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A. Cader Asmal, MD, PhD, MRCP, FCP
Joslin Diabetes Center Harvard Medical School Boston

JAMA. 1985;253(7):978.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

In order to identify the pathogenetic importance of production and removal processes in hypertriglyceridemia, techniques have to be employed that can independently and simultaneously measure both events. Steady-state triglyceride (TG) tracer kinetic studies do not meet these requirements.¹ For this reason the article by Grundy and Kesaniemi,² based on multicompartmental analysis of TG tracer kinetics, reporting a dual defect in the metabolism of very-low-density lipoprotein (VLDL) TGs is of interest. The Zech model of multicompartmental analysis they have employed is itself based on data assuming a monoexponential decay of TG-specific activity. In the latter approach,³ the turnover rate (TOR) is estimated as the product of the rate constant (k) and the pool size (P). Of the three kinetic parameters, two are measured, in this instance k and P, and the third, the TOR, is inferred; ie, production and removal are not simultaneously and independently . . . [Full Text PDF of this Article]

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