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Starvation and maluntrition *clinical nutrition and health - Case Study Example


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Starvation and maluntrition *clinical nutrition and health

Glycogen is mobilized mainly from liver. Other storage sites for glycogen are muscles and skin. Boitel would have initially sustained on blood glucose levels maintained through these mechanisms. Glucagon stimulates breakdown of glycogen and causes inhibition of glycogen synthesis by triggering the cascade of cyclic AMP. This ultimately leads to phosphorylation and activation of the enzyme phosphorylase. Glucagon then causes inhibition of the enzyme glycogen synthetase. This prevents synthesis of glycogen and its storage into muscle and liver. Glucagon also causes inhibition of the synthesis of fatty acids by diminishing pyruvate production and by decreasing the activity of acetyl CoA carboxylase (Berg, 2002). This, it does by keeping it in unphosphorylated state. All this is aimed to mobilize glycogen and decrease conversion of glucose in the blood to glycogen so that the glucose levels in the blood are maintained in adequate ranges for functioning of vital organs like brain and heart which, at this stage are still dependent on glucose alone for energy. Glycogen releases glucose-6-phosphate and this is hydrolyzed to release large amounts of glucose. Liver is the main source of glycogen in this context in a starvation patient like Boitel. Since insulin levels are low, glucose cannot enter into the fat tissue and muscle (Berg, 2002). Thus, decreased insulin levels and increased glucagon levels help maintain blood sugar levels during early starvation. Also, another important aspect is; both

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the liver and muscle use fatty acids are source of energy to preserve glucose levels. All these mechanisms would have amounted to decrease in the glycogen stores of the liver of Boitel. Though gluconeogenesis continues, it only helps restore the glucose that was converted by peripheral tissues to lactate and alanine. The brain however, oxidizes glucose completely, the end-products being H2O and CO2 (Berg, 2002) (Refer to Fig.1). Fig.1: Choice of fuel during starvation (Berg, 2002) Gradual increase in the concentrations of citrate and acetyl CoA causes decrease in glycolysis in a starving patient like Boitel after about a week of starving. Alanine, lactate and pyruvate are eventually shifted to the liver to get converted to glucose. Triacylglycerols can get cleaved and glycerol derived from this is used for synthesis of glucose (Cahill and Veech, 2003). For about a week to ten days after initiation of fasting, Boitel’s body would have metabolically adapted the above mechanisms for functioning of vital organs and survival. In prolonged starvation, as in case of Boitel who starved for 53 days, further depletion of carbon skeletons for glucose production decreases, leading to proteolysis for the purpose of gluconeogenesis. In such a situation, proteins that are degraded are not replenished, instead; they are used as sources of carbon for synthesis of glucose. Secretions of pancreas and also intestinal epithelium proteins are initial protein sources. They actually turn over rapidly. Later muscle proteins are used. After about 3-4 days of starvation, large amounts of 3-hydroxybutyrate and acetoacetate, known as ketone bodies are produced in the liver. Synthesis of these ketone bodies increases dramatically from the liver as the duration of starvation increases like in the Cuban poet and these are released into the
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Metabolic Adaptations during Starvation The Cuban poet Pedro Luis Boitel had been on a hunger strike for 53 days. He died of starvation. When somebody is starving, several metabolic adaptations and changes occur to preserve functioning of vital organs. An understanding of various metabolic pathways related to functioning of the body during various phases of starvation is essential to understand the survival crux of the Cuban poet for 53 days…
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