Metal ions effect on L ‐carnitine activity: A new research direction with a possible mitigating effect of dietary cellulose

Abstract

Disturbance of L-carnitine (LC) activity dissipates metabolic energy production in living cells. LC deficiency regards to malabsorption and biosynthetic and transport deficiencies, either due to dietary or metabolic factors. Metal ions interact with LC molecule or its metabolic system elements such as building blocks (lysine and methionine), biosynthetic enzymes (trimethyllysine hydroxylase, TMLH; γ-butyrobetaine dioxygenase, γ-BBD) and LC transporters (carnitine acetyl transferase, CAT; organic cation transporter novel 2, OCTN2). Metals such as Cu2+, Ca2+ and Mg2+ form complexes with LC, while Pb2+ and Ni form complexes with methionine and lysine. Also, Mg2+ and Mn ions inhibit TMLH and γ-BBD activities. On the other hand, Ca2+ ions induce TMLH activity while LC forms a complex with it. Also, boron stabilizes B6 and C vitamins as they are co-enzymes for LC biosynthetic enzymes activity. Metals affect LC homeostasis via affecting its transporters CAT and OCTN2, that Na+ shortage affects OCTN2 activity, while Cu2+ inhibit CAT activity. Dietary fibres mediate ions toxicity by forming complexes with ions, which increase LC absorption in small intestine, while fibre fermentation liberates the bounded minerals and enrich bacterial biomass in large intestine, but the microbiome sequent metals intra- and extracellularly increasing LC absorption, in addition to the dietary sparing effect on LC from bacterial consumption as nitrogen source. This review aimed to illustrate effect of metal ions toxicity on LC activity and the mediating effect of dietary fibres. To the best of our knowledge, this is the first review to illustrate the ion toxicity on LC activity in monogastrics and fish.