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JANUVIA® (sitagliptin)

Dynamics of the disease

Learn more about the normal, complex process of glucose homeostasis and the mechanisms that lead to type 2 diabetes, including the role of incretins in this process.

Understanding Incretins

Incretins play an active role in mediating pancreatic beta- and alpha-cell responses in healthy individuals. However, this effect is diminished in type 2 diabetes.

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Insulin Secretion

The coordinated functioning of pancreatic beta and alpha cells is essential to normal glycemic control.

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Insulin Secretion Abnormalities

Although insulin resistance is found in almost all patients with type 2 diabetes, the defect in insulin secretion accounts for the development of hyperglycemia and progression of the disease. 12

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DPP-4 Inhibition

DPP-4 inhibition has been shown to slow the degradation of incretins, therefore prolonging their actions in glucose regulation. 13,14,15

Evolution of Incretin Science

The area of diabetes research is rapidly evolving. In recent years, scientific attention has been directed to incretin hormones and their role in glycemic control.

Selected Important Risk Information About JANUMET

JANUMET is contraindicated in patients with renal disease or renal dysfunction (serum creatinine levels >1.5 mg/dL in males and >1.4 mg/dL in females) or abnormal creatinine clearance; acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma; or history of a serious hypersensitivity reaction to JANUMET or sitagliptin (one of the components of JANUMET), such as anaphylaxis or angioedema.

Please read the Boxed Warning for JANUMET about lactic acidosis.

Selected Important Risk Information About JANUVIA

When JANUVIA was used in combination with a sulfonylurea or insulin, medications known to cause hypoglycemia, the incidence of hypoglycemia was increased over that of placebo. Therefore, a lower dose of sulfonylurea or insulin may be required to reduce the risk of hypoglycemia.

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12.
Del Prato S, Marchetti P. Beta- and alpha-cell dysfunction in type 2 diabetes. Horm Metab Res. 2004;36:775–781.
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13.
Ahrén B. Gut peptides and type 2 diabetes mellitus treatment. Curr Diab Rep. 2003;3:365–372.
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14.
Drucker DJ. Therapeutic potential of dipeptidyl peptidase IV inhibitors for the treatment of type 2 diabetes. Expert Opin Investig Drugs. 2003;12:87–100.
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15.
Pospisilik JA, Stafford SG, Demuth H-U, et al. Long-term treatment with the dipeptidyl peptidase IV inhibitor P32/98 causes sustained improvements in glucose tolerance, insulin sensitivity, hyperinsulinemia, and beta-cell glucose responsiveness in VDF (fa/fa) Zucker rats. Diabetes. 2002;51:943–950.