The Influence of Diabetes and Metabolic Syndrome on Liver Fatty Acid Profile: What can we Learn from Animal Models

Tomislav Mašek

University of Zagreb, Faculty of Veterinary Medicine, Heinzelova 55, Zagreb, Croatia

Dr. Tomislav Mašek, University of Zagreb, Faculty of Veterinary Medicine, Heinzelova 55, Zagreb, Croatia.

Keywords: Diabetes; Autoimmunity; Hormonal Modulation

Abstract

Whole body fatty acids can originate from three different sources: food, de novo lipogenesis and bioconversion. Fatty acids generated de novo, as well as fatty acids derived from food can be bioconverted to longer-chain fatty acids with more carbon atoms and/or double bonds, by a series of steps of desaturation and elongation, or shortened by β oxidation steps and recycled between peroxisomes and the endoplasmatic reticulum. Regulation of these steps involves desaturases (Δ9D, Δ6D, Δ5D) and elongases (Elovl2, Elovl5 and Elovl6), as well as different metabolites (glucose), hormones (insulin) and transcriptional factors (peroxisome proliferator activated receptors α PPAR α sterol response element-binding protein-1c, SREBP-1c; liver X receptor, LXR; carbohydrate-regulatory element binding protein, ChREBP; MAX-like factor X, MLX) and microRNA. Nutrition (substrate availability) and competition for rate-limiting enzymes for desaturation, as well as partitioning into oxidation could substantially contribute or even override other regulatory mechanisms.

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