PHARMACOLOGICAL PROPERTIES

Identifying the Pharmacological Properties and Actual/Potential Effects of Metformin on the Patient

Abstract

Metformin is used in the treatment of diabetes mellitus type 2, especially in people with overweight and obesity, and thus preserved normal renal function. Metformin helps to reduce cholesterol LDL and triglycerides and is not associated with weight gain and this is the only anti-diabetic drug that can reduce mortality from cardiovascular complications in diabetes mellitus. When properly administered metformin causes few side effects (some of which are more common gastrointestinal disorder) and is associated with lower risk of hypoglycemia.

Identifying the Pharmacological Properties and Actual/Potential Effects on the Patient

Introduction

Metformin, or metformin hydrochloride commercial preparation is a antidiabetic drug for oral administration. It is used commonly in the treatment and prevention of type 2 diabetes mellitus, also known as noninsulin-dependent diabetes, particularly in patients with overweight as well as in children and people with normal renal function (Salpeter, Greyber, Pasternak & Salpeter 2003). The drug is indicated as an adjunct to diet and physical exercise in patients whose hyperglycemia cannot be controlled only with diet modification (Bailey 2007). FDA recommends doctors not to exceed metformin by 2.0 g per day (Wulffele´ 2004). The recommendation emphasizes physician to minimize its use if adverse reactions are found. Some commercial preparations combine metformin with chlorpropamide or nateglinide (Palomba, Pasquali, Orio & Nestler 2009). In this paper, I identify its pharmacological properties and actual/potential effects on the patient.

Pharmacological Properties

Metformin is an antihyperglycemic but does not act as hypoglycemic therefore does not produce hypoglycemia. The mechanism in which the drug responds (in the treatment of diabetes) is unknown. However, the drug has given widely known therapeutic benefit. Metformin is not recommended affect secretion of pancreas. However, is not activated in the absence of insulin (Palomba, Pasquali, Orio & Nestler 2009). It acts primarily by reducing gluconeogenesis and liver glycogenolysis. It also reduces the absorption of glucose from the gastrointestinal tract while increasing sensitivity to insulin by increasing the use of glucose by peripheral tissues, and by increasing the activity of the insulin receptors (Bailey 2007). The average diabetic patient with type 2 diabetes has a rate of gluconeogenesis three times higher than normal, and apparently metformin reduces this situation in more than a third. Metformin is not metabolized but is excreted in the urine with an elimination half-life of 6 and 2 hours (Salpeter, Greyber, Pasternak & Salpeter 2003).

Effects on Patients

Metformin improves hyperglycemia primarily through inhibition of hepatic glucose production, ie, gluconeogenesis liver. Metformin activates protein kinase-dependent AMPK, an enzyme that plays an important role in the signaling pathway of insulin, energy management and whole body glucose metabolism and fat. The activation of AMPK is necessary for the inhibitory effect of metformin on glucose production by liver cells (Wulffele´ 2004). (Bailey 2007).

The use of this medicine by women with abnormal ovulation causes weight loss improvement in both ovulation and in fertility, a decrease in the rate of abortions and gestational diabetes. In these patients, metformin reduces levels of luteinizing hormone and ...