Short-term dietary magnesium deficiency downregulates the expression of bone formation-related genes in rats.

Dietary magnesium deficiency increases osteoclastic bone resorption and decreases osteoblastic bone formation. Increased bone resorption due to dietary magnesium deficiency can be explained by increased expression of the receptor activator of nuclear factor kB ligand. However, the detailed mechanisms underlying decreased bone formation remain unclear. Thus, in the present study, to determine the mechanism underlying decreased bone formation induced by dietary magnesium deficiency, we investigated the effects of short-term dietary magnesium deficiency on the mRNA expression of genes related to bone formation in rats. Male Wistar rats were fed a control or magnesium-deficient diet for eight days. The mRNA expression level of Runx2, Sp7, Bglap, Alpl, Col1a1, Igf1, and Bmp2 in the femur was significantly lower in magnesium-deficient rats than in control rats. These results suggest that short-term dietary magnesium deficiency decreases the gene expression of insulin-like growth factor-1 and bone morphogenetic protein 2, which, in turn, decreases osteoblastic bone formation through the downregulation of osteoblastogenesis-related gene expression.

Subclinical hypomagnesemia: Prevalence and causes in dairy cows in the semiarid region of the state of Paraíba, Brazil / Hipomagnesemia subclínica: Prevalência e causas em vacas leiteiras da região semiárida no estado da Paraíba, Brasil

In dairy farming, cows display important metabolic changes during the transition period, particularly high-production cows, which need nutrients in greater quantity to meet the required demand. The aim of this study was to determine the prevalence of subclinical hypomagnesemia in pre- and post-partum dairy cows inserted in milk-production systems in the Sousa microregion and the district of São João do Rio do Peixe, both in the State of Paraíba, Brazil. As such, visits were made every two weeks to 34 rural properties, where the team collected 357 blood samples by venepuncture, 106 from pre-partum lactating cows and 251 from lactating cows in the post-partum period. It was found that the properties supplied three types of mineral supplement: a single supplement of NaCl, a supplement of NaCl + mineral base, and a commercial supplement. The cows receiving the commercial mineral supplement had the highest prevalence (10.53%) of the disorder, even showing a significant difference (P .05) between the two. Studies such as this are fundamental for alerting rural and technical producers to the occurrence of subclinical hypomagnesemia in the region, in addition to the damage caused by metabolic disorders.

Na bovinocultura leiteira, as vacas apresentam mudanças metabólicas importantes durante o período de transição, principalmente aquelas de alta produção, que necessitam de nutrientes em maior quantidade para suprir a demanda requerida. Este estudo teve como objetivo determinar a prevalência de hipomagnesemia subclínica no pré e pós-parto em vacas leiteiras inseridas em sistemas de produção de leite na microrregião de Sousa-PB e município de São João do Rio do Peixe-PB. Para isso foram realizadas visitas quinzenais a 34 propriedades rurais, onde a equipe coletou 357 amostras de sangue por meio de punção venosa, sendo 106 provenientes de vacas em lactação que se encontravam no período de pré-parto e 251 de vacas em lactação inseridas no período de pós-parto. Verificou-se que as propriedades forneciam três tipos de suplemento mineral: suplementação exclusiva com NaCl; suplementação com NaCl + núcleo mineral; e suplementação comercial. As vacas que recebiam a suplementação mineral do tipo comercial corresponderam aquelas com maior prevalência (10,53%) de ocorrência do distúrbio, apresentando ainda diferença significativa (P 0,05) entre ambas. Estudos como esse tornam-se fundamentais para alertar produtores rurais e técnicos sobre a ocorrência da hipomagnesemia subclínica na região, além dos prejuízos que os distúrbios metabólicos acarretam.

Magnesium Deficiency and Cardiometabolic Disease.

Magnesium (Mg2+) has many physiological functions within the body. These include important roles in maintaining cardiovascular functioning, where it contributes to the regulation of cardiac excitation-contraction coupling, endothelial functioning and haemostasis. The haemostatic roles of Mg2+ impact upon both the protein and cellular arms of coagulation. In this review, we examine how Mg2+ homeostasis is maintained within the body and highlight the various molecular roles attributed to Mg2+ in the cardiovascular system. In addition, we describe how nutritional and/or disease-associated magnesium deficiency, seen in some metabolic conditions, has the potential to influence cardiac and vascular outcomes. Finally, we also examine the potential for magnesium supplements to be employed in the prevention and treatment of cardiovascular disorders and in the management of cardiometabolic health.

The Response of the Human Umbilical Vein Endothelial Cell Transcriptome to Variation in Magnesium Concentration.

Vascular endothelial cells have a critical role in the maintenance of cardiovascular function. Evidence suggests that endothelial function may be compromised under conditions of magnesium deficiency, which increases vulnerability to inflammation. Whole genome transcription analysis was used to explore the acute (24 h) effects of magnesium on human umbilical vascular endothelial cells (HUVEC) cultured in low (0.1 mM) or high (5 mM) concentrations. With low magnesium 2728 transcripts were differentially expressed compared to the 1 mM control cultures and 3030 were differentially expressed with high magnesium. 615 transcripts were differentially expressed under both conditions, of which only 34 showed a concentration-dependent response. Analysis indicated that cellular organisation and biogenesis and key cellular processes such as apoptosis were impacted by both low and high conditions. High magnesium also influenced protein binding functions, intracellular signal transduction, metabolic and catalytic processes. Both conditions impacted on stress-related processes, in particular the inflammatory response. Key mediators of calcium-dependent regulation of gene expression were responsive to both high and low magnesium conditions. The HUVEC transcriptome is highly sensitive to acute changes in the concentration of magnesium in culture medium. The findings of this study support the view that whilst inflammation is an important process that is responsive to magnesium, the function of the endothelium may be impacted by other magnesium-induced changes including maintenance of cellular integrity, receptor expression and metabolic functions. The high proportion of transcripts that did not show a concentration-dependent response suggests variation in magnesium may elicit indirect changes, possibly mediated by other ions.

Two transporters mobilize magnesium from vacuolar stores to enable plant acclimation to magnesium deficiency.

Magnesium (Mg) is an essential metal for chlorophyll biosynthesis and other metabolic processes in plant cells. Mg is largely stored in the vacuole of various cell types and remobilized to meet cytoplasmic demand. However, the transport proteins responsible for mobilizing vacuolar Mg2+ remain unknown. Here, we identified two Arabidopsis (Arabidopsis thaliana) Mg2+ transporters (MAGNESIUM TRANSPORTER 1 and 2; MGT1 and MGT2) that facilitate Mg2+ mobilization from the vacuole, especially when external Mg supply is limited. In addition to a high degree of sequence similarity, MGT1 and MGT2 exhibited overlapping expression patterns in Arabidopsis tissues, implying functional redundancy. Indeed, the mgt1 mgt2 double mutant, but not mgt1 and mgt2 single mutants, showed exaggerated growth defects as compared to the wild type under low-Mg conditions, in accord with higher expression levels of Mg-starvation gene markers in the double mutant. However, overall Mg level was also higher in mgt1 mgt2, suggesting a defect in Mg2+ remobilization in response to Mg deficiency. Consistently, MGT1 and MGT2 localized to the tonoplast and rescued the yeast (Saccharomyces cerevisiae) mnr2Δ (manganese resistance 2) mutant strain lacking the vacuolar Mg2+ efflux transporter. In addition, disruption of MGT1 and MGT2 suppressed high-Mg sensitivity of calcineurin B-like 2 and 3 (cbl2 cbl3), a mutant defective in vacuolar Mg2+ sequestration, suggesting that vacuolar Mg2+ influx and efflux processes are antagonistic in a physiological context. We further crossed mgt1 mgt2 with mgt6, which lacks a plasma membrane MGT member involved in Mg2+ uptake, and found that the triple mutant was more sensitive to low-Mg conditions than either mgt1 mgt2 or mgt6. Hence, Mg2+ uptake (via MGT6) and vacuolar remobilization (through MGT1 and MGT2) work synergistically to achieve Mg2+ homeostasis in plants, especially under low-Mg supply in the environment.

Increased Wnt/ß-catenin signaling contributes to autophagy inhibition resulting from a dietary magnesium deficiency in injury-induced osteoarthritis.

BACKGROUND: Dietary magnesium deficiency, which is common in modern diet, has been associated with osteoarthritis (OA) susceptibility. Despite this clinical association, no study has addressed if dietary magnesium deficiency accelerates OA development, especially at molecular level. This study aimed to explore aggravating effects of dietary magnesium deficiency on cartilage damage in an injury-induced murine OA model and to determine the underlying mechanism. METHODS: Twelve-week-old C57BL/6J mice subject to injury-induced OA modeling were randomized into different diet groups in which the mice were fed a diet with daily recommended magnesium content (500 mg/kg) or diets with low magnesium content (100 or 300 mg/kg). Articular cartilage damage was evaluated using the OARSI score. To determine molecular mechanisms in vitro, mouse chondrocytes were treated with media of low magnesium conditions at 0.1 and 0.4 mM, compared with normal magnesium condition at 0.7 mM as control. Anabolic and catabolic factors, autophagy markers, ß-catenin, Wnt ligands, and a magnesium channel transient receptor potential cation channel subfamily member 7 (TRPM7) were analyzed by quantitative real-time PCR and immunoblotting. Autolysosomes were detected by DALGreen staining via fluorescence microscopy and autophagosomes were evaluated by transmission electron microscopy. Autophagy markers, ß-catenin, and TRPM7 were assessed in vivo in the mouse cartilage, comparing between dietary magnesium deficiency and normal diet, by immunohistochemistry. RESULTS: Dietary magnesium deficiency aggravated injury-induced cartilage damage, indicated by significant higher OARSI scores. Autophagy markers LC3-II and Beclin-1 were decreased both in low magnesium diet-fed mice and low magnesium-treated chondrocytes. The number of autolysosomes and autophagosomes was also reduced under low magnesium conditions. Moreover, magnesium deficiency induced decreased anabolic and increased catabolic effect of chondrocytes which could be restored by autophagy activator rapamycin. In addition, reduced autophagy under low magnesium conditions is mediated by activated Wnt/ß-catenin signaling. The expression of TRPM7 also decreased in low magnesium diet-fed mice, indicating that downstream changes could be regulated through this channel. CONCLUSIONS: Dietary magnesium deficiency contributes to OA development, which is mediated by reduced autophagy through Wnt/ß-catenin signaling activation. These findings indicated potential benefits of adequate dietary magnesium for OA patients or those individuals at high risk of OA.

The redox modulatory effects of SP/NK1R system: Implications for oxidative stress-associated disorders.

Oxidative stress which refers to redox imbalance with increased generation of reactive oxygen species (ROS) has been associated with the pathophysiology of diverse disease conditions. Recently, a close, yet not fully understood, relation between oxidative stress and neuropeptides, in particular, substance P (SP), has been reported in certain conditions. SP has been shown to affect the cellular redox environment through activation of neurokinin-1receptor (NK1R). It seems that SP/NK1R system and oxidative stress can act either synergistically or antagonistically in a context-dependent manner, thereby, influencing the pathology of various clinical disorders either destructively or protectively. Importantly, the interactions between oxidative stress and SP/NK1R system can be pharmacologically targeted. Therefore, a better understanding of the redox modulatory properties of SP/NK1R signaling will pave the way for identifying new therapeutic possibilities for attenuating oxidative stress-mediated damage. Towards this end, we performed a comprehensive search through PubMed/Medline and Scopus databases and discussed all related existing literature regarding the interplay between oxidative stress and SP/NK1R system as well as their implication in various clinical disorders, to provide a clear view and hence better management of oxidative damage.

Hypomagnesemia in beef cattle from the central region of Argentina: retrospective study / Hipomagnesemia em bovinos de corte da região central da Argentina: estudo retrospectivo

Hypomagnesaemia (grass tetany) is a metabolic disorder of ruminants due to a reduced dietary intake of magnesium (primary deficiency), incorrect digestibility or associated metabolic factors reducing Mg intake (secondary deficiency). Grass tetany is a production disease responsible for important economic losses in beef herds from Argentina. Several factors influence the development of grass tetany in cattle, including physiological status, weather, soil and forage. This research described a retrospective analysis over the past 20 years, revising the cases of beef cattle clinical hypomagnesaemia registered at the Veterinary Diagnostic Service in INTA Balcarce, Argentina.

Hipomagnesemia é um distúrbio metabólico de ruminantes devido a uma redução na absorção de magnésio (deficiência primária), digestibilidade incorreta ou fatores metabólicos associados que reduzem a ingestão de Mg (deficiência secundária). Hipomagnesemia é uma doença de produção responsável por importantes perdas econômicas em rebanhos de corte da Argentina. Vários fatores influenciam o desenvolvimento da hipomagnesemia em bovinos, incluindo fatores fisiológicos, clima, solo e forragem. Este trabalho descreve uma análise retrospectiva dos últimos 20 anos, revisando os casos de hipomagnesemia clínica em bovinos de corte registrados no Serviço de Diagnóstico Veterinário do INTA Balcarce, Argentina.

Combined analyses of translatome and transcriptome in Arabidopsis reveal new players responding to magnesium deficiency.

Translational control of gene expression, including recruitment of ribosomes to messenger RNA (mRNA), is particularly important during the response to stress. Purification of ribosome-associated mRNAs using translating ribosome affinity purification (TRAP) followed by RNA-sequencing facilitates the study of mRNAs undergoing active transcription and better proxies the translatome, or protein response, to stimuli. To identify plant responses to Magnesium (Mg) deficiency at the translational level, we combined transcriptome and translatome analyses. Excitingly, we found 26 previously unreported Mg-responsive genes that were only regulated at the translational level and not the transcriptional level, during the early response to Mg deficiency. In addition, mutants of the transcription factor ELONGATED HYPOCOTYL 5 (HY5), the H+ /CATION EXCHANGER 1 and 3 (CAX1 and CAX3), and UBIQUITIN 11 (UBQ11) exhibited early chlorosis phenotype under Mg deficiency, supporting their functional involvement in ion homeostasis. Overall, our study strongly supports that TRAP-seq combined with RNA-seq followed by phenotype screening could facilitate the identification of novel players during stress responses.

Editorial of Special Issue "Magnesium in Human Health and Disease".

The fundamental role of magnesium in human health is extensively discussed in the review by Fiorentini and colleagues [...].

Effect of oral administration of Magnesium N-Acetyltaurinate on synaptic plasticity in rodents.

While magnesium deficiency is common and its effects well known on the nervous system, very few studies has been dedicated to the efficiency of magnesium replacement treatments on the central nervous system. In this study, the effects of oral administration of magnesium salts of acetyl-taurinate on the central manifestations of magnesium deficiency is described in rats submitted to low-magnesium diet and in a murine model of Alzheimer's disease. We tested the effect of ATA Mg®, a salt combining magnesium and taurine, on the hippocampus, a critical component of cognition. 7-10-month-old rats were submitted to dietary magnesium deprivation for 64 days. The effect of magnesium deficiency was studied in ex vivo hippocampal slices. We showed that long-term potentiation of synaptic transmission in the hippocampus was significantly improved by the oral administration of ATA Mg® at a dose of 50 mg/kg bw/day, which is comparable to the recommended dose in humans. 7-10-months-old transgenic APP/PS1 mice, a model of Alzheimer's disease, received ATA Mg® during 24 days at a dose of 700 mg/kg bw/day which is the dose used in previous studies demonstrating the positive effect of magnesium supplementation. We showed that long-term potentiation was significantly improved in the treated mice. Moreover, the expression of NR2B subunit of NMDA receptors, known to be involved in synaptic plasticity, was significantly increased in the hippocampus. These results demonstrate the ability of ATA Mg® to improve the symptoms related to chronic magnesium deficiency at the level of the hippocampus suggesting its bioavailability and effectiveness in reaching the central nervous system.

Long-term Clinical Follow-up of Patients with Familial Hypomagnesemia with Secondary Hypocalcemia

Objective: Familial hypomagnesemia with secondary hypocalcemia (HSH) is an autosomal recessive disease caused by a mutation in the transient receptor potential melastatin 6 (TRPM6) gene and is characterized by selective magnesium malabsorption. Affected cases are usually diagnosed during infancy and usually present with seizures due to hypocalcemia and hypomagnesemia. Irreversible neurological deficits and arrhythmias can be observed without appropriate treatment. The aim was to evaluate the long-term follow-up of patients with genetically confirmed HSH. Methods: A total of six patients with HSH, two of whom were siblings, were included. Age at diagnosis, clinical, laboratory and follow-up data on admission were recorded. All 39 exons of the TRPM6 gene and flanking exon-intron junctions from genomic DNA were amplified and sequenced in all cases. Results: The median (range) follow-up duration was 12.1 (7.6-21.7) years. All cases were diagnosed in infancy. Four different mutations, three of which had not been previously reported, were detected in the TRPM6 gene. Treatment compliance was good and there were no severe complications in the long-term follow-up of cases. However, mental retardation, specific learning difficulty and attention deficit/hyperactive disorder were observed as comorbidities. Conclusion: Of the four different TRPM6 mutations in this small cohort, three had not been previously reported. The long-term prognosis of HSH appears to be good, given early diagnosis and good treatment compliance. This long-term follow-up and prognostic data and the three novel mutations will contribute to the published evidence concerning this rare condition, HSH, and it is hoped will prevent negative outcomes.

Magnesium Deficiency Induces Lipid Accumulation in Vascular Endothelial Cells via Oxidative Stress-The Potential Contribution of EDF-1 and PPARγ.

BACKGROUND: Magnesium deficiency contributes to atherogenesis partly by promoting the dysfunction of endothelial cells, which are critical in vascular homeostasis and diseases. Since EDF-1 and PPARγ regulate crucial endothelial activities, we investigated the modulation of these proteins involved in lipogenesis as well the deposition of lipids in human endothelial cells cultured in different concentrations of magnesium. METHODS: Human endothelial cells from the umbilical vein were cultured in medium containing from 0.1 to 5 mM magnesium for 24 h. The levels of EDF-1 and PPARγ were visualized by Western blot. Reactive oxygen species (ROS) were measured by DCFDA. Lipids were detected after O Red Oil staining. RESULTS: Magnesium deficiency leads to the accumulation of ROS which upregulate EDF-1. Further, PPARγ is increased after culture in low magnesium, but independently from ROS. Moreover, lipids accumulate in magnesium-deficient cells. CONCLUSIONS: Our results suggest that magnesium deficiency leads to the deposition of lipids by inducing EDF-1 and PPARγ. The increase in intracellular lipids might be interpreted as an adaptive response of endothelial cells to magnesium deficiency.

Magnesium in Infectious Diseases in Older People.

Reduced magnesium (Mg) intake is a frequent cause of deficiency with age together with reduced absorption, renal wasting, and polypharmacotherapy. Chronic Mg deficiency may result in increased oxidative stress and low-grade inflammation, which may be linked to several age-related diseases, including higher predisposition to infectious diseases. Mg might play a role in the immune response being a cofactor for immunoglobulin synthesis and other processes strictly associated with the function of T and B cells. Mg is necessary for the biosynthesis, transport, and activation of vitamin D, another key factor in the pathogenesis of infectious diseases. The regulation of cytosolic free Mg in immune cells involves Mg transport systems, such as the melastatin-like transient receptor potential 7 channel, the solute carrier family, and the magnesium transporter 1 (MAGT1). The functional importance of Mg transport in immunity was unknown until the description of the primary immunodeficiency XMEN (X-linked immunodeficiency with Mg defect, Epstein-Barr virus infection, and neoplasia) due to a genetic deficiency of MAGT1 characterized by chronic Epstein-Barr virus infection. This and other research reporting associations of Mg deficit with viral and bacterial infections indicate a possible role of Mg deficit in the recent coronavirus disease 2019 (COVID-19) and its complications. In this review, we will discuss the importance of Mg for the immune system and for infectious diseases, including the recent pandemic of COVID-19.

Magnesium and inflammation: Advances and perspectives.

Magnesium is an essential element of life, involved in the regulation of metabolism and homeostasis of all the tissues. It also regulates immunological functions, acting on the cells of innate and adaptive immune systems. Magnesium deficiency primes phagocytes, enhances granulocyte oxidative burst, activates endothelial cells and increases the levels of cytokines, thus promoting inflammation. Consequently, a low magnesium status, which is often underdiagnosed, potentiates the reactivity to various immune challenges and is implicated in the pathophysiology of many common chronic diseases. Here we summarize recent advances supporting the link between magnesium deficiency, inflammatory responses and diseases, and offer new hints towards a better understanding of the underlying mechanisms.

Magnesium deficiency with high calcium-to-magnesium ratio promotes a metastatic phenotype in the CT26 colon cancer cell line.

Magnesium (Mg) plays important roles in maintaining genomic stability and cellular redox. Mg also serves as nature's physiological calcium (Ca) channel antagonist, controlling intracellular Ca entry. Because Ca is the most important second messenger, its intracellular concentration is tightly regulated. Excess intracellular Ca can activate aberrant signaling pathways leading to the acquisition of pathological characteristics and cell injury. Several epidemiological studies have linked Mg deficiency (MgD) and increased Ca:Mg ratios with higher incidences of colon cancer and increased mortality. While it is estimated that less than 50% of the US population consumes the recommended daily allowance for Mg, Ca supplementation is widespread. Therefore, we studied the effect of MgD, with variable Ca:Mg ratios on cellular oxidative stress, cell migration, calpain activity, and associated signaling pathways using the CT26 colon cancer cell line. MgD (with Ca:Mg ratios >1) elevated intracellular Ca levels, calpain activity and TRPM7 expression, as well as oxidative stress and cell migration, consistent with observed degradation of full-length E-cadherin, ß-catenin, and N-terminal FAK. MgD was accompanied by enhanced degradation of IκBα and the transactivation domain containing the C-terminus of NF-κB p65 (RelA). MgD-exposed CT26 cells exhibited increased p53 degradation and aneuploidy, markers of genomic instability. By contrast, these pathological changes were not observed when CT26 were cultured under MgD conditions where the Ca:Mg ratio was kept at 1. Together, these data support that exposure of colon cancer cells to MgD with physiological Ca concentrations (or increasing Ca:Mg ratios) leads to the acquisition of a more aggressive, metastatic phenotype.

[Pathogenetic aspects of magnesium deficiency in connective tissue dysplasia syndrome].

The problem of connective tissue dysplasia is currently becoming particularly relevant because of significant increase of individuals with characteristic abnormalities in the structure of connective tissue. The lack of some micronutrients, arising during ontogenesis in the organism, can determine a high risk of worsening connective tissue homeostasis. Recently, the decisive role of magnesium deficiency in the progression of this disease has been demonstrated. The aim of the study was to substantiate the need for magnesium diet therapy in individuals with connective tissue dysplasia basing on the study of the pathogenetic significance of magnesium deficiency in this pathology. Material and methods. The electronic resources of the portals PubMed-NCBI, MEDLINE, the Scientific Electronic Library eLIBRARY.RU, CyberLeninka and the Google Academy were used. Results and discussion. The analysis of the obtained data made it possible to identify fundamentally new provisions on the main mechanisms of the magnesium influence on the metabolic state of all components of connective tissue. It was proved that magnesium deficiency is a predictor of worsening connective tissue homeostasis, increasing in the number of dysplastic symptoms and their severity. This pathogenetically justifies prescribing a balanced diet to patients with connective tissue dysplasia, including products rich in magnesium, taking into account its recommended daily intake, depending on age of patients. Conclusion. Adequate daily intake of magnesium will increase the mechanical properties and functionality of the connective tissue, and should be recommended for patients with connective tissue dysplasia to prevent the development of complications, maintain the quality of life and improve the prognosis for this disease.

SARS-CoV-2: influence of phosphate and magnesium, moderated by vitamin D, on energy (ATP) metabolism and on severity of COVID-19.

The use of vitamin D to reduce the severity of COVID-19 complications is receiving considerable attention, backed by encouraging data. Its purported mode of action is as an immune modulator. Vitamin D, however, also affects the metabolism of phosphate and Mg, which may well play a critical role in SARS-CoV-2 pathogenesis. SARS-CoV-2 may induce a cytokine storm that drains ATP whose regeneration requires phosphate and Mg. These minerals, however, are often deficient in conditions that predispose people to severe COVID-19, including older age (especially males), diabetes, obesity, and usage of diuretics. Symptoms observed in severe COVID-19 also fit well with those seen in classical hypophosphatemia and hypomagnesemia, such as thrombocytopenia, coagulopathy, dysfunction of liver and kidneys, neurologic disturbances, immunodeficiency, failure of heart and lungs, delayed weaning from a respirator, cardiac arrhythmia, seizures, and, finally, multiorgan failure. Deficiencies of phosphate and Mg can be amplified by kidney problems commonly observed in patients with COVID-19 resulting in their wastage into urine. Available data show that phosphate and Mg are deficient in COVID-19, with phosphate showing a remarkable correlation with its severity. In one experiment, patients with COVID-19 were supplemented with a cocktail of vitamin D3, Mg, and vitamin B12, with very encouraging results. We, thus, argue that patients with COVID-19 should be monitored and treated for phosphate and Mg deficiencies, ideally already in the early phases of infection. Supplementation of phosphate and Mg combined with vitamin D could also be implemented as a preventative strategy in populations at risk.

Subclinical hypomagnesemia: Prevalence and causes in dairy cows in the semiarid region of the state of Paraíba, Brazil / Hipomagnesemia subclínica: Prevalência e causas em vacas leiteiras da região semiárida no estado da Paraíba, Brasil

In dairy farming, cows display important metabolic changes during the transition period, particularly high-production cows, which need nutrients in greater quantity to meet the required demand. The aim of this study was to determine the prevalence of subclinical hypomagnesemia in pre- and post-partum dairy cows inserted in milk-production systems in the Sousa microregion and the district of São João do Rio do Peixe, both in the State of Paraíba, Brazil. As such, visits were made every two weeks to 34 rural properties, where the team collected 357 blood samples by venepuncture, 106 from pre-partum lactating cows and 251 from lactating cows in the post-partum period. It was found that the properties supplied three types of mineral supplement: a single supplement of NaCl, a supplement of NaCl + mineral base, and a commercial supplement. The cows receiving the commercial mineral supplement had the highest prevalence (10.53%) of the disorder, even showing a significant difference (P < .05) between the other types of supplement. In relation to reproductive period, it was found that the post-partum cows had a higher prevalence of subclinical hypomagnesemia (9.96%) than did the pre-partem cows (8.49%); there was, however, no significant difference (P > .05) between the two. Studies such as this are fundamental for alerting rural and technical producers to the occurrence of subclinical hypomagnesemia in the region, in addition to the damage caused by metabolic disorders.(AU)

Na bovinocultura leiteira, as vacas apresentam mudanças metabólicas importantes durante o período de transição, principalmente aquelas de alta produção, que necessitam de nutrientes em maior quantidade para suprir a demanda requerida. Este estudo teve como objetivo determinar a prevalência de hipomagnesemia subclínica no pré e pós-parto em vacas leiteiras inseridas em sistemas de produção de leite na microrregião de Sousa-PB e município de São João do Rio do Peixe-PB. Para isso foram realizadas visitas quinzenais a 34 propriedades rurais, onde a equipe coletou 357 amostras de sangue por meio de punção venosa, sendo 106 provenientes de vacas em lactação que se encontravam no período de pré-parto e 251 de vacas em lactação inseridas no período de pós-parto. Verificou-se que as propriedades forneciam três tipos de suplemento mineral: suplementação exclusiva com NaCl; suplementação com NaCl + núcleo mineral; e suplementação comercial. As vacas que recebiam a suplementação mineral do tipo comercial corresponderam aquelas com maior prevalência (10,53%) de ocorrência do distúrbio, apresentando ainda diferença significativa (P < 0,05) entre as demais formas de suplementação. Em relação ao período reprodutivo em que as vacas se encontravam, notou- se que aquelas do pós-parto apresentaram maior prevalência de hipomagnesemia subclínica (9,96%) em relação às vacas do pré-parto (8,49%). Porém não houve diferença significative (P > 0,05) entre ambas. Estudos como esse tornam-se fundamentais para alertar produtores rurais e técnicos sobre a ocorrência da hipomagnesemia subclínica na região, além dos prejuízos que os distúrbios metabólicos acarretam.(AU)