Batool Kereem Mohammed

Huda H.Al-Hasnawy

  Safaa sahib Naji Sultan

Alya A.Rahi

Abstract :

Gentamicin, an aminoglycoside antibiotic used to treat severe bacterial infections, is not directly associated with hyperglycemia; however, its administration in diabetic patients may indirectly lead to elevated blood glucose levels through several mechanisms. The stress response to infection induces hormonal changes that enhance gluconeogenesis and reduce insulin sensitivity, while gentamicin’s known nephrotoxic effects may further compromise renal function in diabetic individuals. Impaired kidney function alters glucose clearance and insulin metabolism, exacerbating hyperglycemia. Additionally, gentamicin may influence insulin secretion by inhibiting calcium-dependent pathways in pancreatic β-cells and disrupting gut microbiota, which in turn elevates branched-chain amino acids linked to insulin resistance. Electrolyte imbalances, particularly hypokalemia, commonly observed during gentamicin therapy, also impair insulin secretion and glucose tolerance. Inflammatory responses to infection and antibiotic-induced endotoxin release may temporarily worsen insulin resistance. Moreover, drug interactions between gentamicin and antidiabetic agents such as metformin pose further challenges, as renal impairment can affect drug clearance and increase toxicity risks. Therefore, effective management of diabetic patients receiving gentamicin necessitates close monitoring of blood glucose and renal function, careful adjustment of antidiabetic therapies, and proactive management of hydration and electrolyte levels. This approach is essential to mitigate the metabolic complications and optimise therapeutic outcomes in this vulnerable population.