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Serum intestinal alkaline phosphatase activity is increased by fat feeding, but the mechanism of this increase is not fully understood. Fasting rats were fed a single feed of either corn oil (12 kcal) or an isocaloric elemental feed (Vivonex 100 HN). Changes in enzyme activity in the small bowel mucosa and serum were followed for 20 h. Only the fat-fed rats had increased serum enzyme activity, being maximal at 7 h and three times the fasting level. This resulted from an increase in the amount of enzyme protein in the serum and not from an increase in its catalytic efficiency. The serum biological half-life of 125I-labeled intestinal alkaline phosphatase was the same in fasted (2.51 min) and fat-fed rats (2.55 min). Both types of feed caused a quantitatively similar increase in brush-border-bound alkaline phosphatase activity. However, levels of soluble intracellular alkaline phosphatase in intestinal mucosa were affected differently: the elemental diet caused a substantial rise, whereas no significant change was seen after fat feeding. The isoelectric pattern of phosphatase activity in serum after fat feeding was identical to that of soluble intracellular and not membranous alkaline phosphatase. Therefore, serum intestinal alkaline phosphatase activity rises in response to a single fat feed as a result of increased delivery of the enzyme to the blood and not as a result of an increase in its normally short biological half-life. This rise cannot be directly linked to an increase in the amount of brush-border-bound enzyme, and it appears that the serum enzyme is derived directly from a pool of soluble intracellular enzyme in the small bowel mucosa.

Bilateral thoracoscopic repair of pectus excavatum with left-to-right mediastinal dissection is a safe alternative to the traditional approach, as it allows a more complete visualization of the mediastinum and eliminates the need for additional safety measures such as subxiphoid dissection and elevation.

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