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A Review on Metformin: Clinical Significance and Side Effects
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| Author:
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AVIJIT MAZUMDER, ASHINI SINGH, SUJEET JHA
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| Abstract:
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Metformin is a biguanide that has been used extensively worldwide for the treatment of type II diabetes
mellitus. It improves glycaemic control by enhancing insulin sensitivity in liver and muscle. An advantage of
metformin treatment is the tendency of weight reduction and the absence of significant hypoglycaemia; blood
glucose levels are reduced only to normal as it does not stimulate insulin secretion. Metformin also has a
beneficial effect on several cardiovascular risk factors including dyslipidemia, elevated plasminogen activator
inhibitor 1 levels, other fibrinolytic abnormalities, hyperinsulinemia, and insulin resistance. Metformin enhances
muscle and adipocyte insulin receptor number and/or affinity, increases insulin receptor tyrosine kinase
activity, stimulates glucose transport and glycogen synthesis, and reduces both hepatic gluconeogenesis and
glycogenolysis. The disadvantages are confined to the gastro-intestinal side effects and the potential risk of
vitamin B 12 and folic acid deficiency during long-term use. These side effects can be minimized by slow
titration and consumption with meals. The under lying mechanism for gastrointestinal intolerance are
proposed to be stimulation of intestinal secretion of serotonin, alteration in incretin and metabolism of
glucose, and malabsorption of bile salts. Lactic acidosis is rare contraindication associated with metformin.
Most reported cases of lactic acidosis occur in patients with contraindications, particularly impaired renal
function. Metformin has a good safety profile, efficacy and comparatively reduced cost. Its ability to improve
insulin sensitivity and the cardiovascular risk profile of type II diabetic patients has enhanced its clinical use as
first-line therapy.
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| Keyword:
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Metformin, Type 2 diabetes mellitus, Insulin, Gastrointestinal, Glycemic, Lactoacidosis.
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| EOI:
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| DOI:
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https://doi.org/10.31838/ijpr/2021.13.03.020
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| Download:
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