Advanced glycation end products in infant formulas do not contribute to insulin resistance associated with their consumption.

<h4>Introduction</h4>Infant formula-feeding is associated with reduced insulin sensitivity. In rodents and healthy humans, advanced glycation end product (AGE)-rich diets exert diabetogenic effects. In comparison with human breast-milk, infant formulas contain high amounts of AGEs. We as...

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Autores principales:	Kristína Simon Klenovics, Peter Boor, Veronika Somoza, Peter Celec, Vincenzo Fogliano, Katarína Sebeková
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/db910f4986424abf9f8c14658cf0b74a
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spelling	oai:doaj.org-article:db910f4986424abf9f8c14658cf0b74a2021-11-18T08:02:52ZAdvanced glycation end products in infant formulas do not contribute to insulin resistance associated with their consumption.1932-620310.1371/journal.pone.0053056https://doaj.org/article/db910f4986424abf9f8c14658cf0b74a2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23301020/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Introduction</h4>Infant formula-feeding is associated with reduced insulin sensitivity. In rodents and healthy humans, advanced glycation end product (AGE)-rich diets exert diabetogenic effects. In comparison with human breast-milk, infant formulas contain high amounts of AGEs. We assessed the role of AGEs in infant-formula-consumption-associated insulin resistance.<h4>Methods</h4>Total plasma levels of N(ε)-(carboxymethyl)lysine (CML), AGEs-associated fluorescence (λ(ex) = 370 nm/λ(em) = 445 nm), soluble adhesion molecules, markers of micro- binflammation (hsCRP), oxidative stress (malondialdehyde, 8-isoprostanes) and leptinemia were determined, and correlated with insulin sensitivity in a cross-sectional study in 166 healthy term infants aged 3-to-14 months, subdivided according to feeding regimen (breast-milk- vs. infant formula-fed) and age (3-to-6-month-olds, 7-to-10-month-olds, and 11-to-14-month-old infants). Effects of the consumption of low- vs. high-CML-containing formulas were assessed. 36 infants aged 5.8 ± 0.3 months were followed-up 7.5 ± 0.3 months later.<h4>Results</h4>Cross-sectional study: 3-to-6-month-olds and 7-to-10-month-old formula-fed infants presented higher total plasma CML levels and AGEs-associated fluorescence (p<0.01, both), while only the 3-to-6-month-olds displayed lower insulin sensitivity (p<0.01) than their breast-milk-fed counterparts. 3-to-6-month-olds fed low-CML-containing formulas presented lower total plasma CML levels (p<0.01), but similar insulin sensitivity compared to those on high-CML-containing formulas. Markers of oxidative stress and inflammation, levels of leptin and adhesion molecules did not differ significantly between the groups. Follow-up study: at initial investigation, the breast-milk-consuming infants displayed lower total plasma CML levels (p<0.01) and AGEs-associated fluorescence (p<0.05), but higher insulin sensitivity (p<0.05) than the formulas-consuming infants. At follow-up, the groups did not differ significantly in either determined parameter.<h4>Conclusions</h4>In healthy term infants, high dietary load with CML does not play a pathophysiological role in the induction of infant formula-associated insulin resistance. Whether a high load of AGEs in early childhood affects postnatal programming remains to be elucidated.Kristína Simon KlenovicsPeter BoorVeronika SomozaPeter CelecVincenzo FoglianoKatarína SebekováPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 1, p e53056 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Kristína Simon Klenovics Peter Boor Veronika Somoza Peter Celec Vincenzo Fogliano Katarína Sebeková Advanced glycation end products in infant formulas do not contribute to insulin resistance associated with their consumption.
description	<h4>Introduction</h4>Infant formula-feeding is associated with reduced insulin sensitivity. In rodents and healthy humans, advanced glycation end product (AGE)-rich diets exert diabetogenic effects. In comparison with human breast-milk, infant formulas contain high amounts of AGEs. We assessed the role of AGEs in infant-formula-consumption-associated insulin resistance.<h4>Methods</h4>Total plasma levels of N(ε)-(carboxymethyl)lysine (CML), AGEs-associated fluorescence (λ(ex) = 370 nm/λ(em) = 445 nm), soluble adhesion molecules, markers of micro- binflammation (hsCRP), oxidative stress (malondialdehyde, 8-isoprostanes) and leptinemia were determined, and correlated with insulin sensitivity in a cross-sectional study in 166 healthy term infants aged 3-to-14 months, subdivided according to feeding regimen (breast-milk- vs. infant formula-fed) and age (3-to-6-month-olds, 7-to-10-month-olds, and 11-to-14-month-old infants). Effects of the consumption of low- vs. high-CML-containing formulas were assessed. 36 infants aged 5.8 ± 0.3 months were followed-up 7.5 ± 0.3 months later.<h4>Results</h4>Cross-sectional study: 3-to-6-month-olds and 7-to-10-month-old formula-fed infants presented higher total plasma CML levels and AGEs-associated fluorescence (p<0.01, both), while only the 3-to-6-month-olds displayed lower insulin sensitivity (p<0.01) than their breast-milk-fed counterparts. 3-to-6-month-olds fed low-CML-containing formulas presented lower total plasma CML levels (p<0.01), but similar insulin sensitivity compared to those on high-CML-containing formulas. Markers of oxidative stress and inflammation, levels of leptin and adhesion molecules did not differ significantly between the groups. Follow-up study: at initial investigation, the breast-milk-consuming infants displayed lower total plasma CML levels (p<0.01) and AGEs-associated fluorescence (p<0.05), but higher insulin sensitivity (p<0.05) than the formulas-consuming infants. At follow-up, the groups did not differ significantly in either determined parameter.<h4>Conclusions</h4>In healthy term infants, high dietary load with CML does not play a pathophysiological role in the induction of infant formula-associated insulin resistance. Whether a high load of AGEs in early childhood affects postnatal programming remains to be elucidated.
format	article
author	Kristína Simon Klenovics Peter Boor Veronika Somoza Peter Celec Vincenzo Fogliano Katarína Sebeková
author_facet	Kristína Simon Klenovics Peter Boor Veronika Somoza Peter Celec Vincenzo Fogliano Katarína Sebeková
author_sort	Kristína Simon Klenovics
title	Advanced glycation end products in infant formulas do not contribute to insulin resistance associated with their consumption.
title_short	Advanced glycation end products in infant formulas do not contribute to insulin resistance associated with their consumption.
title_full	Advanced glycation end products in infant formulas do not contribute to insulin resistance associated with their consumption.
title_fullStr	Advanced glycation end products in infant formulas do not contribute to insulin resistance associated with their consumption.
title_full_unstemmed	Advanced glycation end products in infant formulas do not contribute to insulin resistance associated with their consumption.
title_sort	advanced glycation end products in infant formulas do not contribute to insulin resistance associated with their consumption.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/db910f4986424abf9f8c14658cf0b74a
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Advanced glycation end products in infant formulas do not contribute to insulin resistance associated with their consumption.

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