RESUMO
Maternal severe zinc (Zn) deficiency resulted in growth retardation and high mortality during embryonic development in human. Therefore, this study is aimed at evaluating the effect of maternal marginal Zn deficiency on the development and redox status to avoid severe Zn deficiency using an avian model. A total of 324 laying duck breeders at 214 days old were randomly allotted into 3 dietary Zn levels with 6 replicates of 18 ducks per replicate. The birds were fed experimental diets including 3 dietary supplemental Zn levels of 0 mg/kg (maternal Zn-deficient group, 29.2 mg Zn/kg diet), 60 mg/kg (maternal Zn-adequate group), and 120 mg/kg (maternal Zn-high group) for 6 weeks. Dietary Zn levels had on effect on egg production and fertility (P > 0.05), whereas dietary Zn deficiency decreased breeder plasma Zn concentration and erythrocytic alkaline phosphatase activity at week 6 and inhibited erythrocytic 5'-nucleotidase (5'-NT) activity at weeks 2, 4, and 6 (P < 0.05), indicating that marginal Zn-deficient status occurred after Zn depletion. Maternal marginal Zn deficiency increased embryonic mortality and contents of superoxide anion radical, MDA, and PPC and reduced MT content and CuZnSOD activity in duck embryonic livers on E29. The MDA content was positively correlated with embryonic mortality. Maternal marginal Zn deficiency increased BCL2-associated X protein and Caspase-9 mRNA expressions as well as decreased B-cell lymphoma-2 and MT1 mRNA and signal AKT1 and ERK1 protein expressions (P < 0.05). Breeder plasma Zn concentration and erythrocytic 5'-NT activities at week 6 were positively correlated with GSH-Px activity and GPx, MT1, and BCL2 mRNA expressions in embryonic livers on E29. In conclusion, erythrocytic 5'-NT activity could be more rapid and reliable to monitor marginal Zn-deficient status. Marginal Zn deficiency impaired hatchability and antioxidant defense system and then induced oxidative damage and apoptosis in the embryonic liver, contributing to the greater loss of duck embryonic death.
Assuntos
Apoptose , Deficiências Nutricionais/metabolismo , Patos/embriologia , Embrião não Mamífero/metabolismo , Fenômenos Fisiológicos da Nutrição Materna , Estresse Oxidativo , Zinco/deficiência , 5'-Nucleotidase/sangue , Animais , Apoptose/genética , Proteínas Reguladoras de Apoptose/genética , Proteínas Reguladoras de Apoptose/metabolismo , Deficiências Nutricionais/genética , Deficiências Nutricionais/patologia , Deficiências Nutricionais/fisiopatologia , Modelos Animais de Doenças , Embrião não Mamífero/patologia , Eritrócitos/enzimologia , Feminino , Regulação da Expressão Gênica no Desenvolvimento , Fígado/embriologia , Fígado/enzimologia , Estado Nutricional , Oxirredução , Estresse Oxidativo/genéticaRESUMO
Chronic arsenic exposure via drinking water is associated with diabetes in human pop-ulations throughout the world. Arsenic is believed to exert its diabetogenic effects via multiple mechanisms, including alterations to insulin secretion and insulin sensitivity. In the past, acute arsenicosis has been thought to be partially treatable with selenium supplementation, though a potential interaction between selenium and arsenic had not been evaluated under longer-term exposure models. The purpose of the present study was to explore whether selenium status may augment arsenic's effects during chronic arsenic exposure. To test this possibility, mice were exposed to arsenic in their drinking water and provided ad libitum access to either a diet replete with selenium (Control) or deficient in selenium (SelD). Arsenic significantly improved glucose tolerance and decreased insulin secretion and ß-cell function in vivo. Dietary selenium deficiency resulted in similar effects on glucose tolerance and insulin secretion, with significant interactions between arsenic and dietary conditions in select insulin-related parameters. The findings of this study highlight the complexity of arsenic's metabolic effects and suggest that selenium deficiency may interact with arsenic exposure on ß-cell-related physiological parameters.
Assuntos
Arsenitos/toxicidade , Glicemia/efeitos dos fármacos , Deficiências Nutricionais/metabolismo , Resistência à Insulina , Células Secretoras de Insulina/efeitos dos fármacos , Insulina/sangue , Selênio/deficiência , Compostos de Sódio/toxicidade , Animais , Biomarcadores/sangue , Glicemia/metabolismo , Deficiências Nutricionais/sangue , Deficiências Nutricionais/etiologia , Dieta , Modelos Animais de Doenças , Células Secretoras de Insulina/metabolismo , Masculino , Camundongos Endogâmicos C57BLRESUMO
BACKGROUND: Selenium deficiency appears to limit antioxidant defense in obese individuals. This study evaluated the association between adiposity indices, selenium status, and oxidative stress in obese women. METHODS: This was a cross-sectional study involving 139 women who were divided into the following two groups: the case group (obese women, n = 63) and the control group (normal-weight women, n = 76). Plasma, erythrocyte, and urinary selenium levels were determined using inductively coupled plasma optical emission spectrometry. Body weight, height, waist circumference, hip circumference and neck circumference were measured. Body mass index, waist/height ratio, conicity index, body fat index, body adiposity index, body circularity index, and visceral adiposity index were calculated. Plasma levels of thiobarbituric acid reactive substances were determined. The erythrocyte glutathione peroxidase activity was determined using an automatic biochemical analyzer and Ransel kit. RESULTS: Obese women had selenium deficiency characterized by reduction in plasma and erythrocyte concentrations (P < .001). The urinary selenium excretion was higher in the case group compared to the control group (P < .001). Adiposity indices values and plasma concentrations of thiobarbituric acid reactive substances were significantly elevated in obese women (P < .001). There was a significant association between adiposity indices and selenium status (P < .001), and between erythrocyte selenium and erythrocyte glutathione peroxidase activity (P < .001). CONCLUSION: Obese women evaluated in the study have reduced plasma and erythrocyte concentrations of selenium and an increased urinary excretion of selenium. The correlation analysis reveals an association between intra-abdominal fat accumulation and selenium metabolism and oxidative stress.
Assuntos
Eritrócitos/metabolismo , Glutationa Peroxidase/metabolismo , Obesidade/metabolismo , Estresse Oxidativo , Selênio/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Adulto , Índice de Massa Corporal , Deficiências Nutricionais/metabolismo , Eritrócitos/enzimologia , Feminino , Humanos , Obesidade Abdominal/metabolismo , Selênio/sangue , Selênio/deficiência , Selênio/urina , Circunferência da Cintura , Razão Cintura-EstaturaRESUMO
Objective: Placental iodide transport is necessary for maintaining an adequate iodide supply to the developing fetus. We hypothesized that compounds from the placental barrier can compensate for decreases in maternal iodine intake and normalize fetal iodine levels. Methods: Pregnant rats administered different amounts of iodine (1.24, 2.5, 5, or 10 µg/day) were evaluated on gestational day (gd) 16 and 20. The iodine levels in maternal blood, amniotic fluid (AF), and placental tissue were estimated using As-Ce catalytic spectrophotometry. The protein and/or messenger RNA (mRNA) levels of sodium iodide symporter (NIS), pendrin, alpha-smooth muscle actin (α-SMA), and CD31 in the placental labyrinth, trophoblast cells isolated using laser capture microdissection (LCM), and/or fetomaternal thyroid were detected using immunoblotting, real-time polymerase chain reaction, and/or immunohistochemistry. Results: When iodine intake was reduced, iodine levels in maternal blood gradually decreased; however, placental iodine levels were not significantly different between groups on gd16 and gd20. Minimal changes were observed in AF iodine levels on gd16, and a mild decreasing trend was observed (iodine dose, 10 to 1.24 µg/day) on gd20. NIS protein, which was linearly distributed along the basolateral membrane of maternal-fetal thyroid follicles, gradually increased with decreasing iodine levels. Regarding iodine deficiency in the placental labyrinth on gd16 and gd20, pendrin and glycosylated NIS proteins were significantly upregulated in a dose-dependent manner. However, the mRNA levels were unchanged. Furthermore, the conversion of NIS protein from the nonglycosylated to the glycosylated form increased. In trophoblast cells isolated using LCM, PDS mRNA levels increased in the 1.24-µg/day group on gd16 but not NIS mRNA levels. There was a smaller α-SMA+ area in the labyrinth zone on gd16 and gd20; however, the proportional CD31+ area increased on gd16 and reduced on gd20 with decreased iodine levels. Conclusions: All mechanisms upregulating the expression of iodine transporters and changes in villous stroma and microvessel area in the placental labyrinth can promote iodide transfer from mother to fetus in iodine deficiency, especially before the onset of fetal thyroid function. Compensatory NIS protein regulation in the placenta against decreased iodine intake mainly occurs during translation and glycosylation modification after translation. Pendrin may be more important than NIS in the mediation of placental iodide transport.
Assuntos
Deficiências Nutricionais/tratamento farmacológico , Feto/metabolismo , Iodo/deficiência , Troca Materno-Fetal , Placenta/metabolismo , Iodeto de Potássio/farmacologia , Actinas/metabolismo , Fenômenos Fisiológicos da Nutrição Animal , Animais , Antiportadores de Cloreto-Bicarbonato/genética , Antiportadores de Cloreto-Bicarbonato/metabolismo , Deficiências Nutricionais/metabolismo , Deficiências Nutricionais/fisiopatologia , Modelos Animais de Doenças , Feminino , Glicosilação , Fenômenos Fisiológicos da Nutrição Materna , Estado Nutricional , Molécula-1 de Adesão Celular Endotelial a Plaquetas/metabolismo , Iodeto de Potássio/metabolismo , Gravidez , Ratos Wistar , Transportadores de Sulfato/genética , Transportadores de Sulfato/metabolismo , Simportadores/genética , Simportadores/metabolismoRESUMO
Background: Although substantial progress has been made in recent decades in eliminating iodine deficiency, iodine deficiency disorders (IDDs) are still prevalent in European countries. Challenges include ineffective public health programs and discontinuation of IDD prevention. However, the barriers against the implementation and continuation of prevention and monitoring of IDD remain unclear. Therefore, the objective of our study was to identify potential barriers against pan-European IDD prevention and monitoring programs and to find solutions for the different challenges. Methods: We conducted a Delphi study consisting of three rounds. We identified potential participants with expertise and experience in relevant fields from all European countries, including policy makers, health care professionals, health scientists, and patient representatives. The Delphi method was conducted with open-ended questions and item ranking to achieve group consensus on potential barriers against national and pan-European IDD prevention and monitoring programs and related solutions to overcome those barriers. The answers of the Delphi rounds were analyzed using qualitative content analysis and descriptive analysis methods. In addition, we conducted two expert interviews to analyze and discuss the study results. Results: Eighty experts from 36 countries and different fields of work participated in the first Delphi round, 52 in the second, and 46 in the third. Potential barriers include challenges in the fields of knowledge and information, implementation and management, communication and cooperation, political support, and differences between the European countries. Ranked solutions addressing these barriers include cooperation with different stakeholders, gaining knowledge, sharing information, the development of a European program with national specification, European guidelines/recommendations, and European monitoring. The ranking gives a first overview as to which of these barriers would need to be solved most urgently and which solutions may be most helpful. Conclusion: In our study, we derived key information and first insights with regard to barriers against IDD prevention programs from a broad range of stakeholders. Most barriers were found in the category of implementation and management. Also a lack of political support seems to play an important role. The findings of our study may help decision makers in health policy to develop more effective IDD prevention and monitoring strategies.
Assuntos
Deficiências Nutricionais/prevenção & controle , Iodo/deficiência , Serviços Preventivos de Saúde , Consenso , Deficiências Nutricionais/diagnóstico , Deficiências Nutricionais/epidemiologia , Deficiências Nutricionais/metabolismo , Técnica Delphi , Europa (Continente)/epidemiologia , Regulamentação Governamental , Necessidades e Demandas de Serviços de Saúde , Humanos , Avaliação das Necessidades , Política , Participação dos InteressadosRESUMO
Zinc (Zn) is the second most abundant necessary trace element in the human body. It is reported that zinc deficiency (ZD) promotes many types of cancer progression through multiple signal pathways. It is well known that oxidative stress, DNA damage, DNA repair, cell cycle, cell apoptosis, metabolic alterations, microRNAs abnormal expression, and inflammation level are closely related to cancer development. Cumulative evidence suggests that ZD influences these biological functions. This review explores the latest advances in understanding the role of ZD in tumorigenesis. Fully comprehending the potential mechanisms of ZD-induced tumors may provide novel clues for prevention and clinical treatment of cancers.
Assuntos
Transformação Celular Neoplásica , Deficiências Nutricionais/complicações , Neoplasias/etiologia , Zinco/deficiência , Animais , Apoptose , Proliferação de Células , Transformação Celular Neoplásica/genética , Transformação Celular Neoplásica/metabolismo , Transformação Celular Neoplásica/patologia , Dano ao DNA , Reparo do DNA , Deficiências Nutricionais/metabolismo , Regulação Neoplásica da Expressão Gênica , Humanos , Mediadores da Inflamação/metabolismo , MicroRNAs/genética , MicroRNAs/metabolismo , Neoplasias/genética , Neoplasias/metabolismo , Neoplasias/patologia , Estresse Oxidativo , Transdução de SinaisRESUMO
Lysine cannot be synthesized by most higher organisms and, therefore, is an indispensable amino acid (IAA) that must be consumed in adequate amounts to maintain protein synthesis. Although lysine is an abundant amino acid in body proteins, lysine is limited in abundance in many important food sources (e.g. grains). Older observations assigned importance to lysine because animals fed a lysine-deficient diet did not lose weight as fast as animals placed upon other IAA-deficient diets, leading to the theory that there may be a special pool of lysine or metabolites that could be converted to lysine. The first step in the lysine catabolic pathway is the formation of saccharopine and then 2-aminoadipic acid, processes that are mitochondrial. The catabolism of 2-aminoadipic acid proceeds via decarboxylation to a series of CoA esters ending in acetyl-CoA. In mammals, the liver appears to be the primary site of lysine catabolism. In humans, the metabolic and oxidative response of lysine to diets either restricted in protein or in lysine is consistent with what has been measured for other IAAs with isotopically labeled tracers. Intestinal microflora are known to metabolize urea to ammonia and scavenge nitrogen (N) for the synthesis of amino acids. Studies feeding 15N-ammonium chloride or 15N-urea to animals and to humans, demonstrate the appearance of 15N-lysine in gut microbial lysine and in host lysine. However, the amount of 15N-lysine transferred to the host is difficult to assess directly using current methods. It is important to understand the role of the gut microflora in human lysine metabolism, especially in conditions where dietary lysine intake may be limited, but better methods need to be devised.
Assuntos
Dieta , Microbioma Gastrointestinal , Lisina/metabolismo , Necessidades Nutricionais , Estado Nutricional , Ácido 2-Aminoadípico/metabolismo , Acetilcoenzima A/metabolismo , Amônia/metabolismo , Animais , Bactérias/metabolismo , Peso Corporal , Deficiências Nutricionais/metabolismo , Humanos , Lisina/análogos & derivados , Lisina/biossíntese , Lisina/deficiência , Nitrogênio/metabolismo , Proteínas/metabolismo , Ureia/metabolismoRESUMO
Histidine is a nutritionally essential amino acid with many recognized benefits to human health, while circulating concentrations of histidine decline in pathologic conditions [e.g., chronic obstructive pulmonary disease (COPD) and chronic kidney disease (CKD)]. The purpose of this review is to examine the existing literature regarding the benefits of histidine intake, the adverse effects of excess histidine, and the upper tolerance level for histidine. Supplementation with doses of 4.0-4.5 g histidine/d and increased dietary histidine intake are associated with decreased BMI, adiposity, markers of glucose homeostasis (e.g., HOMA-IR, fasting blood glucose, 2-h postprandial blood glucose), proinflammatory cytokines, and oxidative stress. It is unclear from the limited number of studies in humans whether the improvements in glucoregulatory markers, inflammation, and oxidative stress are due to reduced BMI and adiposity, increased carnosine (a metabolic product of histidine with antioxidant effects), or both. Histidine intake also improves cognitive function (e.g., reduces appetite, anxiety, and stress responses and improves sleep) potentially through the metabolism of histidine to histamine; however, this relation is ambiguous in humans. At high intakes of histidine (>24 g/d), studies report adverse effects of histidine such as decreased serum zinc and cognitive impairment. There is limited research on the effects of histidine intake at doses between 4.5 and 24 g/d, and thus, a tolerable upper level has not been established. Determining tolerance to histidine supplementation has been limited by small sample sizes and, more important, a lack of a clear biomarker for histidine supplementation. The U-shaped curve of circulating zinc concentrations with histidine supplementation could be exploited as a relevant biomarker for supplemental histidine tolerance. Histidine is an important amino acid and may be necessary as a supplement in some populations; however, gaps in knowledge, which this review highlights, need to be addressed scientifically.
Assuntos
Glicemia/metabolismo , Índice de Massa Corporal , Suplementos Nutricionais , Histidina/farmacologia , Inflamação/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Antioxidantes/efeitos adversos , Antioxidantes/metabolismo , Antioxidantes/farmacologia , Carnosina/metabolismo , Deficiências Nutricionais/tratamento farmacológico , Deficiências Nutricionais/etiologia , Deficiências Nutricionais/metabolismo , Histamina/metabolismo , Histidina/efeitos adversos , Histidina/metabolismo , Histidina/uso terapêutico , Humanos , Inflamação/prevenção & controle , Processos Mentais/efeitos dos fármacos , Obesidade/metabolismo , Obesidade/prevenção & controle , Zinco/deficiênciaRESUMO
Selenium is an essential micronutrient commonly deficient in human populations. Selenium deficiency increases the risks of pregnancy complications; however, the long-term impact of selenium deficiency on offspring disease remains unclear. This study investigates the effects of selenium deficiency during pregnancy on offspring metabolic function. Female C57BL/6 mice were allocated to control (>190 µg selenium/kg, n = 8) or low selenium (<50 µg selenium/kg, n = 8) diets prior to mating and throughout gestation. At postnatal day (PN) 170, mice underwent an intraperitoneal glucose tolerance test and were culled at PN180 for biochemical analysis. Mice exposed to selenium deficiency in utero had reduced fasting blood glucose but increased postprandial blood glucose concentrations. Male offspring from selenium-deficient litters had increased plasma insulin levels in conjunction with reduced plasma thyroxine (tetraiodothyronine or T4) concentrations. Conversely, females exposed to selenium deficiency in utero exhibited increased plasma thyroxine levels with no change in plasma insulin. This study demonstrates the importance of adequate selenium intake around pregnancy for offspring metabolic health. Given the increasing prevalence of metabolic disease, this study highlights the need for appropriate micronutrient intake during pregnancy to ensure a healthy start to life.
Assuntos
Glicemia/metabolismo , Deficiências Nutricionais/metabolismo , Selênio/deficiência , Glândula Tireoide/metabolismo , Hormônios Tireóideos/sangue , Fenômenos Fisiológicos da Nutrição Animal , Animais , Biomarcadores/sangue , Deficiências Nutricionais/sangue , Deficiências Nutricionais/fisiopatologia , Modelos Animais de Doenças , Feminino , Masculino , Fenômenos Fisiológicos da Nutrição Materna , Camundongos Endogâmicos C57BL , Gravidez , Efeitos Tardios da Exposição Pré-Natal , Caracteres Sexuais , Glândula Tireoide/fisiopatologia , Fatores de TempoRESUMO
BACKGROUND: To study the effects of hypoxia and nutrition deficiency mimicking degenerated intervertebral disc on the biological behavior of human nucleus-derived pulposus mesenchymal stem cells (hNP-MSCs) and the role of PI3K/Akt pathway in the process in vitro. METHODS: hP-MSCs were isolated from lumbar disc and were further identified by their immunophenotypes and multilineage differentiation. Then, cells were divided into the control group, hypoxia and nutrition deficiency group, the LY294002 group, and insulin-like growth factor 1 (IGF-1) group. Then cell apoptosis, the cell viability, the caspase 3 activity, and the expression of PI3K, Akt, and functional genes (aggrecan, collagen I, and collagen II) were evaluated. RESULT: Our work showed that isolated cells met the criteria of International Society for cellular Therapy. Therefore, cells obtained from degenerated nucleus pulposus were definitely hNP-MSCs. Our results showed that hypoxia and nutrition deficiency could significantly increase cell apoptosis, the caspase 3 activity, and inhibit cell viability. Gene expression results demonstrated that hypoxia and nutrition deficiency could increase the relative expression of PI3K and Akt gene and inhibit the expression of functional genes. However, when the PI3K/Akt pathway was inhibited by LY294002, the cell apoptosis and caspase 3 activity significantly increased while the cell viability was obviously inhibited. Quantitative real-time PCR results showed that the expression of functional genes was more significantly inhibited. Our study further verified that the above-mentioned biological activities of hNP-MSCs could be significantly improved by IGF1. CONCLUSIONS: PI3K/Akt signal pathway may have protective effects on human nucleus pulposus-derived mesenchymal stem cells against hypoxia and nutrition deficiency.
Assuntos
Degeneração do Disco Intervertebral/metabolismo , Células-Tronco Mesenquimais/metabolismo , Núcleo Pulposo/citologia , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Caspase 3/metabolismo , Deficiências Nutricionais/metabolismo , Humanos , Hipóxia/metabolismo , Fator de Crescimento Insulin-Like I/metabolismo , Células-Tronco Mesenquimais/citologia , Cultura Primária de CélulasRESUMO
Dietary trace minerals are pivotal and hold a key role in numerous metabolic processes. Trace mineral deficiencies (except for iodine, iron, and zinc) do not often develop spontaneously in adults on ordinary diets; infants are more vulnerable because their growth is rapid and intake varies. Trace mineral imbalances can result from hereditary disorders (e.g., hemochromatosis, Wilson disease), kidney dialysis, parenteral nutrition, restrictive diets prescribed for people with inborn errors of metabolism, or various popular diet plans. The Special Issue "Dietary Trace Minerals" comprised 13 peer-reviewed papers on the most recent evidence regarding the dietary intake of trace minerals, as well as their effect toward the prevention and treatment of non-communicable diseases. Original contributions and literature reviews further demonstrated the crucial and central part that dietary trace minerals play in human health and development. This editorial provides a brief and concise overview that addresses and summarizes the content of the Dietary Trace Minerals Special Issue.
Assuntos
Deficiências Nutricionais/prevenção & controle , Dieta Saudável , Doenças não Transmissíveis/prevenção & controle , Estado Nutricional , Oligoelementos/administração & dosagem , Deficiências Nutricionais/epidemiologia , Deficiências Nutricionais/metabolismo , Deficiências Nutricionais/fisiopatologia , Humanos , Doenças não Transmissíveis/epidemiologia , Valor Nutritivo , Fatores de Proteção , Recomendações Nutricionais , Fatores de Risco , Comportamento de Redução do Risco , Oligoelementos/metabolismoRESUMO
Deficiencies in methyl donors, folate, and vitamin B12 are known to lead to brain function defects. Fetal development is the most studied but data are also available for such an impact in elderly rats. To compare the functional consequences of nutritional deficiency in young versus adult rats, we monitored behavioral outcomes of cerebellum and hippocampus circuits in the offspring of deficient mother rats and in adult rats fed a deficient diet from 2 to 8 months-of-age. We present data showing that the main deleterious consequences are found in young ages compared to adult ones, in terms of movement coordination and learning abilities. Moreover, we obtained sex and age differences in the deleterious effects on these functions and on neuronal layer integrity in growing young rats, while deficient adults presented only slight functional alterations without tissue damage. Actually, the cerebellum and the hippocampus develop and maturate according to different time lap windows and we demonstrate that a switch to a normal diet can only rescue circuits that present a long permissive window of time, such as the cerebellum, whereas the hippocampus does not. Thus, we argue, as others have, for supplements or fortifications given over a longer time than the developmental period.
Assuntos
Encéfalo/metabolismo , Encéfalo/fisiopatologia , Deficiências Nutricionais/complicações , Deficiências Nutricionais/metabolismo , Desenvolvimento Fetal , Transtornos do Neurodesenvolvimento/etiologia , Transtornos do Neurodesenvolvimento/metabolismo , Animais , Cognição , Deficiências Nutricionais/etiologia , Dieta , Modelos Animais de Doenças , Feminino , Deficiência de Ácido Fólico/complicações , Deficiência de Ácido Fólico/metabolismo , Hipocampo/metabolismo , Hipocampo/fisiopatologia , Masculino , Aprendizagem em Labirinto , RatosAssuntos
Deficiências Nutricionais , Hipertensão , Zinco , Disponibilidade Biológica , Deficiências Nutricionais/metabolismo , Deficiências Nutricionais/prevenção & controle , Humanos , Hipertensão/metabolismo , Hipertensão/prevenção & controle , Necessidades Nutricionais , Reabsorção Renal/fisiologia , Fatores de Risco , Zinco/deficiência , Zinco/metabolismoRESUMO
GENERAL PURPOSE: To provide information on obesity, bariatric surgery, and the nutrient deficiency-related dermatoses that may result from these surgeries. TARGET AUDIENCE: This continuing education activity is intended for physicians, physician assistants, NPs, and nurses with an interest in skin and wound care. LEARNING OBJECTIVES/OUTCOMES: After participating in this educational activity, the participant should be better able to:1. Examine issues related to obesity and bariatric surgery.2. Identify the sources and role of specific nutrients.3. Recognize the clinical signs and symptoms of nutrient deficiency following bariatric surgery. ABSTRACT: Obesity is a global epidemic that increases the risk of weight-related comorbidities in modern society. It is complex, multifactorial, and largely preventable. Noninvasive treatments for obesity include diet, exercise, and medication. However, bariatric surgeries are becoming popular procedures for those who do not achieve success with noninvasive weight management treatment. Bariatric surgeries often result in dietary restriction and/or malabsorption, which lead to drastic weight loss. Individuals who had bariatric surgeries need lifelong follow-up and monitoring to ensure adequate intake of nutrients. Nutrient deficiencies can ensue when long-term vitamin and mineral supplementation is not followed. Severe nutrient deficiencies may lead to dermatoses that can be corrected by nutrient repletion and careful monitoring. A case report of nutrient deficiency-related dermatoses is followed by a review of obesity and its treatments with a focus on bariatric surgeries.
Assuntos
Cirurgia Bariátrica/efeitos adversos , Deficiências Nutricionais/metabolismo , Deficiências Nutricionais/prevenção & controle , Micronutrientes/deficiência , Obesidade/metabolismo , Deficiências Nutricionais/etiologia , Suplementos Nutricionais , Humanos , Micronutrientes/uso terapêutico , Obesidade/cirurgia , Guias de Prática Clínica como AssuntoRESUMO
OBJECTIVE: The present study aimed to evaluate the effect of mandatory iodine fortification of bread on the iodine status of South Australian populations using newborn thyroid-stimulating hormone (TSH) concentration as a marker. DESIGN: The study used an interrupted time-series design. SETTING: TSH data collected between 2005 and 2016 (n 211 033) were extracted from the routine newborn screening programme in South Australia for analysis. Iodine deficiency is indicated when more than 3 % of newborns have TSH > 5 mIU/l. PARTICIPANTS: Newborns were classified into three groups: the pre-fortification group (those born before October 2009); the transition group (born between October 2009 and June 2010); and the post-fortification group (born after June 2010). RESULTS: The percentage of newborns with TSH > 5 mIU/l was 5·1, 6·2 and 4·6 % in the pre-fortification, transition and post-fortification groups, respectively. Based on a segmented regression model, newborns in the post-fortification period had a 10 % lower risk of having TSH > 5 mIU/l than newborns in the pre-fortification group (incidence rate ratio (IRR) = 0·90; 95 % CI 0·87, 0·94), while newborns in the transitional period had a 22 % higher risk of having TSH > 5 mIU/l compared with newborns in the pre-fortification period (IRR = 1·22; 95 % CI 1·13, 1·31). CONCLUSIONS: Using TSH as a marker, South Australia would be classified as mild iodine deficiency post-fortification in contrast to iodine sufficiency using median urinary iodine concentration as a population marker. Re-evaluation of the current TSH criteria to define iodine status in populations is warranted in this context.
Assuntos
Pão , Deficiências Nutricionais/prevenção & controle , Alimentos Fortificados , Iodo/metabolismo , Triagem Neonatal , Política Nutricional , Tireotropina/sangue , Biomarcadores/sangue , Deficiências Nutricionais/diagnóstico , Deficiências Nutricionais/metabolismo , Feminino , Humanos , Recém-Nascido , Iodo/deficiência , Masculino , Saúde da População , Austrália do SulRESUMO
Zinc plays a central role in skin integrity via barrier and immune mechanisms and may also be relevant in the pathogenesis of atopic dermatitis (AD). However, little is known about the relationship between zinc and AD. We performed a systematic review to determine (i) the association between zinc levels or zinc deficiency and AD and (ii) the efficacy of oral zinc supplementation in the treatment of AD. We searched PubMed, Scopus, Web of Science and article references for observational studies on zinc levels or zinc deficiency in participants with AD vs. controls and for randomized control trials (RCTs) on zinc supplementation in AD. For observational studies, we calculated pooled standardized mean differences (SMDs) or odds ratios (ORs) along with 95% confidence intervals (CIs) using a random effects model. We included 14 observational studies and two RCTs. The pooled SMD demonstrated significantly lower serum (SMD 0.66, 95% CI 0.21-1.10, P = 0.004), hair (SMD 0.95, 95% CI 0.38-1.52, P = 0.001) and erythrocyte (SMD 0.95, 95% CI 0.38-1.52, P = 0.001) zinc levels in participants with AD compared to controls. Pooled unadjusted data from three studies showed a non-significant increased odds of AD in those with zinc deficiency compared with those without zinc deficiency (OR = 1.50, 95% CI 0.71-3.16, P = 0.28). One RCT of oral zinc supplementation among AD patients with zinc deficiency showed improvement in extent and severity of AD, while another RCT among all AD patients showed no significant improvement. All the studies were of low or moderate quality. We conclude that low serum, hair and erythrocyte zinc levels are associated with AD. However, the poor quality of included studies makes interpretation of these results problematic. High-quality observational studies are needed to confirm the association between low zinc levels and AD, and RCTs are required to evaluate the merit of zinc supplementation for the treatment or prevention of AD.
Assuntos
Deficiências Nutricionais/metabolismo , Dermatite Atópica/metabolismo , Zinco/metabolismo , Dermatite Atópica/tratamento farmacológico , Dermatite Atópica/prevenção & controle , Suplementos Nutricionais , Humanos , Ensaios Clínicos Controlados Aleatórios como Assunto , Zinco/administração & dosagem , Zinco/deficiênciaRESUMO
Multiscale modeling provides a very powerful means of studying complex biological systems. An important component of this strategy involves coarse-grained (CG) simplifications of regions of the system, which allow effective exploration of complex systems. Here we studied aspects of CG modeling of the human zinc transporter ZnT2. Zinc is an essential trace element with 10% of the proteins in the human proteome capable of zinc binding. Thus, zinc deficiency or impairment of zinc homeostasis disrupt key cellular functions. Mammalian zinc transport proceeds via two transporter families: ZnT and ZIP; however, little is known about the zinc permeation pathway through these transporters. As a step towards this end, we herein undertook comprehensive computational analyses employing multiscale techniques, focusing on the human zinc transporter ZnT2 and its bacterial homologue, YiiP. Energy calculations revealed a favorable pathway for zinc translocation via alternating access. We then identified key residues presumably involved in the passage of zinc ions through ZnT2 and YiiP, and functionally validated their role in zinc transport using site-directed mutagenesis of ZnT2 residues. Finally, we use a CG Monte Carlo simulation approach to sample the transition between the inward-facing and the outward-facing states. We present our structural models of the inward- and outward-facing conformations of ZnT2 as a blueprint prototype of the transporter conformations, including the putative permeation pathway and participating residues. The insights gained from this study may facilitate the delineation of the pathways of other zinc transporters, laying the foundations for the molecular basis underlying ion permeation. This may possibly facilitate the development of therapeutic interventions in pathological states associated with zinc deficiency and other disorders based on loss-of-function mutations in solute carriers.
Assuntos
Proteínas de Transporte de Cátions/metabolismo , Modelos Teóricos , Zinco/metabolismo , Proteínas de Transporte de Cátions/genética , Biologia Computacional/métodos , Deficiências Nutricionais/metabolismo , Deficiências Nutricionais/terapia , Homeostase , Humanos , Método de Monte Carlo , Mutagênese Sítio-Dirigida , Permeabilidade , Zinco/deficiênciaRESUMO
Decreased protein breakdown in pregnant women results in lower concentration of methionine (Met) in plasma, causing pregnancy-related metabolic disturbance. Its dipeptide methionyl-methionine (Met-Met) may exert positive influence in fetal development. This study mainly investigated whether Met-Met can be used as part of free Met to promote reproductive outcomes in mice and the underlying mechanisms. Met-deficient pregnant mice were treated with Met alone or with Met-Met during pregnancy. Daily intraperitoneal injection of 35% dietary Met in pregnant mice was the best dose among the 15â»45% doses. Embryo development and newborn birth weight were enhanced when 25% of the Met in the 35% Met group was replaced with Met-Met. Met-Met replacement had higher plasma insulin, glucose, and free amino acids (AA) concentrations. Besides, in the placenta, the AA transporter mRNA abundances and peptide transporters (PhT1 and PepT1) protein levels were higher in Met-Met treatment group. Moreover, Met-Met increased 4E-BP1, S6K1 and AKT/mTOR phosphorylation. These results suggest that Met-Met could be used as a partial source of Met to promote reproductive outcomes in Met-restricted pregnant mice, which might be mediated by promoting nutrient availability and activating AKT/mTOR-mediated signaling pathway.
Assuntos
Deficiências Nutricionais/tratamento farmacológico , Suplementos Nutricionais , Dipeptídeos/administração & dosagem , Metionina/administração & dosagem , Metionina/deficiência , Complicações na Gravidez/tratamento farmacológico , Reprodução/efeitos dos fármacos , Fenômenos Fisiológicos da Nutrição Animal , Animais , Biomarcadores/sangue , Deficiências Nutricionais/metabolismo , Deficiências Nutricionais/fisiopatologia , Dipeptídeos/farmacocinética , Modelos Animais de Doenças , Feminino , Desenvolvimento Fetal/efeitos dos fármacos , Injeções Intraperitoneais , Fenômenos Fisiológicos da Nutrição Materna , Proteínas de Membrana Transportadoras/metabolismo , Camundongos Endogâmicos ICR , Camundongos Nus , Estado Nutricional , Placenta/efeitos dos fármacos , Placenta/metabolismo , Gravidez , Complicações na Gravidez/metabolismo , Complicações na Gravidez/fisiopatologia , Transdução de Sinais/efeitos dos fármacosRESUMO
We investigated whether marginal iron-deficiency (MID) without anemia influences liver lipid accumulation in rats. Ingestion of a MID diet in which the iron concentration was half of AIN-93 formulation (iron-adequate, IA) for 3 weeks decreased liver iron concentration without anemia. We then evaluated the influence of the MID diet on liver lipid accumulation in combination with a high-sucrose (HS) diet and confirmed that the HS-MID diet successfully decreased liver iron concentration without anemia. Additionally, a significant increase in liver triglyceride concentration was found, accompanied by upregulation of hepatic fatty acid synthase expression in the rats fed the HS-MID diet compared to those in the rats fed an HS-IA diet, although no difference was observed in plasma transaminase activity and hepatic interleukin-1ß expression. These results suggest that MID enhances de novo lipid synthesis via upregulation of lipogenic gene expression in combination with sucrose in the diet. Abbreviations: ALT, alanine aminotransferase; AST, aspartate aminotransferase; HS, high sucrose; IA, iron adequate; ID, iron deficiency; MID, marginal irondeficiency; NAFLD, non-alcoholic fatty liver disease.
Assuntos
Sacarose Alimentar/administração & dosagem , Deficiências de Ferro , Fígado/metabolismo , Triglicerídeos/metabolismo , Alanina Transaminase/sangue , Animais , Aspartato Aminotransferases/sangue , Deficiências Nutricionais/genética , Deficiências Nutricionais/metabolismo , Dieta , Ácido Graxo Sintase Tipo I/genética , Ácido Graxo Sintase Tipo I/metabolismo , Comportamento Alimentar , Regulação Enzimológica da Expressão Gênica , Interleucina-18/metabolismo , Fígado/enzimologia , Masculino , Ratos Wistar , Triglicerídeos/biossínteseRESUMO
BACKGROUND: Rising atmospheric carbon dioxide concentrations are anticipated to decrease the zinc and iron concentrations of crops. The associated disease burden and optimal mitigation strategies remain unknown. We sought to understand where and to what extent increasing carbon dioxide concentrations may increase the global burden of nutritional deficiencies through changes in crop nutrient concentrations, and the effects of potential mitigation strategies. METHODS AND FINDINGS: For each of 137 countries, we incorporated estimates of climate change, crop nutrient concentrations, dietary patterns, and disease risk into a microsimulation model of zinc and iron deficiency. These estimates were obtained from the Intergovernmental Panel on Climate Change, US Department of Agriculture, Statistics Division of the Food and Agriculture Organization of the United Nations, and Global Burden of Disease Project, respectively. In the absence of increasing carbon dioxide concentrations, we estimated that zinc and iron deficiencies would induce 1,072.9 million disability-adjusted life years (DALYs) globally over the period 2015 to 2050 (95% credible interval [CrI]: 971.1-1,167.7). In the presence of increasing carbon dioxide concentrations, we estimated that decreasing zinc and iron concentrations of crops would induce an additional 125.8 million DALYs globally over the same period (95% CrI: 113.6-138.9). This carbon-dioxide-induced disease burden is projected to disproportionately affect nations in the World Health Organization's South-East Asia and African Regions (44.0 and 28.5 million DALYs, respectively), which already have high existing disease burdens from zinc and iron deficiencies (364.3 and 299.5 million DALYs, respectively), increasing global nutritional inequalities. A climate mitigation strategy such as the Paris Agreement (an international agreement to keep global temperatures within 2°C of pre-industrial levels) would be expected to avert 48.2% of this burden (95% CrI: 47.8%-48.5%), while traditional public health interventions including nutrient supplementation and disease control programs would be expected to avert 26.6% of the burden (95% CrI: 23.8%-29.6%). Of the traditional public health interventions, zinc supplementation would be expected to avert 5.5%, iron supplementation 15.7%, malaria mitigation 3.2%, pneumonia mitigation 1.6%, and diarrhea mitigation 0.5%. The primary limitations of the analysis include uncertainty regarding how food consumption patterns may change with climate, how disease mortality rates will change over time, and how crop zinc and iron concentrations will decline from those at present to those in 2050. CONCLUSIONS: Effects of increased carbon dioxide on crop nutrient concentrations are anticipated to exacerbate inequalities in zinc and iron deficiencies by 2050. Proposed Paris Agreement strategies are expected to be more effective than traditional public health measures to avert the increased inequality.