ReviewPharmacological reports : PR2021
Altered glucose metabolism and insulin resistance in cancer-induced cachexia: a sweet poison.
Review in Pharmacological reports : PR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 67 citations in OpenAlex.
- A Drosophila tumor model identifies a conserved Upd-JAK/STAT-Akh signaling axis associated with metabolic changes in cancer cachexia.Disease models & mechanisms · 2026Article
- Beyond a waste product: lactate as a master metabolite dictating anti-tumor T-cell fate.Cell death & disease · 2026Review
- Linking metabolism and metastasis: elevated α-hydroxybutyric acid in oral squamous cell carcinoma patients with lymph node metastasis.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- NF-κB Signaling as a Central Driver of Cancer Cachexia.Cancers · 2026Review
- Gut microbiota in cancer cachexia: a new frontier for research and therapy.Genes & nutrition · 2025Review
- Pancreatic Damage in Ovarian Cancer-Associated Cachexia Is Driven by Activin A Signalling.Journal of cachexia, sarcopenia and muscle · 2025Article
- Sarcopenia and fat loss from serial CT predict survival in multiple myeloma patients undergoing stem cell transplantation.World journal of surgical oncology · 2025Article
- Targeting the molecular crosstalk between diabetes and lung cancer for therapeutic intervention.Discover oncology · 2025Review
- Associations between four insulin resistance (IR) surrogates and the risk of small cell lung cancer (SCLC).Scientific reports · 2025Article
- Hallmarks of Cancer Cachexia: Sexual Dimorphism in Related Pathways.International journal of molecular sciences · 2025Review
- The prognostic value of a laboratory cachexia score (LCAS) defined by LDH, CRP and albumin in patients with advanced lung cancer.BMC cancer · 2025Article
- Article
- Effects of diet and ovariectomy onBrain communications · 2025Article
- Discovery of Glucose Metabolism-Associated Genes in Neuropathic Pain: Insights from Bioinformatics.International journal of molecular sciences · 2024Article
- Article
- Article
- Associations Between Adiponectin and the Development of Diabetes in Rheumatoid Arthritis.The Journal of clinical endocrinology and metabolism · 2024Article
- Cancer cachexia: biomarkers and the influence of age.Molecular oncology · 2024Review
- CCL2 signaling promotes skeletal muscle wasting in non-tumor and breast tumor models.Disease models & mechanisms · 2024Article
- The Role of Adipocytes Recruited as Part of Tumor Microenvironment in Promoting Colorectal Cancer Metastases.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cachexia is a wasting disorder characterised by specific skeletal muscle and adipose tissue loss. Cancer cachexia is also driven by inflammation, altered metabolic changes such as increased energy expenditure, elevated plasma glucose, insulin resistance and excess catabolism. In cachexia, host-tumor interaction causes release of the lactate and inflammatory cytokines. Lactate released by tumor cells takes part in hepatic glucose production with the help of gluconeogenic enzymes. Thus, Cori cycle between organs and cancerous cells contributes to increased glucose production and energy expenditure. A high amount of blood glucose leads to increased production of insulin. Overproduction of insulin causes inactivation of PI3K/Akt/m-TOR pathway and finally results in insulin resistance. Insulin is involved in maintaining the vitality of organs and regulate the metabolism of glucose, protein and lipids. Insulin insensitivity decreases the uptake of glucose in the organs and results in loss of skeletal muscles and adipose tissues. However, looking into the complexity of this metabolic syndrome, it is impossible to rely on a single variable to treat patients having cancer cachexia. Hence, it becomes greater a challenge to produce a clinically effective treatment for this metabolic syndrome. Thus, the present paper aims to provide an understanding of pathogenesis and mechanism underlining the altered glucose metabolism and insulin resistance and its contribution to the progression of skeletal muscle wasting and lipolysis, providing future direction of research to develop new pharmacological treatment in cancer cachexia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.