A review of cancer cachexia and abnormal glucose metabolism in humans with cancer.

Abstract

In 1919, glucose intolerance became the earliest recognized metabolic abnormality in cancer patients. Prior to the development of severe malnutrition, colon, gastric, sarcoma, endometrial, prostate, localized head, neck, and lung cancer patients had many of the metabolic abnormalities of type II (noninsulin dependent) diabetes mellitus. These metabolic abnormalities include glucose intolerance, an increase in both hepatic glucose production (HGP) and glucose recycling, and insulin resistance. In a study of over 600 cancer patients, a diabetic pattern of glucose tolerance test was noted in over one-third of the patients. An increased rate of HGP, commonly seen in diabetics, has been noted in almost all types of cancer patients studied to date. Etiology of the increased glucose production in the cancer patient is not known, but abnormalities in the counter regulatory hormones, especially growth hormone, may contribute to the development of abnormal glucose metabolism. A second possible stimulus for the increase in HGP could be the glucose needs of the tumor. Abnormally high glucose utilization rates in small amounts of tumor tissue have recently been described. This suggests that small tumors may have large needs for glucose calories. An increase in anaerobic glycolysis in the tumor tissue can increase lactate production in the tumor-bearing human, thus supplying substrate to the liver to increase glucose production rates. In this paper, the nature of abnormal glucose metabolism in cancer patients is described.

Uncoupling of fatty acid and glucose metabolism in malignant lymphoma: a PET study

“…The depletion of fatty acids from the apidose tissue and increased fasting lactate levels are commonly found in patients even with a small tumour burden (Tayek, 1992). In our patients, the median plasma concentration of both FFA and lactate was very close to the upper normal limit and some individual patients showed high values that possibly reflected increased lipolysis and reduced oxidative metabolism induced by tumour.…”

FDG–PET. A possible prognostic factor in head and neck cancer

“…Secondly, it has been proposed that the abnormal carbohydrate metabolism seen in the cachectic state is responsible for the disproportionate glucose uptake, in tumours of patients with advanced malignancies (Tayek, 1992). An association has been demonstrated between FDG uptake and cellular proliferation and/or tumour growth rate in a number of cancers including head and neck, lung tumours and non-Hodgkin's lymphoma (Minn et al, 1988(Minn et al, , 1997Haberkorn et al, 1991).…”

Proliferating cell nuclear antigen in the cytoplasm interacts with components of glycolysis and cancer

“…Cancer cells generally show an increase in glucose metabolism, compared to normal cells [19][20][21][22]. This may be, in part, due to the increase in the glucose trans-membrane transportation and concentration of glycolytic enzymes in cancer cells [23][24][25].…”