Changes in predominant energy substrate after hepatectomy

Nakatani, Toshio; Ozawa, Kazue; Asano, Michiko; Ukikusa, Minoru; Kamiyama, Yasuo; Tobe, Takayoshi

doi:10.1016/0024-3205(81)90731-1

Cited by 49 publications

(22 citation statements)

References 10 publications

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“…After partial hepatectomy, the decreased liver mass not only must increase rates of gluconeogenesis to meet peripheral glucose requirements, but also must provide ATP to fuel cell division and liver growth. On the basis of the results shown in Table 3, it seems likely that the major energy-utilizing process within the remnant liver is cell growth and division, and others have demonstrated that fatty acid oxidation is essential to DNA synthesis and mitosis [18,19]. It is noteworthy that the administration of medium-chain triacylglycerol to partially hepatectomized rats caused a significant (although modest) rise in blood ketone-body concentrations.…”

Section: Resultsmentioning

confidence: 91%

Ketone-body metabolism after surgical stress or partial hepatectomy. Evidence for decreased ketogenesis and a site of control distal to carnitine palmitoyltransferase I

Schofield¹,

French²,

Sugden³

1987

Biochemical Journal

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Rats were subjected to laparotomy, or laparotomy and partial hepatectomy, at 0-48 h before administration of water or medium-chain-length triacylglycerol, having been starved post-operatively. Functional hepatectomies were performed at intervals after the intragastric load. Blood ketone-body concentrations after medium-chain triacylglycerol administration and/or functional hepatectomy of these rats were compared with values obtained in starved control rats. Decreased ketonaemia in response to medium-chain triacylglycerol was observed for up to 48 h after partial hepatectomy and at 1 and 2 h after laparotomy, but not at 24 or 48 h after laparotomy. Rates of ketone-body clearance after functional hepatectomy were unaffected by prior laparotomy or partial hepatectomy. Ketonaemia after medium-chain-triacylglycerol administration was only partially blocked by inhibition of CPT I (carnitine palmitoyltransferase I). The results demonstrate sustained effects of partial hepatectomy and short-term effects of surgical stress to decrease ketonaemia via inhibition of ketogenesis at site(s) distal to CPT I.

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Section: Resultsmentioning

confidence: 91%

Ketone-body metabolism after surgical stress or partial hepatectomy. Evidence for decreased ketogenesis and a site of control distal to carnitine palmitoyltransferase I

Schofield¹,

French²,

Sugden³

1987

Biochemical Journal

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“…This can be supported by finding that proliferation of primary hepatocytes in cell culture is associated with marked intracellular accumulation of fat (Michalopoulos et al 1982). First two days after major hepatectomy, the remnant liver is mainly dependent upon the oxidation of fatty acids giving evidence for the significance of fat accumulation in the liver (Simek and Sedlácek 1965;Nakatani et al 1981). Moreover, enteral feeding with medium-chain TAG and long-chain TAG supplement actually preserved liver regeneration (Červinková et al 1995;Bláha et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Effect of S-adenosylmethionine on liver regeneration induced by partial hepatectomy

Kohoutek

Červinková²,

Kučera³

et al. 2010

gpb

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Abstract. S-adenosylmethionine (SAMe) is a key metabolite regulating growth, differentiation and death of hepatocytes. Experimentally, exogenous SAMe has been documented to attenuate hepatocarcinogenesis. The aim of our study was to evaluate the effect of SAMe on proliferation of hepatocytes that are not cancerously transformed.Partial 2/3 hepatectomy (PH) was performed in rats, control animals underwent laparotomy. SAMe was injected immediately after the surgery and then at 24 h intervals for two days at 10 or 40 mg/kg. The animals were sacrificed 24, 48 and 72 h after operation and the intensity of liver regeneration was evaluated. SAMe treatment at 10 mg/kg was associated with decrease in the synthesis of liver DNA 48 h after PH, however, it was not reflected in DNA content. SAMe treatment at 40 mg/kg led to the reduction of DNA synthesis 72 h after PH followed by the diminution of DNA content. The results have documented the inhibition of the liver regeneration by SAMe that may be mediated by the suppression of liver fat accumulation. Cell GSH level correlating with the growth rate was not affected by SAMe. Prevention from the decrease in the intracellular content of SAMe, as a factor attenuating regeneration remains to be verified.

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“…The preparation of fro zen hepatic tissue to measure adenine nucleotides was also reported previously [14,15], ATP was deter mined enzymatically with hexokinase and glucose-6-phosphate dehydrogenase by the standard spectrophotometric method reading the absorbance of NADH at 340 nm [9]. ADP and AMP were determined similarly with lactate dehydrogenase, pyruvate kinase and myokinase [8].…”

Section: Methodsmentioning

confidence: 99%

“…Among them, the occurrence of postopera tive hypoglycemia during the phase imme diately after massive hepatic resection has been recognized as one of the most serious [11,12,17], To prevent hypoglycemia, the administration of a glucose solution, often hypertonic, has been generally recommended after major hepatectomy [11,12,17,22] However, it has been found that a marked glucose intolerance develops in the early crit ical period after massive hepatic resection [6,18]. In addition, the remnant liver predomi nantly utilizes fatty acids as an energy sub strate in the phase immediately after major hepatic resection when the hepatic energy charge [(ATP+0.5 ADP)/(ATP+ADP+AMP)] is decreased [14][15][16], Findings suggest the presence of intracellular metabolic blocks which impede glucose utilization.…”

Section: Introductionmentioning

confidence: 99%

Changes in Blood Glucose Levels in Relation to Blood Ketone Body Ratio following Hypertonic Glucose Infusion in 70&percnt; Hepatectomized Rabbits

Nakatani¹,

Yasuda²,

Ozawa³

et al. 1984

Eur Surg Res

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The effects of postoperative infusion of a hypertonic glucose solution on the blood glucose level, blood ketone body ratio (acetoacetate/β-hydroxybutyrate), and plasma alanine and proline levels were studied in 70% hepatectomized rabbits (group A) and in rabbits 70% hepatectomized and, in addition, subjected to bile duct obstruction at 12 h after hepatectomy (group B). Glucose infusion was started at the end of hepatectomy and continued for 20 h. The blood glucose level in group A remained at approximately 300 mg/’dl throughout the study; however, it reached 789 mg/dl in group B at 20 h. The blood ketone body ratio, which reflects hepatic mitochondrial redox potential, decreased from 0.90 ± 0.09 in untreated rabbits to 0.38 ± 0.05 in group A, and to 0.19 ± 0.03 in group B at 20 h. As the blood ketone body ratio decreased, plasma proline and alanine levels increased rapidly (proline, r = –0.601, p < 0.02; alanine, r = –0.640, p < 0.001). In addition, the blood ketone body ratio was positively correlated with the hepatic energy charge level [(ATP + 0.5 ADP)/(ATP + ADP + AMP)] (r = 0.57, p < 0.001). It is suggested that the entry of glucose and amino acids into the Krebs cycle is inhibited as the blood ketone body ratio decreases, and under such conditions the infused glucose tends to accumulate, resulting in severe hyperglycemia.

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Changes in predominant energy substrate after hepatectomy

Cited by 49 publications

References 10 publications

Ketone-body metabolism after surgical stress or partial hepatectomy. Evidence for decreased ketogenesis and a site of control distal to carnitine palmitoyltransferase I

Ketone-body metabolism after surgical stress or partial hepatectomy. Evidence for decreased ketogenesis and a site of control distal to carnitine palmitoyltransferase I

Effect of S-adenosylmethionine on liver regeneration induced by partial hepatectomy

Changes in Blood Glucose Levels in Relation to Blood Ketone Body Ratio following Hypertonic Glucose Infusion in 70&percnt; Hepatectomized Rabbits

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