Biochemical Phases of Cachexia

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The organism has to supply 150-180 g glucose/day for oxidative phosphorylation in the brain and bone marrow.

In the normal fast, hypoglycaemia stimulates the production of glucagon, which induces glycogenolysis in the liver and in the muscle to produce glucose. But if glycogen stores can supply glucose only for 12-18 h, then hypoglycaemia stimulates the production of epinephrine, which in turn starts lipolysis in fat stores. About 160 g fat (triglycerides, FFA, glycerol)/day can be transformed into glucose to maintain vital processes. But, if the requirement for energy is prolonged, then lipids alone are not sufficient to maintain glucose levels, as their use is limited by the accumulation of ketones (ketoacidosis) and by the decrease of insulin. At this point, the organism, which has depleted glycogen stores and is self-limited in using lipids, goes on to use muscular and visceral proteins to produce glucose. About 75 grams of proteins/day are used for gluconeogenesis during normal starvation, with urinary loss of about 12 grams nitrogen/day. If the fast is prolonged, the organism adapts itself to utilise more ketone bodies and to reduce nitrogen loss to between 8 and 3 g/day. Differently from normal starvation, in stressed starvation it is not hypoglycaemia that starts catabolic events, but the increase of hormonal factors, including cortisol, glucagon, epi-nephrine, leptin, cytokines (tumour necrosis factor [TNF], interleukin [IL]-1, IL-2, IL-6, IL-10, interferons [IFNs], and prostaglandins [PGs]). These hormones may not increase in the blood; rather, in metabolically active tissues. Consumption of lean mass of up to 500 g/day, with a urinary loss of nitrogen of 20 g/day, may be reached.

The calorie balance represents an equation in which the energy introduced by food can be used for muscular work and metabolic activity, or it can be saved and stored in the tissues. If the consumption of energy exceeds the intake, the system goes into a condition of caloric deficit and the organism tries to maintain the homeostasis by burning its reserves. The caloric balance can be overturned by causes that alter the availability of nourishment, its absorption, and its metabolism (Table 2).

Table 2. Causes of energetic imbalance

Reduced oral intake: Lack of foods, old age Anorexia, depression, dementia Cerebral disturbances

Functional or organic obstacles to the passing of food

Reduced caloric absorption: Digestive disturbances Malabsorption Diarrhoea

Metabolic disturbances: Protein-synthesis defects Hypermetabolism Futile metabolic cycle Cytokine action

Enzymatic or endocrine disturbances Fever

During serious illness, a normal type of nourishment is not sufficient to balance the intense catabolism and nitrogen loss caused by the pathologic process, in which glucose, lipid, and protein reserves are burnt in order to cover energy needs (self-cannibalism). If self-cannibalism persists, the effect is fatal: the loss of a third of body proteins (= 2 kg proteins or 8 kg cellular mass) in a person of average weight causes death in less than one month. The degree of cachexia itself, independent from its cause, is a mortality factor. If the depletion of cellular mass and total body potassium is examined with reference to the survival time, a linear correlation (Fig. 1) is observed in AIDS and in cancer patients [22-24, 34, 38]. At the time of

Fig. 1. Relationship of ideal body weight (IBW) and total body potassium (TBK) to the timing of death. Death occurs when body weight is about one third below ideal values and TBK just above 50% of normal

death, cellular mass is reduced, on average, to 54% of normal, corresponding to 66% of ideal weight. In voluntary or forced starvation, death occurs when the body weight is reduced to almost a third of the ideal weight [22].

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