Prevalence of anemia among Indigenous children in Latin America: a systematic review

OBJECTIVE: To describe the prevalence pattern of anemia among Indigenous children in Latin America. METHODS: PRISMA guidelines were followed. Records were identified from the databases PubMed, Google Scholar, and LILACS by two independent researchers between May and June 2021. Studies were included if the following criteria were met: a) studied Indigenous people b) was about children (from 0 to 12 years old); c) reported a prevalence estimate of anemia; d) had been conducted in any of the countries of Latin America; e) was published either in English, Portuguese, or Spanish; f) is a peer-reviewed article; and g) was published at any date. RESULTS: Out of 2,401 unique records retrieved, 42 articles met the inclusion criteria. A total of 39 different Indigenous communities were analyzed in the articles, and in 21 of them (54.0%) child anemia was a severe public health problem (prevalence ≥ 40%). Those communities were the Aymara (Bolivia); Aruak, Guaraní, Kamaiurá, Karapotó, Karibe, Kaxinanuá, Ma-cro-Jê, Suruí, Terena, Xavante (Brazil); Cabécar (Costa Rica), Achuar, Aguaruna, Awajún, Urarina, Yomybato (Peru); Piaroa and Yucpa (Venezuela); and Quechua (Peru and Bolivia). Children below two years had the highest prevalence of anemia (between 16.2% and 86.1%). Among Indigenous people, risk factors for anemia include nutrition, poor living conditions, access to health services, racism, and discrimination. Bolivia and Guatemala are scarcely studied, despite having the highest proportion of Indigenous communities in Latin America. CONCLUSIONS: Anemia constitutes a poorly documented public health problem among Indigenous children in 21 Indigenous communities in Bolivia, Brazil, Colombia, Costa Rica, Ecuador, Guatemala, Mexico, and Peru. In all Indigenous communities included in this study child anemia was an issue, especially in younger children

Structure and function of the plasma phospholipid transfer protein

International audienceRecent cloning and sequencing of plasma phospholipid transfer protein complementary DNA revealed that phospholipid transfer protein belongs to the lipid transfer/lipopolysaccharide binding protein family that includes the cholesteryl ester transfer protein, the bactericidal permeability increasing protein and the lipopolysaccharide-binding protein. In addition to structural similarities, members of the lipid transfer/lipopolysaccharide-binding protein family might share some common functional properties, and recent studies demonstrated that phospholipid transfer protein can act in several distinct metabolic processes. In particular, the molecular transfer of phospholipids, unesterified cholesterol, alpha-tocopherol and lipopolysaccharides by phospholipid transfer protein suggests that it might be involved both in lipoprotein metabolism and in antimicrobial defence, resulting in a growing interest in this protein

New therapeutic horizons for plasma phospholipid transfer protein (PLTP): targeting endotoxemia, infection and sepsis

International audiencePhospholipid Transfer Protein (PLTP) transfers amphiphilic lipids between circulating lipoproteins and between lipoproteins, cells and tissues. Indeed, PLTP is a major determinant of the plasma levels, turnover and functionality of the main lipoprotein classes: very low-density lipoproteins (VLDL), low-density lipoproteins (LDL) and high-density lipoproteins (HDL). To date, most attention has been focused on the role of PLTP in the context of cardiometabolic diseases, with additional insights in neurodegenerative diseases and immunity. Importantly, beyond its influence on plasma triglyceride and cholesterol transport, PLTP plays a key role in the modulation of the immune response, with immediate relevance to a wide range of inflammatory diseases including bacterial infection and sepsis. Indeed, emerging evidence supports the role of PLTP, in the context of its association with lipoproteins, in the neutralization and clearance of bacterial lipopolysaccharides (LPS) or endotoxins. LPS are amphipathic molecules originating from Gram-negative bacteria which harbor major pathogen-associated patterns, triggering an innate immune response in the host. Although the early inflammatory reaction constitutes a key step in the anti-microbial defense of the organism, it can lead to a dysregulated inflammatory response and to hemodynamic disorders, organ failure and eventually death. Moreover, and in addition to endotoxemia and acute inflammation, small amounts of LPS in the circulation can induce chronic, low-grade inflammation with long-term consequences in several metabolic disorders such as atherosclerosis, obesity and diabetes. After an updated overview of the role of PLTP in lipid transfer, lipoprotein metabolism and related diseases, current knowledge of its impact on inflammation, infection and sepsis is critically appraised. Finally, the relevance of PLTP as a new player and novel therapeutic target in the fight against inflammatory diseases is considered

Prevention of LDL a-tocopherol consumption, cholesterol oxidation, and vascular endothelium dysfunction by polyphenolic compounds from red wine

International audienceRed wine polyphenolic compounds (RWPCs) have been demonstrated to possess antioxidant properties, and several studies have suggested that they might constitute a relevant dietary factor in the protection from coronary heart disease. The aim of the present study was to determine further the mechanism by which RWPCs can prevent the formation of vasoactive compounds in oxidized LDL. RWPCs were obtained from the Cabernet-Sauvignon grape variety. Human LDL was oxidized in the presence of CuSO 4 (ox-LDL). Vascular reactivity studies were conducted on rabbit aortic rings. RWPCs significantly reduced the formation of 7bhydroxycholesterol and 7-ketocholesterol and in a lower extent the emergence of lysophosphatidylcholine in ox-LDL. The ability of RWPCs to prevent cholesterol oxide formation was directly dependent on the LDL a-tocopherol content. Once the LDL atocopherol has been consumed, RWPCs were no longer effective, indicating that RWPCs act by sparing endogenous a-tocopherol. As a consequence of the preservation of the endogenous a-tocopherol content of LDL, RWPCs could prevent the inhibition of the acetylcholine-mediated endothelium-dependent relaxation of rabbit aorta which was linked to a direct effect on NO release. Independently of a treatment with ox-LDL, RWPC exerted a concentration-dependent and persistent inhibitory effect on the norepinephrine-induced contraction of rabbit aorta. In conclusion, RWPCs can preserve a normal vascular reactivity by acting at different stages of the cascade that leads to lipid oxidation, endothelium dysfunction and vasospasm

Plasma phospholipid transfer protein prevents vascular endothelium dysfunction by delivering α-tocopherol to endothelial cells

International audienceα-tocopherol, the most potent antioxidant form of vitamin E, is mainly bound to lipoproteins in plasma and its incorporation into the vascular wall can prevent the endothelium dysfunction at an early stage of atherogenesis. In the present study, the plasma phospholipid transfer protein (PLTP) was shown to promote the net mass transfer of α-tocopherol from high density lipoproteins (HDL) and α-tocopherol-albumin complexes toward α-tocopherol-depleted, oxidized low density lipoproteins (LDL). The facilitated transfer reaction of α-tocopherol could be blocked by specific anti-PLTP antibodies. These observations indicate that PLTP may restore the antioxidant potential of plasma LDL at an early stage of the oxidation cascade that subsequently leads to cellular damages. In addition, the present study demonstrated that the PLTP-mediated net mass transfer of α-tocopherol can constitute a new mechanism for the incorporation of α-tocopherol into the vascular wall in addition to the previously recognized LDL receptor and lipoprotein lipase pathways. In ex vivo studies on rabbit aortic segments, the impairment of the endothelium-dependent arterial relaxation induced by oxidized LDL was found to be counteracted by a pretreatment with purified PLTP and α-tocopherol-albumin complexes, and both the maximal response and the sensitivity to acetylcholine were significantly improved. We conclude that PLTP, by supplying oxidized LDL and endothelial cells with α-tocopherol through a net mass transfer reaction may play at least two distinct beneficial roles in preventing endothelium damage, i.e., the antioxidant protection of LDL and the preservation of a normal relaxing function of vascular endothelial cells

Lysophosphatidylcholine and 7-oxocholesterol modulate Ca2+ signals and inhibit the phosphorylation of endothelial NO synthase and cytosolic phospholipase A2.

The oxidation of plasma LDLs (low-density lipoproteins) is a key event in the pathogenesis of atherosclerosis. LPC (lysophosphatidylcholine) and oxysterols are major lipid constitutents of oxidized LDLs. In particular, 7-oxocholesterol has been found in plasma from cardiac patients and atherosclerotic plaque. In the present study, we investigated the ability of 7-oxocholesterol and LPC to regulate the activation of eNOS (endothelial nitric oxide synthase) and cPLA2 (cytosolic phospholipase A2) that synthesize two essential factors for vascular wall integrity, NO (nitric oxide) and arachidonic acid. In endothelial cells from human umbilical vein cords, both 7-oxocholesterol (150 microM) and LPC (20 microM) decreased histamine-induced NO release, but not the release activated by thapsigargin. The two lipids decreased NO release through a PI3K (phosphoinositide 3-kinase)-dependent pathway, and decreased eNOS phosphorylation. Their mechanisms of action were, however, different. The NO release reduction was dependent on superoxide anions in LPC-treated cells and not in 7-oxocholesterol-treated ones. The Ca2+ signals induced by histamine were abolished by LPC, but not by 7-oxocholesterol. The oxysterol also inhibited (i) the histamine- and thapsigargin-induced arachidonic acid release, and (ii) the phosphorylation of both cPLA2 and ERK1/2 (extracellular-signal-regulated kinases 1/2). The results show that 7-oxocholesterol inhibits eNOS and cPLA2 activation by altering a Ca2+-independent upstream step of PI3K and ERK1/2 cascades, whereas LPC desensitizes eNOS by interfering with receptor-activated signalling pathways. This suggests that 7-oxocholesterol and LPC generate signals which cross-talk with heterologous receptors, effects which could appear at early stage of atherosclerosis

Cholesterol Accumulation Is Increased in Macrophages of Phospholipid Transfer Protein-Deficient Mice

International audienceObjective-Phospholipid transfer protein (PLTP) is a multifunctional, extracellular lipid transport protein that plays a major role in lipoprotein metabolism and atherosclerosis. Recent in vivo studies suggested that unlike systemic PLTP, macrophage-derived PLTP would be antiatherogenic. The present study aimed at characterizing the atheroprotective properties of macrophage-derived PLTP. Methods and Results-Peritoneal macrophages were isolated from PLTP-deficient and wild-type mice and their biochemical characteristics were compared. It is shown that macrophages isolated from PLTP-deficient mice have increased basal cholesterol content and accumulate more cholesterol in the presence of LDL compared with wild-type cells. Cholesterol parameters in macrophages of PLTP-deficient mice were normalized by dietary ␣-tocopherol supplementation. Conclusions-The antiatherogenic properties of macrophage-derived PLTP are related at least in part to its ability to reduce cholesterol accumulation in macrophages through changes in the alpha-tocopherol content and oxidative status of the cells

Prevalence of anemia among Indigenous children in Latin America: a systematic review

ABSTRACT OBJECTIVE: To describe the prevalence pattern of anemia among Indigenous children in Latin America. METHODS: PRISMA guidelines were followed. Records were identified from the databases PubMed, Google Scholar, and Lilacs by two independent researchers between May and June 2021. Studies were included if the following criteria were met: a) studied Indigenous people b) was about children (from 0 to 12 years old); c) reported a prevalence estimate of anemia; d) had been conducted in any of the countries of Latin America; e) was published either in English, Portuguese, or Spanish; f) is a peer-reviewed article; and g) was published at any date. RESULTS: Out of 2,401 unique records retrieved, 42 articles met the inclusion criteria. A total of 39 different Indigenous communities were analyzed in the articles, and in 21 of them (54.0%) child anemia was a severe public health problem (prevalence ≥ 40%). Those communities were the Aymara (Bolivia); Aruak, Guaraní, Kamaiurá, Karapotó, Karibe, Kaxinanuá, Ma-cro-Jê, Suruí, Terena, Xavante (Brazil); Cabécar (Costa Rica), Achuar, Aguaruna, Awajún, Urarina, Yomybato (Peru); Piaroa and Yucpa (Venezuela); and Quechua (Peru and Bolivia). Children below two years had the highest prevalence of anemia (between 16.2% and 86.1%). Among Indigenous people, risk factors for anemia include nutrition, poor living conditions, access to health services, racism, and discrimination. Bolivia and Guatemala are scarcely studied, despite having the highest proportion of Indigenous communities in Latin America. CONCLUSIONS: Anemia constitutes a poorly documented public health problem among Indigenous children in 21 Indigenous communities in Bolivia, Brazil, Colombia, Costa Rica, Ecuador, Guatemala, Mexico, and Peru. In all Indigenous communities included in this study child anemia was an issue, especially in younger children

Phospholipid transfer protein (PLTP), lipopolysaccharides detoxification and metabolic diseases: a connection ?

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