AI Article Synopsis

  • The study investigates the causes of low albumin levels (hypoalbuminemia) in a patient using specific biochemical methods to measure albumin production and breakdown rates.
  • Results indicated that the patient had significantly lower plasma albumin compared to healthy controls, with an increased rate of albumin synthesis but reduced overall synthesis due to faster clearance from the bloodstream.
  • The findings suggest that the low albumin levels stem from both increased clearance and impaired synthesis, highlighting potential pitfalls in measuring protein synthesis rates using certain methods.

Article Abstract

Objective: To determine the contribution of albumin synthetic and catabolic rates to steady state levels in a patient with idiopathic hypoalbuminemia.

Methods: Using L-[1-(13)C] valine, both FSR (fractional synthesis rate) as well as FCR (fractional catabolic rate) were studied. Human albumin cDNA analysis and determination of the exact albumin mass by electrospray mass spectrometry were performed.

Results: Compared with controls, plasma albumin concentration in the patient was reduced (6.7 vs. 37.0 +/- 2.6 g/L). Albumin FSR (= FCR in steady state) was increased compared to controls. The ASR (absolute synthesis rate) of albumin was decreased based on the enrichment in plasma valine and KIV, but estimated to be normal based on VLDL apoB100 at plateau compared to controls. Direct estimation of albumin FCR rejected the latter. No mutation was found in the transcribed region of albumin gene. The exact mass of albumin (66.493 Da) was not different from controls.

Conclusion: The hypoalbuminemia was a result of accelerated clearance of albumin from plasma in addition to defective albumin synthesis. This study also shows that the chosen method of the precursor pool could lead to misinterpretation of data in hepatic protein synthesis.

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Source
http://dx.doi.org/10.1016/s0009-9120(02)00357-0DOI Listing

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