TY - JOUR

T1 - Host-related factors explaining interindividual variability of carotenoid bioavailability and tissue concentrations in humans

AU - Bohn, Torsten

AU - Desmarchelier, Charles

AU - Dragsted, Lars Ove

AU - Nielsen, Charlotte Salgaard

AU - Stahl, Wilhelm

AU - Rühl, Ralph

AU - Keijer, Jaap

AU - Borel, Patrick

N1 - CURIS 2017 NEXS 072

PY - 2017

Y1 - 2017

N2 - Carotenoid dietary intake and their endogenous levels have been associated with a decreased risk of several chronic diseases. There are indications that carotenoid bioavailability depends, in addition to the food matrix, on host factors. These include diseases (e.g. colitis), life-style habits (e.g. smoking), gender and age, as well as genetic variations including single nucleotide polymorphisms that govern carotenoid metabolism. These are expected to explain interindividual differences that contribute to carotenoid uptake, distribution, metabolism and excretion, and therefore possibly also their association with disease risk. For instance, digestion enzymes fostering micellization (PNLIP, CES), expression of uptake/efflux transporters (SRARB1, CD36, NPC1L1), cleavage enzymes (BCO1/2), intracellular transporters (FABP2), secretion into chylomicrons (APOB, MTTP), carotenoid metabolism in the blood and liver (LPL, APO C/E, LDLR), and distribution to target tissues such as adipose tissue or macula (GSTP1, StARD3) depend on the activity of these proteins. In addition, human microbiota, e.g. via altering bile-acid concentrations, may play a role in carotenoid bioavailability. In order to comprehend individual, variable responses to these compounds, an improved knowledge on intra-/interindividual factors determining carotenoid bioavailability, including tissue distribution, is required. Here, we highlight the current knowledge on factors that may explain such intra-/interindividual differences. This article is protected by copyright. All rights reserved.

AB - Carotenoid dietary intake and their endogenous levels have been associated with a decreased risk of several chronic diseases. There are indications that carotenoid bioavailability depends, in addition to the food matrix, on host factors. These include diseases (e.g. colitis), life-style habits (e.g. smoking), gender and age, as well as genetic variations including single nucleotide polymorphisms that govern carotenoid metabolism. These are expected to explain interindividual differences that contribute to carotenoid uptake, distribution, metabolism and excretion, and therefore possibly also their association with disease risk. For instance, digestion enzymes fostering micellization (PNLIP, CES), expression of uptake/efflux transporters (SRARB1, CD36, NPC1L1), cleavage enzymes (BCO1/2), intracellular transporters (FABP2), secretion into chylomicrons (APOB, MTTP), carotenoid metabolism in the blood and liver (LPL, APO C/E, LDLR), and distribution to target tissues such as adipose tissue or macula (GSTP1, StARD3) depend on the activity of these proteins. In addition, human microbiota, e.g. via altering bile-acid concentrations, may play a role in carotenoid bioavailability. In order to comprehend individual, variable responses to these compounds, an improved knowledge on intra-/interindividual factors determining carotenoid bioavailability, including tissue distribution, is required. Here, we highlight the current knowledge on factors that may explain such intra-/interindividual differences. This article is protected by copyright. All rights reserved.

KW - Faculty of Science

KW - Absorption

KW - Biodistribution

KW - Intestine

KW - Macula lutea

KW - Genetic polymorphisms

U2 - 10.1002/mnfr.201600685

DO - 10.1002/mnfr.201600685

M3 - Review

C2 - 28101967

VL - 61

JO - Molecular Nutrition & Food Research

JF - Molecular Nutrition & Food Research

SN - 1613-4125

IS - 6

M1 - 1600685

ER -