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Anatomy & Physiology: Current Research

Anatomy & Physiology: Current Research
Open Access

ISSN: 2161-0940

+44 1300 500008

Abstract

The Relation between Non-adipose Muscle Fat and Hepatic Steatosis Studied with Localized 1H Magnetic Resonance Spectroscopy (1H MRS) and LC-MS Techniques

van Ginneken VJT, Ronald Booms, Elwin Verheij, Evert de Vries and Jan van der Greef

Aim/objective: In this study we investigated ectopic fat storage in the muscle and the liver using 1H Magnetic Resonance Spectroscopy (1H-MRS). The inability to store fat in adipose tissue leads to ectopic Triacylglycerol (TG) accumulation in muscle followed by the liver: the so called “overflow hypothesis”. It is assumed that when steatosis occurs in organs like the liver we can speak from “Metabolic Syndrome”.

Methods: We compared the effects of two different diet interventions, 24 h-starvation and 40 days High-fat diet (+0.25% cholesterol and 45% energy from bovine lard) with control mice. Characterization of lipid molecular species in non-adipose muscle homogenate was performed by comparing the groups using liquid chromatography coupled to mass spectrometry (LC-MS) techniques following a Systems Biology lipidomics based approach. Reversed phase liquid chromatography coupled to mass spectrometry (LC-MS) were used to quantify and qualify the rearrangement and repartitioning of the triacylglycerol compound in the liver organ.

Results: The major message of this manuscript is the interaction of remnant organ/tissue called “carcass” in the absorption capacity of lipids and the spill-over of these lipid compounds (mainly TG’s) to the liver. Our data suggest that if the remnant muscle compartment is saturated with lipids until ≈500 g/kg dry matter there is no TGs accumulation in the liver, but above this level there is a spill over in the plasma resulting in fat accumulation in the liver.

Conclusion: We demonstrated in this study that fat can be stored in the muscle but when this compartment is saturated the liver takes over the function as a fat sink, the "overflow hypothesis" resulting finally in hepatic steatosis and ‘Metabolic Syndrome’.

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