Assessment of energy status and fructose metabolism of liver in obstructive jaundice by ³¹P magnetic resonance spectroscopy

Abstract

The effect of cholestasis on hepatic energy status and fructose metabolism in jaundiced rats and patients was investigated using 31P magnetic resonance spectroscopy. Rats with obstructive jaundice (OJ group) were studied 7 days after bile duct ligation. Drainage rats were studied at 3 days (DR3 group) and 7 days (DR7 group) after the relief of 1 week obstruction of the common bile duct. In the bile duct ligated rat, the beta-adenosine triphosphate (ATP)/Pi (inorganic phosphate) ratio was significantly lower than in sham-operated controls. This ratio recovered rapidly in the DR3 and DR7 groups. The maximum increase in the phosphomonoester peak (PMEmax) after an intravenous bolus of fructose was significantly reduced in both the OJ and DR3 groups, and was accompanied by a decrease in hepatic fructokinase activity. The PMEmax and the fructokinase activity recovered in the DR7 group. In a clinical study, the beta-ATP/Pi ratio in six healthy volunteers was comparable to that of 15 patients with obstructive jaundice, regardless of their biliary drainage status. The PMEmax in all patients (serum bilirubin > or = 5 mg/dL), irrespective of biliary drainage, was significantly lower than in volunteers. Furthermore, the PMEmax in four of the eight patients with biliary drainage (serum bilirubin < 5 mg/dL) was lower than in volunteers. It is concluded that while energy status in jaundiced patients is well maintained, fructose phosphorylation is inhibited and recovery is delayed after the relief of obstruction compared with serum bilirubin. For the non-invasive evaluation of damaged liver function in jaundice, 31P magnetic resonance spectroscopy is a useful technique.

Clinical Magnetic Resonance Spectroscopy

“…Fructose injection leads to phosphorylation of fructose to fructose‐1‐phosphate, resulting in immediate PME increases and reductions of ATP and Pi levels that partly resolve over the next hour (67, 68). Patients with cirrhosis, hereditary glucose intolerance or jaundice exhibited little or no response (68–70), while patients with non‐alcoholic steatohepatitis showed an impaired recovery of ATP level (71). Alanine infusion stimulates gluceogenesis leading to increased levels of hepatic phosphorylated glucose intermediates such as (the PME) glucose‐6‐phosphate.…”