Oral antihyperglycemic therapy for type 2 diabetes mellitus - PubMed (original) (raw)

Review

Oral antihyperglycemic therapy for type 2 diabetes mellitus

Alice Y Y Cheng et al. CMAJ. 2005.

Abstract

Diabetes mellitus is a chronic disease that is growing in prevalence worldwide. Pharmacologic therapy is often necessary to achieve optimal glycemic control in the management of diabetes. Orally administered antihyperglycemic agents (OHAs) can be used either alone or in combination with other OHAs or insulin. The number of available OHAs has increased significantly in the last decade, which translates into more therapeutic options and complex decision-making for physicians. This review article is designed to help with these decisions. We review the mechanism of action, efficacy and side effects of the different classes of OHAs (alpha-glucosidase inhibitors, biguanides, insulin secretagogues, insulin sensitizers and intestinal lipase inhibitor) and discuss the current recommendations for their use.

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Figures

Fig. 1: Overview of the pathogenesis of type 2 diabetes mellitus. FFA = free fatty acids. Photo: Lianne Friesen and Nicholas Woolridge

Fig. 2: Major target organs and actions of orally administered antihyperglycemic agents in type 2 diabetes mellitus. TZD = thiazolidinedione; FFA = free fatty acid; AGI = α-glucosidase inhibitor. Photo: Lianne Friesen and Nicholas Woolridge

Fig. 3: Metformin activates AMPK in liver and muscle to improve glucose and lipid metabolism in type 2 diabetes. (A) shows the ion channel in a resting pancreatic β cell. (B) shows the action of insulin secretagogues on the cell. AMPK = adenosine monophosphate-activated protein kinase; ACC = acetyl-CoA carboxylase; SREPB-1 = sterol-regulatory-element-binding-protein-1; VLDL = very low density lipoprotein. Photo: Lianne Friesen and Nicholas Woolridge

Box 1

Fig. 4: Insulin secretagogues mimic glucose to close adenosine triphosphate-sensitive potassium channels (kir6.2) and stimulate insulin secretion. Photo: Lianne Friesen and Nicholas Woolridge

Fig. 5: Mechanism of action of thiazolidinediones. PPARγ = peroxisome proliferator-activated receptor-gamma; TNF-α = tumour necrosis factor-α. *There is recent evidence in rodents that skeletal muscle PPARγis an important mediator of the beneficial effects of TZDs on insulin sensitivity. Photo: Lianne Friesen and Nicholas Woolridge

Fig. 6: Management of hyperglycemia in type 2 diabetes. BMI = body mass index. *When used in combination with insulin, insulin sensitizers may increase the risk of edema of congestive heart failure. The combination of an insulin sensitizer and insulin is currently not an approved indication in Canada. †If using preprandial insulin, do not add an insulin secretagogue. Reprinted with permission from Can J Diabetes 2003;27(Suppl 2):S39.

Comment in

Effect of thiazolidinediones on lipid profile.
Madan P. Madan P. CMAJ. 2005 Aug 16;173(4):344; author reply 344-5. doi: 10.1503/cmaj.1050034. CMAJ. 2005. PMID: 16103495 Free PMC article. No abstract available.

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Oral antihyperglycemic therapy for type 2 diabetes mellitus - PubMed (original) (raw)