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Experimental Observations of Starvation
Sqadia video is the demonstration of Metabolism in Starvation. Total starvation includes complete deprivation of foods, salts and water. It results in death of the animal in the shortest possible time. Starvation induces a number of metabolic changes, some occurring within a few days and others occurring late. Ketosis develops, and some retention of salt and water occurs and in prolonged starvation fatty liver develops. The effects of food starvation have been mostly observed in animals. In first few days, there is a craving for foods, particularly at meal times. After a week, the craving subsides, provided water and salts are freely allowed. Gradually, desire for food vanishes. At about this time the subject falls into a state of semi consciousness. The pulse rate and body temperature remain almost normal till before death, these are affected very late. The amount of urine as well as its urea content falls. The body weight is steadily lost. The daily loss in man during the first 10 days, amounts to between 1 to 1.5 per cent of the original body weight. The extracellular fluid in large quantities is also lost. Dissolution of the muscular tissues and protoplasmic structures occurs much later. The more vital organs lose the least weight, whereas the less vital ones lose the most.
Effects on Metabolism
During starvation, the body has to depend upon its own tissue materials to get energy in absence of foods. Even if no physical work is being done, 2000 K. cal (C) are needed daily approximately. Out of the principal three food groups—glycogen, fat, and proteins, the liver glycogen is first mobilized. Due to its limited storage, 6% (108 grams) it cannot last long. This initial stage lasts for not more than 2 to 3 days. 80-90% of energy requirement will be derived from fats and the remainder 10-20% from proteins. Since the adipose tissue represents the largest amount of stored food, the second stage will last for longest period, usually over two weeks. In the third stage, Energy requirement is obtained from the breakdown of tissue proteins. The stage lasts for less than one week. Tissue glycogen is utilized initially for energy production and for maintaining blood sugar level, consequently, the liver glycogen and the blood sugar fall on fasting, the blood sugar may become less than 40-60 mg %. Hypoglycaemia, in turn depresses insulin secretion and thus increases gluconeogenesis. Pyruvate carboxylase, fructose 1,6-bi-phosphatase (FDPase), PEP carboxykinase and glucose 6-P-ase activity is increased manifold in starvation or carbohydrate deprivation, enhancing both gluconeogenesis and glycogenolysis.
Fats of adipose tissue are largely mobilized to the liver as FFA and oxidized for energy purposes. Fat utilised in starvation in the beginning is only triacylglycerol (TG), from fat depots, i.e. the “element variable”. Starvation increases the activities of the “hormone sensitive” TG lipase of the adipose tissue and also increases the enzymes of β-oxidation (beta-oxidation) in Liver. Amounts of FFA progressively rises in the plasma from the very first day of starvation. Glycerol component released from lipolysis acts as a substrate for gluconeogenesis and joins the carbohydrate pool after activation to α-glycero-P. In prolonged starvation the activity of lipoprotein lipase declines in the adipose tissue; but rises in cardiac and skeletal muscle fibres. Starvation ketosis owing to gradual decline in carbohydrate store and lack of carbohydrate, energy is obtained from fat burning. Relative lack of oxaloacetic acid (OAA) is produced when gluconeogenesis is more as OAA is utilised for gluconeogenic pathway and less available for TCA cycle. Availability of more acetyl-CoA increases ketogenesis. Ketosis and ketonuria cause acidosis. There occurs, reduction of [HCO3–] due to buffering of the strong and non-volatile acids. Increased pulmonary ventilation and fall in alveolar CO2 tension. Due to lack of carbohydrate, esterification will be less, α-glycero-P, VLDL formation and elimination will decrease leading to accumulation of fat producing fatty liver. A feedback mechanism has been suggested for controlling FFA output from adipose tissue. As the liver takes up and esterifies a considerable proportion of the FFA output, it plays a regulatory role in removing excess FFA from circulation. Thus, in starvation, two cycles operate: A carbohydrate cycle, involving release of glycerol from adipose tissue, the other is a lipid cycle and involves release of FFA by adipose tissue.
In starvation, tissue proteins are treated as ‘food proteins”. They are hydrolysed to amino acids, but to a larger extent and at an increased scale than that occurs normally. For catabolism of tissue proteins, tissues are not uniformly used. The breakdown of tissue proteins in starvation is controlled possibly through the action of adrenal cortex (Glucocorticoids). The released amino acids from amino acid pool are utilized as follows: On the First call Utilised for the maintenance of the structural and functional efficiency of vital organs, and in the Second call the amino acids also undergo de-amination in the liver and the non-nitrogenous part helps in the maintenance of blood sugar. Amino acid breakdown pathways join mainstream carbon utilization at different points of entry. The amount of N2 excretion in urine during first few days is directly proportional to the amount of protein intake before starvation. The average daily excretion in the first week of starvation is about 10 grams daily. During second and third weeks of starvation, there is a gradual decline in N2 excretion and the values are very low. But just before death, when tissue proteins are being catabolised for energy, the urinary N2 excretion again rises (“pre-mortal” rise). The end-products of endogenous protein metabolism, i.e. creatine/creatinine, neutral sulphur compounds and uric acid are the main other nitrogenous products. Increased protein catabolism lowers the secretion of insulin, thyroxine, gonadotrophins.
Water and Mineral Metabolism
The ECF is reduced during the first few days, due to stoppage of water intake and continued obligatory losses. On prolonged starvation, the ICF volume may also fall by 25 per cent or more, because of cellular breakdown. Due to cellular disintegration, there is loss of intracellular K+ thus reducing the total body K+. Na+ in the ECF may be maintained in the normal range. The need for drinking water is reduced due to increase in “metabolic water” and relative expansion of ECF by reduced glomerular filtration. Edema may appear due to relative expansion of EC compartment and ‘decline’ in serum albumin level (starvation oedema).