• Darren V Mann, Wynnie W M Lam, N Magnus Hjelm, Nina M C So, David K W Yeung, Constantine Metreweli, and Wan Y Lau.
• Department of Surgery, Prince of Wales Hospital, Chinese University of Hong Kong, Shatin, New Territories, Hong Kong. d_v_mann@hotmail.com
• Ann. Surg. 2002 Mar 1; 235 (3): 408416408-16.

ObjectiveTo elucidate the metabolic changes occurring within hepatocytes during acute phase reaction and liver regeneration.Summary Background DataThe metabolic events occurring within the liver during the hepatic stress response are poorly understood. The authors used in vivo 31-phosphorus magnetic resonance spectroscopy to study hepatic metabolism after surgical trauma with and without loss of liver cell mass.MethodsThree groups were studied: five patients undergoing partial hepatectomy; five patients in whom laparotomy and colonic resection was performed; and five patients treated by thyroidectomy. Hepatic metabolism was evaluated by 31-phosphorus magnetic resonance spectroscopy before surgery and serially thereafter on postoperative days 2, 4, 6, 14, and 28. Estimation of liver volume by magnetic resonance imaging and blood sampling for biochemistry were performed at the same time points.ResultsThe authors found that alterations in hepatocyte phospholipid metabolism occurred after surgery that were correlated with changes in circulating acute phase proteins. Liver regeneration after hepatectomy was also associated with a derangement in energy metabolism, measured by a decrease in the ratio of ATP to its hydrolysis product inorganic phosphate. The depleted energy status was mirrored in biochemical indices of liver function, and restitution paralleled the course of restoration of hepatic cell mass.ConclusionsThese findings indicate that changes in liver metabolism after surgery reflect the magnitude of tissue injury and the quantity of functioning liver cells. Acute phase responses dominate the initial recovery period at the expense of less important endergonic functions. When liver parenchyma is lost, the acute phase reaction is maintained and further supported by a rapid replenishment of hepatocytes, which can even be considered a continuation of acute phase physiology. Modulation of liver function within the framework of overall hepatic energy economy is one mechanism for matching energy supply with increased demands during these processes.

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