In vivo measurement of hepatic lipid composition by proton magnetic resonance spectroscopy

N.A. Johnson,¹ D.W. Walton,² T. Sachinwalla,² C.H. Thompson,³ K. Smith,¹ P. Ruell,¹ S.R. Stannard⁴ and J. George,⁵ ¹Discipline of Exercise and Sport Science, The University of Sydney, East Street, Lidcombe, NSW 2141, Australia, ²Department of Magnetic Resonance, Rayscan Imaging, 41-43 Goulburn Street Liverpool, NSW 2170, Australia, ³Department of Medicine, Flinders University, Bedford Park, SA 5042, Australia, ⁴Institute of Food, Nutrition and Human Health, Massey University, Palmerston North Private Bag 11222, New Zealand and ⁵Storr Liver Unit Westmead Millennium Institute, The University of Sydney, Westmead Hospital, Westmead, NSW 2145, Australia.

Non-alcoholic fatty liver is frequently observed in obese individuals, yet the factors which predict its development and progression to liver disease are poorly understood. It has been proposed that an increase in hepatic saturated fatty acids and/or a decrease in polyunsaturated fatty acids predisposes to hepatic triglyceride accumulation and inflammation.

We assessed the efficacy of using proton magnetic resonance spectroscopy (¹H-MRS) to non-invasively measure hepatic lipid composition. Hepatic lipid unsaturation index (UI), a surrogate saturation index (SI) and polyunsaturation index (PUI) measured by ¹H-MRS were in agreement with those expected in oils of known composition. Hepatic triglyceride concentration (HTGC) and composition were then measured in vivo in healthy lean (LEAN) men (n = 10), obese men with normal HTGC (OB) (n = 8) and obese men with hepatic steatosis (OB+HS) (n = 9).

HTGC was significantly higher in OB+HS (14.9 ± 3.2 %) versus OB (2.4 ± 0.4 %) and LEAN (0.4 ± 0.1 %) (Figure A; p < 0.01 for both). SI was significantly higher in OB+HS (0.94 ± 0.01) and OB (0.91 ± 0.01) versus LEAN (0.80 ± 0.02) (Figure B; p < 0.01 for both). PUI was significantly lower in OB+HS (0.003 ± 0.001) and OB (0.029 ± 0.001) versus LEAN (0.102 ± 0.013) (p < 0.01), and significantly lower in OB+HS versus OB (Figure C; p < 0.05).

These findings demonstrate that hepatic lipid composition can be non-invasively measured by ¹H-MRS, and that obese men with and without hepatic steatosis exhibit a significant increase in SI and a decrease in PUI when compared with healthy lean men. Furthermore, obese men with hepatic steatosis showed specific depletion of polyunsaturated fatty acids (PUFAs) when compared with obese men with normal HTGC. These data are consistent with those derived by needle biopsy and histology by Araya et al. (2004). While a cause-effect relationship cannot be inferred from our cross-sectional research design, our finding is consistent with the postulation that dilution of hepatic lipid PUFAs promotes triglyceride accumulation by reducing triglyceride export and inhibiting lipid oxidation (Videla et al., 2004). Further longitudinal research is required to confirm this hypothesis and the suggestion that this phenotype might further predispose to inflammation (Videla et al., 2004).

Araya J, Rodrigo R, Videla LA, Thielemann L, Orellana M, Pettinelli P & Poniachik J. (2004) Clinical Science, 106: 635-643.

Videla LA, Rodrigo R, Araya J & Poniachik J. (2004) Free Radical Biology and Medicine, 37: 1499-1507.