Anticancer drugs effects on glucose metabolism
| Class/Agent | Glycaemia | HbA1c | c-peptide/insulin | Mechanisms |
|---|---|---|---|---|
| Hormonal agents - GnRH agonists (triptorelin, leuprorelin) - Anti-androgens (cyproterone acetate, flutamide, bicalutamide, nilutamide) | ↑ [73] | ↑ [78] | Increased Ins-Res | |
| Glucocorticoids (prednisone, prednisolone, methylprednisolone, dexamethasone) | ↑ [80, 81] | ↑ [67, 81] | Increased Ins-Res | |
| mTOR inhibitors (everolimus, sirolimus, temsirolimus) | ↑ [87] | ↑ [67] | Increased Ins-Res | |
| ICIs - Anti-CTLA-4 antibodies (ipilimumab) - PDL-1 inhibitors (atezolizumab, avelumab) - PD-1 inhibitors (nivolumab, pembrolizumab) | ↑ [89] | ↑ [89] | ↓ [89] | Reduced IP/S |
| Somatostatin analogues (octreotide, lanreotide, pasireotide) | ↑ (pasireotide) [93]↓ (octreotide) [94] | ↑ [93] | Reduced IP/SReduced GP/S | |
| L-asparaginase | ↑ [95, 96] | Reduced IP/S | ||
| Alkylating agents (cisplatin, carboplatin, oxaliplatin, cyclophosphamide, etc.) | ↑ [97–99] | ↑ [67] | Reduced IP/S | |
| Anti-microtubules (docetaxel, paclitaxel, vinorelbine, vincristine, etc.) | ↑ [97, 100] | ↑ [67] | Reduced IP/S | |
| Antimetabolites (5-fluorouracil, gemcitabine, capecitabine, methotrexate, etc.) | ↑ [98, 101] | ↑ [67] | ↓ [101] | Reduced IP/S |
| Antracyclines (doxorubicin, epirubicin, etc.) | ↑ [97] | Reduced IP/S |
indicates the uncertainty of the evidence on this item; GnRH: gonadotropin-releasing hormone; Ins-Res: insulin resistance; HbA1c: glycated haemoglobin; mTOR: mammalian target of rapamycin; ICIs: immune checkpoint inhibitors; CTLA-4: cytotoxic T-lymphocyte 4-antigen; PDL-1: programmed cell death ligand-1; PD-1: programmed cell death-1; IP/S: insulin production/secretion; GP/S: glucagon production/secretion