Pathophysiology of cancer cachexia

Abstract

Cancer cachexia is a frequent complication observed in patients with malignant tumors. Although several decades have passed since the first focus on the metabolic dysfunction's associated with cancer, few effective therapeutic interventions have been successfully introduced into the medical armamentarium. The present study thoroughly reviews the basic pathophysiology of cancer cachexia and the treatment options already investigated in that field. Experimental and clinical studies were evaluated individually in order to clarify the intricate alterations observed in tumor-bearing patients. The difficulties in introducing sound and effective nutritional support or metabolic manipulation to reverse cancer cachexia are outlined in this review.

Metformin reduces the Walker-256 tumor development in obese-MSG rats via AMPK and FOXO3a

“…The tumor cells use glucose as an energy source converting it to lactate by glycolysis, consequently the lactate is converted to glucose in the liver by gluconeogenesis, which may be used by both the host and the tumor cells [36,70]. In this process, there is significant energy expenditure because only two molecules of ATP are produced by glycolysis, whereas six molecules of ATP are consumed by gluconeogenesis.…”

“…In this process, there is significant energy expenditure because only two molecules of ATP are produced by glycolysis, whereas six molecules of ATP are consumed by gluconeogenesis. Then, this contributes to the degradation of the tissue as a result of the increased lipolysis and proteolysis as well as to weight and body mass loss leading to cachexia [4,66,67,70].…”

A pilot study of Auron Misheil Therapy in patients with advanced cervical cancer: Tumor response and its correlation with clinical benefit response, and preliminary quality of life data

“…Cancer patients, due to the high energy requirements of tumors, often have changes in their carbohydrate metabolism, characterized by a higher glucose production, glucose intolerance, increased whole-body glucose turnover rate and insulin resistance (14,15). Glucose intolerance is one of the earliest recognized metabolic alterations in patients with cancer (15).…”

“…Glucose intolerance is one of the earliest recognized metabolic alterations in patients with cancer (15). Insulin treatment may have two beneficial mechanisms of action.…”

Anti-tumor effects of AMT in the renal cell carcinoma model

“…Cancer patients often experience deregulated glucose metabolism (4). Exogenous addition of insulin can help to normalize glucose levels (5) and, more importantly, insulin is regarded as a potent biologic response modifier when its role in the insulin potentiation therapy concept is discussed (6).…”