The metabolic system is one of the important systems in human body. It processes the complex carbohydrate and sugar molecules from food and transforms them into glucose for storage and metabolism. The system comprises the stomach, pancreas, liver and cells where each organ has specific roles in digesting or storing glucose from food. Hormones, such as insulin and glucagon, assist the process by providing signals to the cells for releasing stored glucose or the liver for storing glucose from bloodstream.
After food is consumed, the body reduces complex carbohydrate and sugar molecules to the simple six-carbon sugar known as glucose. Glucose is the body’s fuel, and upon the reduction by the body, it is either utilised or stored. Sensing glucose in the bloodstream leads the β-cells in the pancreas to produce insulin. The concentration of insulin acts as the body’s signal to manage storage and transportation, and thus determines the utilisation or storage rate of glucose.
Insulin is a protein that consists of 51 amino acids in two closely connected chains. Insulin molecules and their connecting fragments are then packed together in small granules in the β- cells, which are secreted on demand through the islets of Langerhans in the pancreas. Along with β-cells, the 1 to 2 million islets of Langerhans contain α and δ cells, which secrete glucagon and somatostatin, respectively, and act as additional blood glucose regulatory hormones. The α, β and δ cells are approximately 25%, 60% and 10% of the total islets and are all very closely related (Guyton and Hall, 2000)
The level of insulin in the bloodstream is the signal that facilitates the proper metabolic response as shown in Figure 1.1 . A high insulin level promotes storage of glucose, and a low insulin and glucose level signals the need for the release of glucose fuels, currently in storage, back into the blood stream. A meal results in an increase of insulin concentration in the blood, due to the increased secretion of insulin by the β-cells, and signals the liver and
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muscles to consume the extra fuel (glucose) available. The liver stores glucose as glycogen or fat, and the muscles utilise glucose primarily to repair damaged muscle cells, for energy storage as glycogen and lastly storage in fat cells.
Figure 1.1: Model of Glucose-Insulin Regulatory System. The schematic shows the effect of
high and low blood glucose levels in the body. Adapted from health.howstuffworks.com
Counter regulatory hormones, such as glucagon and adrenaline, signal the liver to release glucose. Too much glucose removal from the blood-stream can result in low blood glucose levels. When the glucose available is not sufficient enough to supply the brain’s requirements, hypoglycaemic symptoms including hunger, anxiousness, restlessness, agitation, perspiration, tachycardia (racing pulse) and palpitation (irregular and/or forced heart-beats) occur. These symptoms are partly a result of the release of adrenaline by the body as a counter regulatory measure to restore normal blood glucose levels. When the amount of insulin released is suddenly reduced, the signal is not available to the body to indicate it should remove glucose from the blood stream. The blood glucose level therefore
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rises until there is hyperglycaemia, requiring further insulin. It is thus a natural feedback system using glucose raising / glucagon and adrenaline, and lowering insulin hormones.
Insulin is an anabolic hormone and promotes growth, while lowering glucose levels (Vander, 2001). Insulin also increases the activity of other enzymes, primarily those involved in glycogen, lipid and protein synthesis, and inhibit the activity of those that catalyse glucose degradation. However, all these digestive and metabolic activities involving secretion of insulin, glycogen and other related hormones and enzymes are optimum only during normal body temperature between 36oC and 37.5oC (Lehninger, 1970, Wilson, 1988). At body temperature of higher or lower than normal range, the production of hormones and enzymes from the pancreas and other organs shows some decay and can eventually affect the metabolic rate and physiological condition of the body (Benz-Woerner et al., 2012).
To date, there is no scientific evidence explaining human glucose-insulin kinetics during hypothermia. However, by use of a newly developed technique, substrate profiles and their regulation by insulin were examined in hypothermic rats over 24h (Hoo-Paris et al., 1988, Cueni-Villoz et al., 2011), resulting in the following outcomes:
i) Plasma glucose concentrations increased during cooling and remained high thus reducing glucose utilization throughout the period of hypothermia (Escolar et al., 1990).
ii) Plasma insulin decreased dramatically during cooling and remained very low during the whole period of hypothermia, reflecting the suppression of endogenous insulin secretion seen in isolated islets at low temperatures (Escolar et al., 1987).
iii) Resistance to exogenous insulin is increased (Torlinska et al., 2002).
The role of pancreas in producing insulin and glycogen hormones is vital and its ability to perform at optimum level is important in regulating blood glucose level at normal glycaemic range. However, during hypothermia, the pancreas is unable to function normally, which can lead to increased or decreased blood glucose levels (Benz-Woerner et al., 2012). In general, hypothermia can be life threatening. However, it also benefits patients with recent heart attack.
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