Long-Term Dose-Response Condensed Tannin Supplementation Does Not Affect Iron Status or Bioavailability

Citation: Delimont, N. M., Fiorentino, N. M., Kimmel, K. A., Haub, M. D., Rosenkranz, S. K., & Lindshield, B. L. (2017). Long-Term Dose-Response Condensed Tannin Supplementation Does Not Affect Iron Status or Bioavailability. Current Developments in Nutrition, 1(10), e001081. https://doi.org/10.3945/cdn.117.001081Background: Repeated phytic acid consumption leads to iron absorption adaptation but, to the best of our knowledge, the impact of repeated tannin consumption has not yet been established. Salivary proline-rich proteins (PRPs) may improve iron absorption by precipitating tannins. Objectives: This study aimed to determine the effect of long-term, dose-response condensed tannin supplementation on iron bioavailability and status and to assess the effect of salivary proteins on iron bioavailability during prolonged condensed tannin consumption. A secondary objective was to assess astringency as a potential marker for adaptation to tannins and iron bioavailability. Methods: Eleven nonanemic women were enrolled in a double-blind 3-dose crossover trial. Three (1.5, 0.25, or 0.03 g) condensed tannin supplements were consumed 3 times/d for 4 wk in random order, with 2-wk washouts in between. Meal challenges were employed before and after supplementation to assess iron bioavailability, iron status, salivary PRP changes, and astringency. Results: Tannin supplementation in any dose did not change iron bioavailability at any dose (P . 0.82) from weeks 0 to 4. Hemoglobin (P = 0.126) and serum ferritin (P = 0.83) were unchanged by tannin dose from weeks 0 to 4. There were significant correlations among tannin supplementation and iron bioavailability, basic proline-rich proteins (bPRPs) (r = 0.366, P = 0.003), and cystatin production (r = 0.27, P = 0.03). Astringency ratings did not change significantly within or between tannin doses (P . 0.126), but there were negative relations among bPRP (r , 20.32, P , 0.21), cystatin production (r , 20.2, P , 0.28), and astringency ratings. Conclusions: Condensed tannin consumption did not affect iron bioavailability or status regardless of the supplementation period in premenopausal nonanemic women. Correlation analyses suggest that bPRPs and cystatins are associated with improved iron bioavailability and that lower ratings of astringency may predict improved iron absorption with repeated tannin consumption. Curr Dev Nutr 2017;1:e001081

Role for a Novel Usher Protein Complex in Hair Cell Synaptic Maturation

The molecular mechanisms underlying hair cell synaptic maturation are not well understood. Cadherin-23 (CDH23), protocadherin-15 (PCDH15) and the very large G-protein coupled receptor 1 (VLGR1) have been implicated in the development of cochlear hair cell stereocilia, while clarin-1 has been suggested to also play a role in synaptogenesis. Mutations in CDH23, PCDH15, VLGR1 and clarin-1 cause Usher syndrome, characterized by congenital deafness, vestibular dysfunction and retinitis pigmentosa. Here we show developmental expression of these Usher proteins in afferent spiral ganglion neurons and hair cell synapses. We identify a novel synaptic Usher complex comprised of clarin-1 and specific isoforms of CDH23, PCDH15 and VLGR1. To establish the in vivo relevance of this complex, we performed morphological and quantitative analysis of the neuronal fibers and their synapses in the Clrn1−/− mouse, which was generated by incomplete deletion of the gene. These mice showed a delay in neuronal/synaptic maturation by both immunostaining and electron microscopy. Analysis of the ribbon synapses in Ames waltzerav3J mice also suggests a delay in hair cell synaptogenesis. Collectively, these results show that, in addition to the well documented role for Usher proteins in stereocilia development, Usher protein complexes comprised of specific protein isoforms likely function in synaptic maturation as well

The Impact of Tannin Consumption on Iron Bioavailability and Status: A Narrative Review

Iron deficiency remains a global health issue, and antinutritional factors, such as tannins, are often cited as contributors to the high prevalence of deficiency. Despite this, tannin-rich diets may have potential beneficial cardiovascular and cancer-fighting properties because of the antioxidant activity of tannins. Furthermore, epidemiologic studies and long-term trials involving participants who consumed diets rich in antinutritional factors, particularly tannins, conflict with single-meal bioavailability studies. The purpose of this narrative review is to determine the effect of tannins on iron bioavailability and status and establish whether adaptation to tannins reduces the antinutritional effects of tannins over time. We also aimed to compare tannins used in iron studies. Common themes related to iron bioavailability and iron status with tannin consumption were collected and collated for summary and synthesis based on models and subjects used. Overall, there was dissonance between iron bioavailability and status in studies. Single-meal studies with hydrolyzable and oligomeric catechin and epicatechin tannins (tea and tannic acid) generally support reductions in bioavailability related to tannin consumption but not consumption of condensed tannin, which are more commonly found in food. Long-term animal model, epidemiologic, and multimeal studies generally do not support changes in iron status related to tannin intake. Studies suggest that long-term tannin consumption may impact iron status in a different manner than single-meal studies or bioavailability iron models predict. Furthermore, iron bioavailability studies that use condensed tannins, which are more commonly consumed, may better predict mealtime iron bioavailability. More research is needed to develop representative antinutritional iron studies and investigate mechanisms underlying the adaptation to tannins and other antinutritional factors that occur over time

Molecular Brain Research

2-Jan137-1498

Molecular Brain Research

2-JanThis is a erratum reprint - with original pagination of the original title - placed at the front of issue: Molecular Brain Research. 2000,.DEC 28. V.85:(1-2).137-1498

Salivary proline-rich protein may reduce tannin-iron chelation: a systematic narrative review

Abstract Background Tannins are often cited for antinutritional effects, including chelation of non-heme iron. Despite this, studies exploring non-heme iron bioavailability inhibition with long-term consumption have reported mixed results. Salivary proline-rich proteins (PRPs) may mediate tannin-antinutritional effects on non-heme iron bioavailability. Aim To review evidence regarding biochemical binding mechanisms and affinity states between PRPs and tannins, as well as effects of PRPs on non-heme iron bioavailability with tannin consumption in vivo. Methods Narrative systematic review and meta-analysis. Common themes in biochemical modeling and affinity studies were collated for summary and synthesis; data were extracted from in vivo experiments for meta-analysis. Results Thirty-two studies were included in analysis. Common themes that positively influenced tannin-PRP binding included specificity of tannin-PRP binding, PRP and tannin stereochemistry. Hydrolyzable tannins have different affinities than condensed tannins when binding to PRPs. In vivo, hepatic iron stores and non-heme iron absorption are not significantly affected by tannin consumption (d = −0.64-1.84; −2.7-0.13 respectively), and PRP expression may increase non-heme iron bioavailability with tannin consumption. Conclusions In vitro modeling suggests that tannins favor PRP binding over iron chelation throughout digestion. Hydrolyzable tannins are not representative of tannin impact on non-heme iron bioavailability in food tannins because of their unique structural properties and PRP affinities. With tannin consumption, PRP production is increased, and may be an initial line of defense against tannin-non-heme iron chelation in vivo. More research is needed to compare competitive binding of tannin-PRP to tannin-non-heme iron complexes, and elucidate PRPs’ role in adaption to non-heme iron bioavailability in vivo

Progressive morphological and functional defects in retinas from alpha1 integrin-null mice.

PURPOSE: The role of integrin/cell matrix interactions between the RPE and the basement membrane in retinal maintenance and function is not well characterized. In this study the functional importance of alpha1beta1 integrin for retinal pigment epithelial cell homeostasis and retinal health was assessed by comparing alpha1 integrin knockout mice with strain- and age-matched wild-type mice. METHODS: Immunolocalization and Western blot analysis of retinas and ARPE19 cells were performed to examine the expression of alpha1beta1 integrin in the RPE. Retinal abnormality was assessed by funduscopy, histology, and transmission electron microscopy. Progressive retinal damage was quantified by direct counting of rod photoreceptors. Light-induced translocation of arrestin and alpha-transducin was documented by immunohistochemical analysis of retinal cryosections. RESULTS: Integrin alpha1beta1 localizes to the basal aspect of retinal pigment epithelial cells colocalizing with the basal lamina of the RPE. Integrin alpha1-null mice have delayed-onset progressive retinal degeneration associated with thickening of the basement membrane, dysmorphology of basal processes, synaptic malformations, and funduscopic abnormalities. Integrin alpha1-null mice display marked delays in transducin translocation compared with dark-adapted wild-type mice after exposure to light. CONCLUSIONS: Collectively, these data suggest an essential role for alpha1beta1 integrin/basement membrane interactions in the RPE in basement membrane metabolism and translocation of transducin in photoreceptors. This is the first report describing evidence supporting an essential role for integrin/basement membrane interaction in the RPE. Further, this report demonstrates a direct link between integrin alpha1beta1 function in retinal pigment epithelial and molecular defects in photoreceptor cell function before retinal abnormality is apparent