Prolonged fasting

With increasing metabolism of fat through p oxidation, much of the mitochondrial CoA pool may become tied up as acyl- or acetyl-CoA. In such cases, the supply of free CoA can be diminished, and this may limit the rate of p oxidation. Upon prolonged fasting and heavy reliance on fat for energy, the liver induces the enzymes required for the formation of ketone bodies and brain induces enzymes required for their metabolism. 

Avoid prolonged fasting. Glucose infusion during acute episode... 

Extreme muscle weakness associated with endurance exercise and/or exercise after prolonged fasting... 

Oxidized in cardiac skeletal muscle, renal cortex, and brain (prolonged fast)... 

Table 7.5 Arteriovenous differences of oxygen, glucose, fatty acids, acetoacetate and hydroxybutyrate across the brain of obese females during prolonged fasting...

D13. Drenick, E. J., The relationship of BSP retention during prolonged fasts to changes in plasma volume. Metab. Clin. Exp. 17, 522-527 (1968). 

C. In prolonged fasting, triacylglycerol degradation in adipose tissue becomes maximal and sustained. 

B. During a prolonged fast, glucose can be synthesized from various precursors,... 

Which of the following organs or tissues does NOT need to be supplied with glucose for energy production during a prolonged fast ... 

Deficiency of which of the following enzymes would impair the body s ability to maintain blood glucose concentration during the first 24 hours of a prolonged fast ... 

Alanine Pyruvate/lactate defects Hyperammonemias Fasting Prolonged fasting, ketosis... 

FIGURE 23-28 Fuel metabolism in the liver during prolonged fasting or in uncontrolled diabetes mellitus. After depletion of stored carbohydrates, to proteins become an important source of glucose, produced from glucogenic amino acids by gluconeogenesis. ... 

Triacylglycerol molecules stored in adipose tissue represent the major reserve of substrate providing energy during a prolonged fast. During such a fast ... 

Responses to hormonal manipulations and fasting. Activities responded in a parallel fashion to glucocorticoid administration (93-96, 113), alloxan diabetes and insulin therapy (41, 113, 117), growth hormone treatment (118), and acute and prolonged fasting (90, 98, 118, 121). 

Co-trimoxazole can cause reversible hypoglycemia, which may be prolonged, particularly in patients with risk factors for hypoglycemia. Common risk factors include compromised renal function, prolonged fasting, malnutrition, and the use of excessive doses. It has been postulated that the sulfonamide mimics the action of sul-fonylureas, stimulating pancreatic islet cells to secrete insulin. In elderly people, co-trimoxazole-induced hypoglycemia can cause altered mental state (1146,1147). 

The term ketone bodies refers primarily to two compounds acetoacetate and P-hydroxy-butyrate, which are formed from acetyl-CoA when the supply of TCA-cycle intermediates is low, such as in periods of prolonged fasting. They can substitute for glucose in skeletal muscle, and, to some extent, in the brain. The first step in ketone body formation is the condensation of two molecules of acetyl-CoA in a reverse of the thiolase reaction. 

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