| |
Diabetes medications and risk of HCC
|
| |
| |
Download the PDF here
Abstract
Type 2 diabetes mellitus is a recognized risk factor for HCC in patients with liver disease, independent from the etiology of their liver disease. Hence, prevention and treatment of type 2 diabetes mellitus and its underlying cause, insulin resistance, should be considered a treatment target for patients with liver disease. The drug armamentarium for diabetes is wide and consists of agents with insulin-sensitizing activity, agents that stimulate insulin secretion, insulin itself, and agents that reduce gastrointestinal and urinary glucose absorption. From an endocrinology perspective, the main goal of treatment is the achievement of euglycemia; however, in patients at risk of, or with known underlying liver disease, the choice of diabetic medication as it relates to potential hepatic carcinogenesis remains complex and should be carefully considered. In the last decade, increasing evidence has suggested that metformin may reduce the risk of HCC, whereas evidence for other classes of diabetic medications, particularly some of the newer agents including the sodium glucose cotransporter-2 inhibitors and glucagon-like peptide-1 receptor agonists, is fewer and often inconsistent. In this review, we aim to summarize the current evidence on the potential effects of the most widely used diabetic agents on liver cancer tumorigenesis.
Insulin
As described previously, insulin is a potent mitogen associated with up-regulation of various growth factors that lead to stimulation of cytokine pathways related to cell proliferation and inhibition of apoptosis.[82] In the past decade, increasing evidence has shown a higher risk of HCC incidence in diabetic patients treated with insulin. Indeed, high fasting serum insulin levels (> 6.10 µU/ml) have been associated with a 2.36-fold risk of HCC when compared with low fasting insulin levels (< 2.75 µU/ml).[83]
| |
| |
| |
|
|
|
