Altered glucose metabolism and insulin resistance in cancer-induced cachexia: a sweet poison.
Level 5 - mechanism / opinion, no new human data
Narrative review detailing mechanistic pathways without primary data
PubMed 33141425 · doi:10.1007/s43440-020-00179-y
What was done
This narrative review synthesized the proposed mechanisms linking altered glucose metabolism, the Cori cycle, and insulin resistance to muscle wasting and lipolysis in cancer-induced cachexia.
What was found
The abstract reports no numerical data. It outlines a mechanistic pathway wherein tumor-derived lactate fuels hepatic gluconeogenesis via the Cori cycle, elevating blood glucose and stimulating excess insulin production. This chronic hyperinsulinemia is described as leading to inactivation of the PI3K/Akt/mTOR pathway and systemic insulin resistance, impairing organ glucose uptake and driving skeletal muscle and adipose tissue breakdown.
Why it matters
Understanding the metabolic and endocrine cross-talk between tumors and host tissues helps identify multi-target strategies for treating cancer cachexia, which cannot be adequately managed by addressing single metabolic pathways.
Limits
As a narrative review, it provides no primary clinical or experimental data, presents no statistical findings in the abstract, and lacks a systematic search methodology or sample size evaluation.
Cited by
- supports Cancer cachexia involves the mobilization of skeletal muscle proteins for gluconeogenesis and direct tumor utilization of glutamine.