A Metabolic Shift from Normal to Cancer Metabolism

Authors

  • Maurice Israël Institut Alfred Fessard CNRS 2 Av., Terrasse 91190 Gif-sur-Yvette, France
  • Guy Tenenbaum 5558 E Leitner Drive Coral Springs, FL 33067, USA

DOI:

https://doi.org/10.14738/bjhr.1301.19878

Keywords:

cancer metabolism, pancreas in cancer, ketones in cancer, AMP deaminase, AMP kinase, DAG lipase

Abstract

This work compares cancer metabolism to other metabolic situations elicited by catabolic, or anabolic hormones, or by Growth hormone. The comparison suggests that hormonal controls allowing shifting from catabolism to anabolism partially fail in cancer, leading to a hybrid metabolic situation in cancer, with enzymes phosphorylated as for catabolism, while others shift to anabolism.  Markers such as AMP and DAG, differentiate the metabolic situations studied. To get markers opposite to those of cancer metabolism, a DAG lipase was implicated. This enzyme forms endocannabinoids with anti-proliferative effects.

References

Israël, M., Signalling and metabolism in Cancer: Endocrine pancreas deficiency and hybrid Anabolism-catabolism, drugs that undo the process. Cancer Therapy, 2014. 10:p1-10.

Israël, M., E. Berg, and G. Tenenbaum, Cancer Metabolism: Fasting reset, The Keto-Paradox and drugs for undoing. Journal of Clinical Medicine, 2023. 12: p 1589-1602.

Mazurek, S., E. Eigenbrodt, The tumor metabolome. Anticancer Res., 2003, 23: p 1149-1154.

Hitosugi, T., et al., Tyrosine phosphorylation of mitochondrial Pyruvate dehydrogenase kinase 1 Is important for cancer metabolism. Molecular Cell, 2011. 44: p 864-877. Scholar Publishing

Israël, M., L. Schwartz, Inhibition of the ketolytic acetyl CoA supply to tumors could be their”Achilles heel”. Int. J. Cancer, 2020, 147: p1755-1757.

Israël, M., E. Berg, and G. Tenenbaum, Branched Chain Amino Acid Ketones, or Ketolysis of Beta hydroxybutyrate support Lipogenesis and tumour growth. British Journal of Healthcare and Medical research, 2024, 11(4): p 69-74.

Yoshino,M., E. Miyajima, and K. Tsushima, Kinetics of the interactions of AMPdeaminase with Fatty acids. J. Biol. Chem., 1979, 254: p1521-1525

Yoshino,M., E.Miyajima, AMP Deaminase as a Control System of Glycolysis in Yeast. J. Biol. Chem., 1982, 257(18):p10644-10649.

Ouyang, J., R.A.Parakhia, and R.S. Ochs. Metformin activates AMP kinase through inhibition of AMPdeaminase. Journal of Biological Chemistry, 2011, 286(1): p 1-11.

Warburg, O., On the respiratory impairment in cancer cells. Science, 1956, 124: p 269-370.

Mendizabal-Zubiaga, J., et al., Cannabinoid CB1 Receptors are localized in striated muscle mitochondria and regulate mitochondrial respiration. Front. Physiol., 2016, 7: p476

De Petrocellis, L. et al., The endogenous cannabinoid anandamine inhibits human breast cancer cell proliferation. Proc Natl Acad Sci., 1998, 95(14): p 8375-380. ,

Klement, RJ. , Wilhelm Brünings forgotten contribution to the metabolic treatment of cancer Utilizing hypoglycaemia and very low carbohydrate (ketogenic) diet. J. Tradit. Complement Med., 2019, 9 p: 192-200.

Vegari, E., et al., Insulin inhibits glucagon release by SCTL- induced stimulation of somatostatin secretion. Nat. Commun., 2019,10: p 139-50.

Gernez, A., in, Néo-postulats biologiques et pathologiques.1975, Editions « La vie Claire ».

Guevara-Aguirre, J., et al. Growth Hormone Receptor Deficiency is associated with a major reduction in Pro Aging signalling, Cancer, and Diabetes in Humans. Science translational Medicine, 2011, 3(70):p.70ra13. Scholar Publishing

Downloads

Published

2026-02-02

How to Cite

Israël, M., & Tenenbaum, G. (2026). A Metabolic Shift from Normal to Cancer Metabolism. British Journal of Healthcare and Medical Research, 13(01), 249–257. https://doi.org/10.14738/bjhr.1301.19878