Metabolism Disorders

The cause of metabolic changes in cancer patients remains unclear. However, several mechanisms that play a role is the presence of a systemic response mediated by hormonal factors distant induced tumors (neuroendocrine axis), the non-specific response to factors released by tumors, the response systemic inflammation mediated by cytokines produced by macrophages. cytokines is a group of various soluble glycoproteins and low molecular weigh peptides that regulate interactions between cells and the function of cells and tissues. In relation with cancer of cachexia, cytokines regulate gastric motility and emptying via the gastrointestinal tract or central nervous system by disrupting efferent signals that regulate satiety. Several hormones and cytokines that play a role in metabolic disorders are: TNF suppress lipoprotein lipase activity in adipocytes, thereby disrupting kliren triglicerida of plasma and cause hypertriglyceridemia; IL-1 causes anorexia through blocking neuropeptide Y (NPY) induced feeding, NPY is a potent feeding stimulatory peptides which are activated by a decrease in leptin levels; TNF and IL-1 increased levels of corticotrophin releasing hormone which is a neurotransmitter in the central nervous and release of glucose-sensitive neurons causes a decrease in the intake food, and IL-6, leukemia inhibitor factor (LIF) produced by cancer cells particularly skeletal muscle causing a potent cachectic effects; IFN-γ also causes of cachexia; lipid-mobilizing factor causing lipolysis and weight loss; proteolysis Inducing factor (PIF) causes the degradation of proteins in skeletal muscle through increased regulation of ubiquitin proteasome proteolytic pathway, reducing the synthesis protein and increase cytokines and acute phase proteins; Leptin controls the intake food and energy expenditure through effector neuropeptic moleculs in hypothalamus, leptin stimulates catabolic pathways and inhibits anabolic pathways, TNF, IL- 1 and LIF increases levels of leptin cause anorexia by preventing normal mechanism of reduction in food intake; uncoupling protein (UPC) 1, 2 and 3 that plays a role in the formation of ATP energy and influential of energy expenditure, its expression is influenced by the product of the tumor (cytokines). For example, in patients with lung cancer small cell obtained an average increase of 37% of basal energy expenditur, so intake of food provided is not sufficient for the body, causing negative energy balance and weight loss.

Hemostasis glucose: glucose is the main energy source for tumor cells and host, increasing use will be accompanied by an increased release of lactate then regenerated into glucose by the liver through coricycle. enhancement coricycle This will increase the energy loss of about 300 kcal per day. Increased gluconeogenesis to maintain glucose hemostasis. Amino acids, glycerol and fat breakdown is used for gluconeogenesis in the liver to to form glucose (plasma levels of alanine, glycine and glutamine decreased). Production of glucose, glucose intolerance and increased insulin resistance. The release of counter regulatory hormones such as glucocorticoid and glucagons increases insulin resistance, so the use of glucose by skeletal muscle decreased.

Protein metabolism: increased muscle catabolism (muscle wasting) caused asthenia or decrease in strength caused by an increase in breakdown protein and a decrease in muscle protein synthesis, increase in liver protein synthesis (acute phase proteins) and tumors. Negative nitrogen balance occurs where there is an increase Whole body protein turnover and turnover aminoacid disorders. Metabolism of fat: the patient will experience a loss of fat tissue due to increased lipolysis and decreased lipogenesis. Turnover of glycerol and free Fathy acid (FFA) increased, decreased levels of lipoprotein lipase causes clearance of plasma triglycerides decreased, increased triglyceride levels, high and low density lipoprotein decreases.