetes. 1981; 30:951-4. https://pubmed.ncbi.nlm.nih.gov/7028548

10. Hayakawa T, Kondo T, Okumura N et al. Enteroglucagon release in disaccharide malabsorption induced by intestinal α-glucosidase inhibition. Am J Gastroenterol. 1989; 84:523-6. https://pubmed.ncbi.nlm.nih.gov/2655436

11. Bristol-Myers Squibb, Princeton, NJ: personal communication on metformin.

12. Scheppach W, Fabian C, Ahrens F et al. Effect of starch malabsorption on colonic function and metabolism in humans. Gastroenterology. 1988; 95:1549-55. https://pubmed.ncbi.nlm.nih.gov/3053313

13. Fölsch UR, Ebert R, Creutzfeldt W. Response of serum levels of gastric inhibitory polypeptide and insulin to sucrose ingestion during long-term application of acarbose. Scand J Gastroenterol. 1981; 16:629-32. https://pubmed.ncbi.nlm.nih.gov/7034156

14. Balfour JA, McTavish D. Acarbose: an update of its pharmacology and therapeutic use in diabetes mellitus. Drugs. 1993; 46:1025-54. https://pubmed.ncbi.nlm.nih.gov/7510610

16. Carlisle BA, Kroon LA, Koda-Kimble MA. Diabetes mellitus. In: Koda-Kimble MA, Young LY, eds. Applied therapeutics: the clinical use of drugs. 8th ed. Philadelphia, PA: Lippincott Williams &Wilkins; 2005: 50-1–50-86.

18. Coniff RF, Shapiro JA, Seaton TB. Long-term efficacy and safety of acarbose in the treatment of obese subjects with non-insulin-dependent diabetes mellitus. Arch Intern Med. 1994; 154:2442-8. https://pubmed.ncbi.nlm.nih.gov/7979840

19. Coniff RF, Shapiro JA, Seaton TB et al. Multicenter, placebo-controlled trial comparing acarbose (BAY g 5421) with placebo, tolbutamide, and tolbutamide-plus-acarbose in non-insulin-dependent diabetes mellitus. Am J Med. 1995; 98:443-51. https://pubmed.ncbi.nlm.nih.gov/7733122

20. Coniff RF, Shapiro JA, Robbins D et al. Reduction of glycosylated hemoglobin and postprandial hyperglycemia by acarbose in patients with NIDDM: a placebo-controlled dose-comparison study. Diabetes Care. 1995; 18:817-24. https://pubmed.ncbi.nlm.nih.gov/7555508

21. Hoffmann J, Spengler M. Efficacy of 24-week monotherapy with acarbose, glibenclamide, or placebo in NIDDM patients: the Essen Study. Diabetes Care. 1994; 17:561-6. https://pubmed.ncbi.nlm.nih.gov/8082525

22. Chiasson J-L, Josse RG, Hunt JA et al. The efficacy of acarbose in the treatment of patients with non-insulin-dependent diabetes mellitus. Ann Intern Med. 1994; 121:928-35. https://pubmed.ncbi.nlm.nih.gov/7734015

23. Bayer, West Haven, CT: Personal communication.

24. Toeller M. Nutritional recommendations for diabetic patients and treatment with α-glucosidase inhibitors. Drugs. 1992; 44(Suppl 3):13- 20. https://pubmed.ncbi.nlm.nih.gov/1280573

25. Coniff RF, Shapiro JA, Seaton TB et al. A double-blind placebo- controlled trial evaluating the safety and efficacy of acarbose for the treatment of patients with insulin-requiring type II diabetes. Diabetes Care. 1995; 18:928-32. https://pubmed.ncbi.nlm.nih.gov/7555551

26. Zimmerman BR. Preventing long term complications: implications for combination therapy with acarbose. Drugs. 1992; 44(Suppl 3):54-60. https://pubmed.ncbi.nlm.nih.gov/1280578

27. Anon. Round-table discussion. Drugs. 1992; 44(Suppl 3):61-5. https://pubmed.ncbi.nlm.nih.gov/1283586

28. Hollander P. Safety profile of acarbose, an α-glucosidase inhibitor. Drugs. 1992; 44(Suppl 3):47-53. https://pubmed.ncbi.nlm.nih.gov/1280577

29. William-Olsson T, Krotkiewski M, Sjöström L. Relapse- reducing effects of acarbose after weight reduction in severely obese subjects. J Obesity Weight Regulation. 1985; 4:20-32.

30. William-Olsson T. α-glucosidase inhibition in obesity. Acta Med Scand Suppl. 1985; 706:1-39. https://pubmed.ncbi.nlm.nih.gov/3914827

31. Shichiri M, Kishikawa H, Ohkubo Y et al. Long-term results of the Kumamoto study on optimal diabetes control in type 2 diabetic patients.Diabetes Care. 2000; 23 (Suppl 2):B21-9. https://pubmed.ncbi.nlm.nih.gov/10860187

33. Hiele M, Ghoos Y, Rutgeerts P et al. Effects of acarbose on starch hydrolysis: study in healthy subjects, ileostomy patients, and in vitro. Dig Dis Sci. 1992; 37:1057-64. https://pubmed.ncbi.nlm.nih.gov/1618053

34. Rodier M, Richard JL, Monnier L et al. Effect of long term acarbose (Bay g 5421) therapy on metabolic control of non insulin dependent (Type II) diabetes mellitus. Diabete Metab. 1988; 14:12-4. https://pubmed.ncbi.nlm.nih.gov/3292303

35. Couet C, Ulmer M, Hamdaoui M et al. Metabolic effects of acarbose in young healthy men. Eur J Clin Nutr. 1989; 43:187-96. https://pubmed.ncbi.nlm.nih.gov/2659314

36. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med. 1993; 329:977-86. https://pubmed.ncbi.nlm.nih.gov/8366922

37. Hanefeld M, Fischer S, Schulze J et al. Therapeutic potentials of acarbose as first-line drug in NIDDM insufficiently treated with diet alone. Diabetes Care. 1991; 14:732-7. https://pubmed.ncbi.nlm.nih.gov/1954810

39. Baron AD, Eckel RH, Schmeiser L et al. The effect of short-term alpha-glucosidase inhibition on carbohydrate and lipid metabolism in type II (noninsulin-dependent) diabetics. Metab Clin Exp. 1987; 36:409-15. https://pubmed.ncbi.nlm.nih.gov/3553848

40. Sailer D, Röder G. Treatment of non-insulin dependent diabetic adults with a new glycoside hydrolase inhibitor (Bay g 5421). Arzneimittelforschung. 1980; 30:2182-5. https://pubmed.ncbi.nlm.nih.gov/7194082

41. Ahr HJ, Boberg M, Krause HP et al. Pharmacokinetics of acarbose: Part I: absorption, concentration in plasma, metabolism and excretion after single administration of [14C]acarbose to rats, dogs and man. Arzneimittelforschung. 1989; 39:1254-60. https://pubmed.ncbi.nlm.nih.gov/2610717

42. Klein R, Klein BEK, Moss SE et al. Glycosylated hemoglobin predicts the incidence and progression of diabetic retinopathy. JAMA. 1988; 260:2864-71. https://pubmed.ncbi.nlm.nih.gov/3184351

43. Scheen AJ, Castillo MJ, Lefèbvre PJ. Combination of oral antidiabetic drugs and insulin in the treatment of non-insulin-dependent diabetes. Acta Clin Belg. 1993; 48:259-68. https://pubmed.ncbi.nlm.nih.gov/8212978

44. Reaven GM, Lardinois CK, Greenfield MS et al. Effect of acarbose on carbohydrate and lipid metabolism in NIDDM patients poorly controlled by sulfonylureas. Diabetes Care. 1990; 13(Suppl 3):32-6. https://pubmed.ncbi.nlm.nih.gov/2209341

45. Gérard J, Luyckx AS, Lefebvre PJ. Improvement of metabolic control in insulin dependent diabetics treated with the α-glucosidase inhibitor acarbose for two months. Diabetologia. 1981; 21:446-51. https://pubmed.ncbi.nlm.nih.gov/7028558

46. Rybka J, Gregorová A, Zmydlená A et al. Clinical study of acarbose. Drug Invest. 1990; 2:264-7.

47. Santeusanio F, Ventura MM, Contadini S et al. Efficacy and safety of two different dosages of acarbose in non-insulin dependent diabetic patients treated by diet alone. Diabetes Nutr Metab. 1993; 6:147-54.

48. Dimitriadis GD, Tessari P, Go VLW et al. α-Glucosidase inhibition improves postprandial hyperglycemia and decreases insulin requirements in insulin-dependent diabetes mellitus. Metabolism. 1985; 34:261-5. https://pubmed.ncbi.nlm.nih.gov/3883097

49. Sachse G, Willms B. Effect of the α-glucosidase-inhibitor BAY-g- 5421 on blood glucose control of sulphonylurea-treated diabetics and insulin- treated diabetics. Diabetologia. 1979; 17:287-90. https://pubmed.ncbi.nlm.nih.gov/387504

51. Calle-Pascual AL, Garcia-Honduvilla J, Martin-Alvarez PJ et al. Comparison between acarbose, metformin, and insulin treatment in type 2 diabetic patients with secondary failure to sulfonylurea treatment. Diabete Metab. 1995; 21:256-60. https://pubmed.ncbi.nlm.nih.gov/8529760

52. Bayer. Product information form for American hospital formulary service: Precose (acarbose tablets). West Haven, CT; 1996 Apr.

54. National Institutes of Health Office of Medical Applications of Research. Consensus development conference statement: diet and exercise in noninsulin-dependent diabetes mellitus. Bethesda, MD: 1986(Dec 10); 6:1-7. Available at National Institutes of Health website. Accessed 2007 Feb 5. http://consensus.nih.gov/1986/1986DietExerciseDiabetesII060html.htm

57. Bailey CJ, Turner RC. Metformin. N Engl J Med. 1996; 334:574-9. https://pubmed.ncbi.nlm.nih.gov/8569826

59. American Diabetes Association. Office guide to diagnosis and classification of diabetes mellitus and other categories of glucose intolerance. Diabetes Care. 1995; 18(Suppl 1):4.

62. American Diabetes Association. Standards of medical care for patients with diabetes mellitus. Diabetes Care. 2006;29 (Suppl 1):S4-42.

63. Knudson PE, Weinstock RS, Henry JB. Carbohydrates. In: Henry JB, ed. Todd-Sanford-Davidsohn clinical diagnosis and management by laboratory methods. 20th ed. Philadelphia: W.B. Saunders Company; 2001:211-23.

64. Polonsky KS, Sturis J, Bell GI. Non-insulin-dependent diabetes mellitus—a genetically programmed failure of the beta cell to compensate for insulin resistance. N Engl J Med. 1996; 334:777-83. https://pubmed.ncbi.nlm.nih.gov/8592553

68. U. K. Prospective Diabetes Study Group. U. K. prospective diabetes study 16: overview of 6 years’ therapy of type II diabetes: a progressive disease. Diabetes. 1995; 44:1249-58. https://pubmed.ncbi.nlm.nih.gov/7589820

70. 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). Lancet. 1998; 352:837-53. https://pubmed.ncbi.nlm.nih.gov/9742976

71. American Diabetes Association. Implications of the United Kingdom Prospective Diabetes Study. Diabetes Care. 1999; 22(Suppl 1):27-31. https://pubmed.ncbi.nlm.nih.gov/10333899

72. Matthews DR, Cull CA, Stratton RR et al. UKPDS 26: sulphonylurea failure in non-insulin-dependent diabetic patients over 6 years. Diabet Med. 1998; 15:297-303. https://pubmed.ncbi.nlm.nih.gov/9585394

75. Genuth S, Brownless MA, Kuller LH et al. Consensus development conference on insulin resistance: Novermber 5-6 1997. Diabetes Care. 1998; 21:310-4. https://pubmed.ncbi.nlm.nih.gov/9540000

78. Nathan DM. Some answers, more controversy, from UKDS. Lancet. 1998; 352:832-3. https://pubmed.ncbi.nlm.nih.gov/9742972

82. UK Prospective Diabetes Study (UKPDS) Group. ffect of intensive blood-glucose control with metfromin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet. 1998; 352:854-65. https://pubmed.ncbi.nlm.nih.gov/9742977

90. American Diabetes Association. Type 2 diabetes in children and adolescents. Pediatrics. 2000; 105:671-80. https://pubmed.ncbi.nlm.nih.gov/10699131

92. United Kingdom Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. BMJ. 1998; 317:703-13. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC28659/ https://pubmed.ncbi.nlm.nih.gov/9732337

93. UK Prospective Diabetes Study (UKPDS) Group. Efficacy of atenolol and captopril in reducing risk of macrovascular complications in type 2 diabetes mellitus: UKPDS 39. BMJ. 1998; 317:713-20. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC28660/ https://pubmed.ncbi.nlm.nih.gov/9732338

99. Buse J. Combining insulin and oral agents. Am J Med. 2000; 108(Suppl 6A):23S-32S. https://pubmed.ncbi.nlm.nih.gov/10764847

101. Yki-Jarvinen H, Dressler A, Ziemen M et al. Less nocturnal hypoglycemia and better post-dinner glucose control with bedtime insulin glargine compared with bedtime HPH insulin during insulin combination therapy in type 2 diabetes. Diabetes Care. 2000; 23:1130-6 (IDIS 451244) https://pubmed.ncbi.nlm.nih.gov/10937510

102. Eli Lilly and Company. Humalog (insulin lispro, rDNA origin) injection prescribing information. Indianapolis, IN; 2000 May 1.

104. Florence JA, Yeager BF. Treatment of type 2 diabetes mellitus. Am Fam Physician. 1999; 59:2835-44. https://pubmed.ncbi.nlm.nih.gov/10348076

105. Bastyr EJ, Johnson ME, Trautman ME et al. Insulin lispro in the treatment of patients with type 2 diabetes mellitus after oral agent failure. Clin Ther. 1999; 21:1703-4. https://pubmed.ncbi.nlm.nih.gov/10566566

106. DeFronzo RA. Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med. 1999; 131:281-303. https://pubmed.ncbi.nlm.nih.gov/10454950

108. Bayer. Managing you diabetes with Precose. Questions/answers to help you get the most out of your diabetes treatment plan. West Haven, CT; 2001 May.

109. American Diabetes Association. Preconception care of women with diabetes. Diabetes Care. 2004; 27(Suppl 1):S76-78.

110. Nathan DM, Buse JB, Davidson MB et al. Medical management of hyperglycemia in type 2 diabetes: a consensus algorithm for the initiation and adjustment of therapy. A consensus statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care. 2009; 32:193-203. https://pubmed.ncbi.nlm.nih.gov/18945920

111. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. Canadian Diabetes Association 2003 clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diabetes. 2003; 27 (Suppl 2):S1-152.

112. Amylin Pharmaceuticals. Symlin (pramlintide acetate) injection prescribing information. San Diego, CA; 2005 Mar.

113. GlaxoSmithKline. Avandia (rosiglitazone maleate) tablets prescribing information. Research Triangle Park, NC; 2006 Jun.

114. SmithKline Beecham Pharmaceuticals, Philadelphia, PA: Personal communication.

698. Garber AJ, Handelsman Y, Grunberger G et al. Consensus statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the comprehensive type 2 diabetes management algorithm 2020 executive summary. Endocr Pract. 2020; 26:107-139. https://pubmed.ncbi.nlm.nih.gov/32022600

699. Zelniker TA, Wiviott SD, Raz I et al. Comparison of the effects of glucagon-like peptide receptor agonists and sodium-glucose cotransporter 2 inhibitors for prevention of major adverse cardiovascular and renal outcomes in type 2 diabetes mellitus. Circulation. 2019; 139(17):2022-2031. https://pubmed.ncbi.nlm.nih.gov/30786725

704. American Diabetes Association. 9. Pharmacologic approaches to glycemic treatment: Standards of Medical Care in Diabetes-2020. Diabetes Care. 2020; 43:S98-S110. https://pubmed.ncbi.nlm.nih.gov/31862752

705. American Diabetes Association. 10. Cardiovascular disease and risk management: Standards of Medical Care in Diabetes-2020. Diabetes Care. 2020; 43:S111-S134. https://pubmed.ncbi.nlm.nih.gov/31862753

706. American Diabetes Association. 11. Microvascular complications and foot care: Standards of Medical Care in Diabetes-2020. Diabetes Care. 2020; 43:S135-S151. https://pubmed.ncbi.nlm.nih.gov/31862754

Medical Disclaimer