Abstract

Introduction

Metformin is the most frequently prescribed medication in the management of Type 2 Diabetes Mellitus.

Metformin belongs to the biguanide class of oral antidiabetic drugs. The main site of metformin action is thought to be in the liver where the drug suppresses glucose production.

It promotes glucose uptake by tissues via the glucose transporters, and inhibits hepatic gluconeogenesis.

A range of additional affects such as improvements in endothelial function, hemostasis and oxidative stress, insulin resistance, lipid profiles, and fat redistribution accompany the primary glycemic function of metformin.

Metformin causes an impairment of calcium-dependent membrane activity in the ileum which leads to malabsorption of Vitamin B12 bound to intrinsic factor leading to vitamin B12 deficiency.

Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the phenotype of hyperglycemia.

Several distinct types of DM are caused by a complex interaction of genetics and environmental factors.

Depending on the etiology of the DM, factors contributing to hyperglycemia include reduced insulin secretion, decreased glucose utilization, and increased glucose production.

The metabolic dysregulation associated with DM causes secondary pathophysiologic changes in multiple organ systems that impose a tremendous burden on the individual with diabetes and on the health care system.

Vitamin B12, also referred to as cobalamin (Cbl), is thought to play a large role in the formation of red blood cells as well as key roles in brain and nerve function.

Vitamin B12 deficiency presents as neuropathy of the feet and development of anemia.

Neuropathy as a result of Vitamin B12 deficiency is particularly difficult to identify as it mimics that of diabetic neuropathy and can take a long period of time to develop.