Effect of Marginal Zinc Intake and Repletion on Essential Fatty Acid Metabolism

Objective To determine the effects of marginal zinc deficiency and repletion on essential fatty acid, sphingolipid, and lipoprotein metabolism. Methods Sixteen apparently healthy male subjects between ages of 18–45 were subjected to three sequential phases of dietary zinc intake modulation: Phase 1:...

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Main Authors: Suh, Jung, Burke, Sarah, Shigenaga, Mark, Killela, David, Holland, Tai, Shenvi, Swapna, Sutherland, Barbara, King, Janet C.
Format: Journal Article
Language:Inglés
Published: 2017
Subjects:
Online Access:https://hdl.handle.net/10568/171044
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author Suh, Jung
Burke, Sarah
Shigenaga, Mark
Killela, David
Holland, Tai
Shenvi, Swapna
Sutherland, Barbara
King, Janet C.
author_browse Burke, Sarah
Holland, Tai
Killela, David
King, Janet C.
Shenvi, Swapna
Shigenaga, Mark
Suh, Jung
Sutherland, Barbara
author_facet Suh, Jung
Burke, Sarah
Shigenaga, Mark
Killela, David
Holland, Tai
Shenvi, Swapna
Sutherland, Barbara
King, Janet C.
author_sort Suh, Jung
collection Repository of Agricultural Research Outputs (CGSpace)
description Objective To determine the effects of marginal zinc deficiency and repletion on essential fatty acid, sphingolipid, and lipoprotein metabolism. Methods Sixteen apparently healthy male subjects between ages of 18–45 were subjected to three sequential phases of dietary zinc intake modulation: Phase 1: Low Zinc intake: 6 mg/day with 1.5 g of phytate (2 wks); Phase II: Zinc Repletion: 10 mg/day with no phytate (4 wks); Phase III: Zinc Supplementation: Ad lib diet supplemented with 20 mg zinc (2 wks). Subject weight, and compliance with diet were monitored every 3–4 days during the first two phases. Plasma free fatty acids and sphingolipids were measured by mass spectrometry. FADS1 and FADS2 activities were calculated by g-linolenic (GLA)/linolenic acid (LA) or arachidonic acid (AA)/dihomo-g-linolenic acid (DGLA) ratios, respectively. Results Plasma zinc levels remained unchanged during Phases I and II in all subjects and increased only at the conclusion of phase III. FADS1 activity significantly (p=0.005) decreased from 5.2 ± 0.5 to 3.6 ± 0.5 (mean ± SEM) following Zn depletion. In contrast, FADS2 activity was insensitive to effects of low zinc intake. As a consequence of FADS1 activity loss, concentrations of AA-containing phosphatidylcholine (PC), phosphatidylethanolamine (PE), sphingomyelins and plasmalogen antioxidant lipids decreased significantly. Furthermore, plasma concentrations of C16:0 ceramide increased following Zn depletion (p = 0.06) and was inversely correlated with FADS1 activity (p = 0.04; r2 = 0.6). Zn depletion also increased plasma triglyceride (TG) by 26 ± 15% (p< 0.05) and decreased high-density lipoprotein (HDL) by 18.5 ± 3%; P<0.05. Interestingly, changes in FADS1 activity observed during the depletion was not normalized by dietary Zn repletion (Phase II) but, it was completely normalized with Zn supplementation (20 mg/day; Phase III). Conclusion Dietary Zn depletion (6 mg/day) decreases FADS1 activity and lowered AA incorporation into major lipid sub-classes. Loss in FADS1 activity was inversely correlated with C16:0 ceramide and was further associated with dyslipidemia as evidenced by significant alterations in plasma TG and HDL. These effects were not corrected with dietary Zn repletion (10 mg/day); supplementation with 20 mg Zn/d for an additional 3 weeks was required. These data suggest that FADS1 activity may be a sensitive biomarker of inadequate zinc intake and they also implicate marginal Zn intake as a novel risk factor for dyslipidemia and insulin resistance. Support or Funding Information Harvest Plus, NIH S10OD0018070-01
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spelling CGSpace1710442025-02-19T14:31:24Z Effect of Marginal Zinc Intake and Repletion on Essential Fatty Acid Metabolism Suh, Jung Burke, Sarah Shigenaga, Mark Killela, David Holland, Tai Shenvi, Swapna Sutherland, Barbara King, Janet C. zinc nutrition methodology Objective To determine the effects of marginal zinc deficiency and repletion on essential fatty acid, sphingolipid, and lipoprotein metabolism. Methods Sixteen apparently healthy male subjects between ages of 18–45 were subjected to three sequential phases of dietary zinc intake modulation: Phase 1: Low Zinc intake: 6 mg/day with 1.5 g of phytate (2 wks); Phase II: Zinc Repletion: 10 mg/day with no phytate (4 wks); Phase III: Zinc Supplementation: Ad lib diet supplemented with 20 mg zinc (2 wks). Subject weight, and compliance with diet were monitored every 3–4 days during the first two phases. Plasma free fatty acids and sphingolipids were measured by mass spectrometry. FADS1 and FADS2 activities were calculated by g-linolenic (GLA)/linolenic acid (LA) or arachidonic acid (AA)/dihomo-g-linolenic acid (DGLA) ratios, respectively. Results Plasma zinc levels remained unchanged during Phases I and II in all subjects and increased only at the conclusion of phase III. FADS1 activity significantly (p=0.005) decreased from 5.2 ± 0.5 to 3.6 ± 0.5 (mean ± SEM) following Zn depletion. In contrast, FADS2 activity was insensitive to effects of low zinc intake. As a consequence of FADS1 activity loss, concentrations of AA-containing phosphatidylcholine (PC), phosphatidylethanolamine (PE), sphingomyelins and plasmalogen antioxidant lipids decreased significantly. Furthermore, plasma concentrations of C16:0 ceramide increased following Zn depletion (p = 0.06) and was inversely correlated with FADS1 activity (p = 0.04; r2 = 0.6). Zn depletion also increased plasma triglyceride (TG) by 26 ± 15% (p< 0.05) and decreased high-density lipoprotein (HDL) by 18.5 ± 3%; P<0.05. Interestingly, changes in FADS1 activity observed during the depletion was not normalized by dietary Zn repletion (Phase II) but, it was completely normalized with Zn supplementation (20 mg/day; Phase III). Conclusion Dietary Zn depletion (6 mg/day) decreases FADS1 activity and lowered AA incorporation into major lipid sub-classes. Loss in FADS1 activity was inversely correlated with C16:0 ceramide and was further associated with dyslipidemia as evidenced by significant alterations in plasma TG and HDL. These effects were not corrected with dietary Zn repletion (10 mg/day); supplementation with 20 mg Zn/d for an additional 3 weeks was required. These data suggest that FADS1 activity may be a sensitive biomarker of inadequate zinc intake and they also implicate marginal Zn intake as a novel risk factor for dyslipidemia and insulin resistance. Support or Funding Information Harvest Plus, NIH S10OD0018070-01 2017 2025-01-29T12:57:38Z 2025-01-29T12:57:38Z Journal Article https://hdl.handle.net/10568/171044 en Limited Access Suh, Jung; Burke, Sarah; Shigenaga, Mark; Killela, David; Holland, Tal; Shenvi, Swapna; Sutherland, Barbara; and King, Janet. 2017. Effect of Marginal Zinc Intake and Repletion on Essential Fatty Acid Metabolism. FASEB Journal 31(1): 802. http://www.fasebj.org/content/31/1_Supplement/802.7.short
spellingShingle zinc
nutrition
methodology
Suh, Jung
Burke, Sarah
Shigenaga, Mark
Killela, David
Holland, Tai
Shenvi, Swapna
Sutherland, Barbara
King, Janet C.
Effect of Marginal Zinc Intake and Repletion on Essential Fatty Acid Metabolism
title Effect of Marginal Zinc Intake and Repletion on Essential Fatty Acid Metabolism
title_full Effect of Marginal Zinc Intake and Repletion on Essential Fatty Acid Metabolism
title_fullStr Effect of Marginal Zinc Intake and Repletion on Essential Fatty Acid Metabolism
title_full_unstemmed Effect of Marginal Zinc Intake and Repletion on Essential Fatty Acid Metabolism
title_short Effect of Marginal Zinc Intake and Repletion on Essential Fatty Acid Metabolism
title_sort effect of marginal zinc intake and repletion on essential fatty acid metabolism
topic zinc
nutrition
methodology
url https://hdl.handle.net/10568/171044
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