Deficient Diet Research Articles

The Epithelial Na+ Channel Is a Zn2+ Sensitive Renal Na+ Reabsorption Pathway that Mediates Zn2+ Deficiency-induced Hypertension

Background: Zinc (Zn2+) deficiency (ZnD) is comorbid with many chronic diseases including kidney disease and diabetes. Individuals in these vulnerable populations have a higher prevalence of hypertension. Recently, we reported that ZnD induces hypertension by promoting renal Na+ reabsorption. However, the renal Na+ reabsorption mechanisms involved continue to be identified. The renal epithelial Na+ channel (ENaC) plays an essential role in regulating whole-body Na+ and water balance and is involved in hypertension. We hypothesize that ENaC is a Zn2+-sensitive channel that mediates ZnD-induced hypertension. Experimental Design: To establish the role of ENaC in ZnD-induced hypertension, WT C57Bl/6 mice were switched from a Zn2+ adequate to a Zn2+ deficient diet for 10 weeks. During weeks 9 and 10, mice were treated with benzamil, an ENaC inhibitor. Systolic blood pressure (BP) was monitored by tail-cuff plethysmography; Renal ENaC expression was examined by immunohistochemistry and Western blot. To authenticate the Zn2+ sensitivity of ENaC, mouse distal convoluted tubule cells (mDCT) were treated with a Zn2+ chelator (TPEN) or vehicle (ethanol) for 24 hours. A subset of TPEN-treated cellular monolayers were supplemented with Zn2+ for 24 hours to replete intracellular Zn2+. Cellular ENaC expression was examined by Western blot analysis. Results: 1) Blood pressure: Compared to Zn2+ adequate mice (101.4 mm Hg ± 4.225), Zn2+ deficient mice had increased BP (154.6 mm Hg ± 2.422). However, benzamil treatment lowered BP (115.0 mm Hg ± 4.626) of Zn2+ deficient mice. 2)Immunohistochemistry: Next, Zn2+ effects on ENaC expression were examined. In Zn2+ deficient mice, αENaC protein abundance significantly increased compared with Zn2+ adequate mice. 3) Western blot analysis: To directly investigate Zn2+effects on ENaC expression, in vitro studies were performed using mDCT cells. Western blot analysis showed that TPEN-induced ZnD stimulated both αENaC and βENaC protein expression. Conclusion: Collectively, our findings reveal that (1) ENaC is a Zn2+ sensitive renal Na+ reabsorption pathway and (2) ENaC mediates ZnD-induced hypertension. Significance: Understanding the renal mechanisms by which Zn2+ regulates blood pressure may have an important therapeutic impact on hypertension. Funding: R21 DK119879, R01 DK-133698 (National Institute of Diabetes and Digestive and Kidney Diseases); R25DK078381 (NIH NIDDK STEP-UP program);1742339 (National Science Foundation ASK Program). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Co-enrichment of selenium and cadmium in soils of southern China and its implication for the safe utilisation of selenium-rich lands

Dietary deficiency of selenium (Se) is a global health threat related to low Se concentrations in crops. Southern China has abundant Se-rich land resources, but the cadmium (Cd) pollution problem is prominent, which may lead to Cd exceeding the safety standard in Se-rich crops. Therefore, it is important to delineate Se-rich land without Cd pollution in order to develop green Se-rich agriculture. Based on soil/sediment geochemical survey data covering 2.3 million km2 of southern China, this study analysed the concentration and spatial distribution of Se and Cd, discussed their enrichment mechanisms and proposed suggestions for the safe use of Se-rich land. The results showed that the soil/sediments in southern China were significantly enriched in Se and Cd, and the median values were 0.31 mg·kg−1 and 221 μg·kg−1, which were 1.8 times and 2.5 times the national soil background values, respectively. In addition, a significant positive correlation was observed between Se and Cd, indicating that Cd contamination in Se-rich soils frequently exceeded the pollution limit. According to statistics, Se-rich land accounted for 32.13 % of southern China. However, due to the co-enrichment of Se and Cd, areas without Cd pollution accounted for only one-third of the total Se-rich area. In particular, the areas with co-enrichment of SeCd are primarily distributed in Yunnan, Guizhou, Guangxi, western Hubei, northwestern Zhejiang, western Hunan, southern Hunan and northern Guangdong. The enrichment of Se is predominantly associated with parent rocks (black and carbonate rocks). At the same time, the enrichment of Cd is influenced by the parent rocks and PbZn mineralisation and mining activities. Three recommendations for managing Se-rich land were proposed: imposing restrictions on the utilisation of heavily contaminated Se-rich land for agricultural production, adopting a rational approach towards utilising lightly polluted Se-rich land and actively promoting the development of Se-rich agriculture in uncontaminated Se-rich areas. In the future, it is necessary to develop technologies that simultaneously enhance Se absorption while inhibiting Cd absorption in order to safely exploit Se-rich lands affected by Cd pollution.

Methionine-choline deficient diet deteriorates DSS-induced murine colitis through disturbance of gut microbes and infiltration of macrophages.

Ulcerative colitis (UC) is associated with changed dietary habits and mainly linked with the gut microbiota dysbiosis, necroptosis of epithelial cells, and mucosal ulcerations. Liver dysfunction and abnormal level of liver metabolism indices were identified in UC patients, suggesting a close interaction between gut and liver disorders. Methionine-choline deficient diet (MCD) has been shown to induce persistent alterations of gut microbiota and metabolome during hepatitis. In this study we further explored the disease phenotypes in UC patients and investigated whether MCD functioned as a trigger for UC susceptibility. After assessing 88 serum specimens from UC patients, we found significant liver dysfunction and dyslipidemia including abnormal ALT, AST, TG, TC, LDL-c and HDL-c. Liver dysfunction and dyslipidemia were confirmed in DSS-induced colitis mice. We fed mice with MCD for 14 days to cause mild liver damage, and then treated with DSS for 7 days. We found that MCD intake significantly exacerbated the pathogenesis of mucosal inflammation in DSS-induced acute, progressive, and chronic colitis, referring to promotion of mucosal ulcers, colon shortening, diarrhea, inflammatory immune cell infiltration, cytokines release, and abnormal activation of inflammatory macrophages in colon and liver specimens. Intraperitoneal injection of clodronate liposomes to globally delete macrophages dramatically compromised the pathogenesis of MCD-triggering colitis. In addition, MCD intake markedly changed the production pattern of short-chain fatty acids (SCFAs) in murine stools, colons, and livers. We demonstrated that MCD-induced colitis pathogenesis largely depended on the gut microbes and the disease phenotypes could be transmissible through fecal microbiota transplantation (FMT). In conclusion, this study supports the concept that intake of MCD predisposes to experimental colitis and enhances its pathogenesis via modulating gut microbes and macrophages in mice.

Fat and proteolysis due to methionine, tryptophan, and niacin deficiency leads to alterations in gut microbiota and immune modulation in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is one of the intractable diseases. Nutritional components associated with IBD have been identified, and it is known that excessive methionine intake exacerbates inflammation, and that tryptophan metabolism is involved in inflammation. Analysis of the gut microbiota has also progressed, where Lactobacillus regulate immune cells in the intestine and suppress inflammation. However, whether the methionine and tryptophan metabolic pathways affect the growth of intestinal Lactobacillus is unknown. Here we show how transient methionine, tryptophan, and niacin deficiency affects the host and gut microbiota in mouse models of colitis (induced by dextran sodium sulfate) fed a methionine-deficient diet (1K), tryptophan and niacin-deficient diet (2K), or methionine, tryptophan, and niacin-deficient diet (3K). These diets induced body weight decrease and 16S rRNA analysis of mouse feces revealed the alterations in the gut microbiota, leading to a dramatic increase in the proportion of Lactobacillus in mice. Intestinal RNA sequencing data confirmed that the expression of several serine proteases and fat-metabolizing enzymes were elevated in mice fed with methionine, tryptophan, and niacin (MTN) deficient diet. In addition, one-carbon metabolism and peroxisome proliferator-activated receptor (PPAR) pathway activation were also induced with MTN deficiency. Furthermore, changes in the expression of various immune-related cytokines were observed. These results indicate that methionine, tryptophan, and niacin metabolisms are important for the composition of intestinal bacteria and host immunity. Taken together, MTN deficiencies may serve as a Great Reset of gut microbiota and host gene expression to return to good health.

Effects of dietary phytase with or without multi-carbohydrase supplementation on growth performance, nutrient digestibility, and bone traits in nursery pigs

The aim was to determine the effects of supplementing increasing doses of phytase alone or in combination with a multi-carbohydrase blend to a phosphorus (P)-deficient diet for nursery pigs on growth performance, nutrient digestibility, and metacarpal bone characteristics. A total of 192 weaned pigs (7.7 ± 0.05 kg) were allotted to one of eight dietary treatments each with eight replicates in a randomized complete block design based on initial body weight. Fecal samples (days 18, 19, and 20) and metacarpal bones (day 21) were collected to determine apparent total tract digestibility (ATTD) of energy and nutrients and bone mineralization, respectively. During week 3 and overall period, increasing doses of phytase quadratically increased ( P < 0.05) average daily gain. The ATTD of ash and P quadratically increased ( P < 0.05) when doses of phytase increased. Phytase had quadratic ( P < 0.05) effects by increasing fat-free dry weight, ash content, and P in metacarpal bone. In conclusion, increasing levels of phytase quadratically improved growth performance in week 2, nutrient digestibility, and bone traits of pigs fed a P-deficient diet. In general, however, there was no effect of multi-carbohydrase supplementation on growth performance and metacarpal characteristics in nursery pigs.

Epigenetic and Coping Mechanisms of Stress in Affective Disorders: A Scoping Review

This review aims to explore the intricate relationship among epigenetic mechanisms, stress, and affective disorders, focusing on how early life experiences and coping mechanisms contribute to susceptibility to mood disorders. Epigenetic factors play a crucial role in regulating gene expression without altering the DNA (deoxyribonucleic acid) sequence, and recent research has revealed associations between epigenetic changes and maladaptive responses to stress or psychiatric disorders. A scoping review of 33 studies employing the PRISMA-S (Preferred Reporting Items for Systematic Reviews and Meta-Analyses—Statement) guidelines investigates the role of stress-induced epigenetic mechanisms and coping strategies in affective disorder occurrence, development, and progression. The analysis encompasses various stress factors, including childhood trauma, work-related stress, and dietary deficiencies, alongside epigenetic changes, such as DNA methylation and altered gene expression. Findings indicate that specific stress-related genes frequently exhibit epigenetic changes associated with affective disorders. Moreover, the review examines coping mechanisms in patients with bipolar disorder and major depressive disorder, revealing mixed associations between coping strategies and symptom severity. While active coping is correlated with better outcomes, emotion-focused coping may exacerbate depressive or manic episodes. Overall, this review underscores the complex interplay among genetic predisposition, environmental stressors, coping mechanisms, and affective disorders. Understanding these interactions is essential for developing targeted interventions and personalized treatment strategies for individuals with mood disorders. However, further research is needed to elucidate specific genomic loci involved in affective disorders and the clinical implications of coping strategies in therapeutic settings.

Non-alcoholic fatty liver disease changes the expression and activity of hepatic drug-metabolizing enzymes and transporters in rats

Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases, which can cause serious complications and gradually increase the mortality rate. However, the effects of NAFLD on drug-metabolizing enzymes and transporters remain unclear, which may cause some confusion regarding patient medication. In this study, a NAFLD rat model was constructed by feeding rats with methionine and choline deficiency diets for 6 weeks, and the mRNA and protein levels of drug-metabolizing enzymes and transporter were analyzed by real-time fluorescent quantitative PCR and Western blot, respectively. The activity of drug-metabolizing enzymes was detected by cocktail methods. In the NAFLD rat model, the mRNA expression of phase I enzymes, phase II enzymes, and transporters decreased. At the protein level, only CYP1A1, CYP1B1, CYP2C11, and CYP2J3 presented a decrease. In addition, the activities of CYP1A2, CYP2B1, CYP2C11, CYP2D1, CYP3A2, UGT1A1, UGT1A3, UGT1A6, and UGT1A9 decreased. These changes may be caused by the alteration of FXR, HNF4α, LXRα, LXRβ, PXR, and RXR. In conclusion, NAFLD changes the expression and activity of hepatic drug-metabolizing enzymes and transporters in rats, which may affect drug metabolism and pharmacokinetics. In clinical medication, drug monitoring should be strengthened to avoid potential risks.

Modest effect of differential dietary vitamin A intake on the pathogenesis of alcohol-associated liver disease.

Chronic alcohol consumption is a major public health issue. The primary organ damaged by alcohol abuse is the liver, leading to alcohol-associated liver disease (ALD). ALD begins with hepatic steatosis and can progress to fibrosis and cirrhosis; however, we have an incomplete understanding of ALD pathogenesis. Interestingly, the liver is also the major organ for vitamin A metabolism and storage, and ALD has previously been linked with altered hepatic vitamin A homeostasis. We hypothesize that alcohol-induced vitamin A depletion disrupts its normal function in the liver, contributing to the pathogenesis of ALD. To test this hypothesis, we postulated that adding copious vitamin A to the diet might alleviate ALD, and conversely, that a vitamin A deficient diet would worsen ALD. We conducted two dietary intervention studies in mice comparing deficient (0 IU/g diet) and copious (25 IU/g diet) dietary vitamin A intake versus control (4 IU/g diet), using the NIAAA chronic-binge model of ALD. Hepatic steatosis was assessed using histopathological and biochemical approaches. Tissue Vitamin A levels were measured using high-performance liquid chromatography. Markers of ALD, hepatic inflammation and lipid metabolism were analyzed by the quantitative polymerase chain reaction and western blotting. As expected, a 0 IU/g Vitamin A diet decreased, and a 25 IU/g Vitamin A diet increased hepatic Vitamin A stores. However, alcohol induced changes in hepatic triglyceride levels, markers of hepatic lipid metabolism, inflammation and fibrosis were not significantly different in mice consuming a copious or deficient vitamin A diet compared to control. Altered vitamin A intake and hepatic vitamin A storage have a minor effect on the pathogenesis of ALD. Thus, given the known link between altered retinoic acid signaling and ALD, future studies that further explore this linkage are warranted.

Interruptible demyelination in avian riboflavin deficient neuropathy

Background and aimsThe evolution of demyelination in individual internodes remains unclear although it has been noticed the paranodal demyelination precedes internodal demyelination in neuropathies with diverse aetiologies. For therapeutic purpose, it is fundamental to know whether the demyelinating procedure in affected internodes can be interrupted. This study aimed to delineate the development of demyelination in individual internodes in avian riboflavin deficient neuropathy.MethodsNewborn broiler meat chickens were maintained either on a routine diet containing 5.0 mg/kg riboflavin, a riboflavin deficient diet containing 1.8 mg/kg riboflavin, or initially a riboflavin deficient diet for 11 days and then routine diet plus riboflavin repletion from day 12. Evolution of demyelination in individual internodes was analyzed by teased nerve fibre studies from day 11 to 21.ResultsIn riboflavin deficient chickens, demyelination was the predominant feature: it was mainly confined to the paranodal region at day 11; extended into internodal region, but less than half of the internodal length in most affected internodes at day 16; involved more than half or whole internode at day 21. In the internode undergoing demyelination, myelin degeneration of varying degrees was noticed in the cytoplasm of the Schwann cell wrapping the internode. Two days after riboflavin repletion, co-existence of remyelination and active demyelination within individual internodes was noticed. Remyelination together with preserved short original internodes was the characteristic feature 4 and 9 days after riboflavin repletion.ConclusionRiboflavin repletion interrupts the progression from paranodal to internodal demyelination in riboflavin deficient chickens and promotes remyelination before complete internodal demyelination.

Personalized Health-Centric Food Recommendation System

People nowadays suffer from a wide range of acute and chronic conditions. It is challenging to properly prescribe a diet in modern world. When a body does not obtain enough nutrients, it might develop nutritional disorders, which can cause a number of different health issues. Chronic conditions including hypertension, cardiovascular disease, diabetes, and others can be caused on by dietary deficiencies or excesses of particular nutrients as well as eating disorders. Primary root cause of these conditions is typically an inadequate or improper diet. We propose a diet suggestion system in this study that takes the user’s physics details and symptoms into account. Machine learning methods (KNN) are used in this study. The system predicts the proposed meal plan for a user by leveraging its training data, which comprises daily calorie requirements and food consumption patterns. According to the evaluation of the dataset, the suggested model outperforms existing diet recommendation systems. Analyzing the user’s dietary and nutritional requirements, the suggested system generates a prediction about the meal plan. It could result in a customized food plan for each person and promote better health

Histamine Intolerance: Symptoms, Diagnosis, and Beyond.

Histamine intolerance is a condition characterized by the accumulation of histamine to a point that exceeds the body's capacity to eliminate it. Researchers have attributed several reasons to this condition, such as genetic factors, alcohol, and dietary deficiencies, among other elements. Symptoms of histamine intolerance have been found to extend beyond the gastrointestinal tract and to the whole body, with these symptoms being sporadic and non-specific. This review will explore various aspects related to histamine intolerance, such as its causes, symptoms, diagnosis, and information related to management.

NASH triggers cardiometabolic HFpEF in aging mice

Both heart failure with preserved ejection fraction (HFpEF) and non-alcoholic fatty liver disease (NAFLD) develop due to metabolic dysregulation, has similar risk factors (e.g., insulin resistance, systemic inflammation) and are unresolved clinical challenges. Therefore, the potential link between the two disease is important to study. We aimed to evaluate whether NASH is an independent factor of cardiac dysfunction and to investigate the age dependent effects of NASH on cardiac function. C57Bl/6 J middle aged (10 months old) and aged mice (24 months old) were fed either control or choline deficient (CDAA) diet for 8 weeks. Before termination, echocardiography was performed. Upon termination, organ samples were isolated for histological and molecular analysis. CDAA diet led to the development of NASH in both age groups, without inducing weight gain, allowing to study the direct effect of NASH on cardiac function. Mice with NASH developed hepatomegaly, fibrosis, and inflammation. Aged animals had increased heart weight. Conventional echocardiography revealed normal systolic function in all cohorts, while increased left ventricular volumes in aged mice. Two-dimensional speckle tracking echocardiography showed subtle systolic and diastolic deterioration in aged mice with NASH. Histologic analyses of cardiac samples showed increased cross-sectional area, pronounced fibrosis and Col1a1 gene expression, and elevated intracardiac CD68+ macrophage count with increased Il1b expression. Conventional echocardiography failed to reveal subtle change in myocardial function; however, 2D speckle tracking echocardiography was able to identify diastolic deterioration. NASH had greater impact on aged animals resulting in cardiac hypertrophy, fibrosis, and inflammation.

Switch of ELF3 and ATF4 transcriptional axis programs the amino acid insufficiency-linked epithelial-to-mesenchymal transition

Epithelial-to-mesenchymal transition (EMT) that endows cancer cells with increased invasive and migratory capacity enables cancer dissemination and metastasis. This process is tightly associated with metabolic reprogramming acquired for rewiring cell status and signaling pathways for survival in dietary insufficiency conditions. However, it remains largely unclear how transcription factor (TF)-mediated transcriptional programs are modulated during the EMT process. Here we reveal that depletion of a key epithelial TF, ELF3, triggers a TGFβ signaling activation-like mesenchymal transcriptomic profile and metastatic features linked to the aminoacyl-tRNA biogenesis pathway. Moreover, the transcriptome alterations elicited by ELF3 depletion perfectly resemble an ATF4-dependent weak response to amino acid starvation. Intriguingly, we observe an exclusive enrichment of ELF3 and ATF4 in epithelial and TGFβ-induced or ELF3 depletion-elicited mesenchymal enhancers, respectively, with rare co-binding on altered enhancers. We also find that the upregulation of aminoacyl-tRNA synthetases and some mesenchymal genes upon amino acid deprivation is diminished in ATF4-depleted cells. In sum, the loss of ELF3 binding on epithelial enhancers and the gain of ATF4 binding on the enhancers of mesenchymal factors and amino acid-deprivation responsive genes facilitate the loss of epithelial cell features and the gain of TGFβ signaling-associated mesenchymal signatures, which further promote lung cancer cell metastasis.

DTYMK is an essential gene in mice and heterozygosity does not cause neural tube defects

Regulation of nucleotide biosynthesis is necessary for maintaining cellular processes including DNA replication and repair. A key enzyme in this process is deoxythymidylate kinase (dTYMK), which catalyzes the initial step in the production of dTTP from dTMP. This gene constitutes the first merged step of dTTP synthesis from the de novo and salvage pathways which regulate dTMP biosynthesis. Decreased de novo dTMP biosynthesis causes dysregulated dTTP:dUTP pools, and leads to increased uracil in DNA and neural tube closure defect (NTD) development in mice. The goal of this research was to investigate if dTYMK, the downstream enzyme in dTTP production, is an essential gene in mice and if impairments in dTYMK play a causal role in development including NTD pathology in mice. Dtymk+/− C57BL/6J females were weaned onto either a control, excess folic acid, or folic acid deficient diet and timed breeding was performed after 8 weeks on diet. The offspring were analyzed for NTDs and other reproductive outcomes at embryonic day 12.5 (E12.5). Dtymk–/– mice were confirmed to be embryonic lethal before E12.5, and Dtymk+/− mice on all three experimental diets did not show the presence of open neural tube defects, spina bifida or exencephaly. However, the expression of dTYMK in Dtymk+/− mouse embryos was confirmed to be decreased by approximately 3-fold compared to Dtymk+/+ embryos. Although dTYMK was demonstrated to be an essential gene in mice and is required for the regulation of nucleotide pools in vitro, there was no evidence of increased risk of NTDs because of a reduction in expression of this enzyme during embryonic development. It is possible that a further reduction in expression may be required to see developmental anomalies in C57BL/6J mice.

A 5-Year-Old Boy with Scurvy, Severe Anemia, and Severe Malnutrition: A Challenge

Background: Scurvy is a rare disease caused by a severe vitamin C deficiency in the diet. Due to its rarity compared to other dietary deficiencies, it is seldom recognized, resulting in a typical delay in diagnosis. This issue is more common in children with physical disabilities or poor eating habits. This study aims to examine the medical history of a healthy young individual who was unexpectedly diagnosed with scurvy. Case description: We report a five-year-old male with hearing impairment presented to our clinic with a movement limitation in lower limbs in one week. The patient's dietary history indicated that meat, fruits, and vegetables were strictly limited. Based on the X-ray results of the right and left genu, there is evidence of spur formation accompanied by sclerosis and irregular metaphysis in the femur and tibia of both sides (known as Pelken's spur). Additionally, there are dense areas with calcification on the surface of the spur (referred to as the Frankel line), as well as reduced bone trabeculation and thinning of the outer layer of the bone (referred to as pencil thin cortex). The presence of radiographic characteristics indicated osteopenia raises suspicions of scurvy. According to the complete blood count examination, the patient had severe anemia. The patient is severely malnourished. Based on the dietary history, clinical symptoms, and radiographic evidence, scurvy was diagnosed. Conclusion: Our case demonstrates the importance of emphasizing the need for dietary screening to reduce over-examination in patients with non-specific complaints.

Effects of dietary iron deficiency or overload on bone: Dietary details matter

PurposeBone is susceptible to fluctuations in iron homeostasis, as both iron deficiency and overload are linked to poor bone strength in humans. In mice, however, inconsistent results have been reported, likely due to different diet setups or genetic backgrounds. Here, we assessed the effect of different high and low iron diets on bone in six inbred mouse strains (C57BL/6J, A/J, BALB/cJ, AKR/J, C3H/HeJ, and DBA/2J). MethodsMice received a high (20,000 ppm) or low-iron diet (∼10 ppm) after weaning for 6–8 weeks. For C57BL/6J males, we used two dietary setups with similar amounts of iron, yet different nutritional compositions that were either richer (“TUD study”) or poorer (“UCLA study”) in minerals and vitamins. After sacrifice, liver, blood and bone parameters as well as bone turnover markers in the serum were analyzed. ResultsAlmost all mice on the UCLA study high iron diet had a significant decrease of cortical and trabecular bone mass accompanied by high bone resorption. Iron deficiency did not change bone microarchitecture or turnover in C57BL/6J, A/J, and DBA/2J mice, but increased trabecular bone mass in BALB/cJ, C3H/HeJ and AKR/J mice. In contrast to the UCLA study, male C57BL/6J mice in the TUD study did not display any changes in trabecular bone mass or turnover on high or low iron diet. However, cortical bone parameters were also decreased in TUD mice on the high iron diet. ConclusionThus, these data show that cortical bone is more susceptible to iron overload than trabecular bone and highlight the importance of a nutrient-rich diet to potentially mitigate the negative effects of iron overload on bone.

Omega-3 fatty acids mitigate skin damage caused by ultraviolet-B radiation

Mice fed a diet containing an adequate amount of ω-3 fatty acids (ω-3 Adq) or a deficient diet (ω-3 Def) were irradiated with ultraviolet-B (UV-B) and were measured daily changes in transepidermal water loss (TEWL). TEWL was significantly increased in ω-3 Def mice with repeated UV-B irradiation, but this increase was significantly reduced in ω-3 Adq mice. The epidermal layers revealed thickening of the spinous and basal layers induced by UV-B irradiation in both groups. Moreover, the ω-3 Def mice had a disturbed epidermal structure and a coarser stratum corneum. And the granule cell layer is significantly reduced, and abnormal layer formation (parakeratosis) occurred in the stratum corneum. These results suggest that continuous UV-B irradiation promotes epidermal turnover and leads to epidermal thickening, but ω-3 fatty acids protect the body from UV-B-induced stress.

Perspectives on Iron Deficiency as a Cause of Human Disease in Global Public Health

Abstract: Iron (Fe) is a necessary trace element in numerous pathways of human metabolism. Therefore, Fe deficiency is capable of causing multiple health problems. Apart from the well-known microcytic anemia, lack of Fe can cause severe psychomotor disorders in children, pregnant women, and adults in general. Iron deficiency is a global health issue, mainly caused by dietary deficiency but aggravated by inflammatory conditions. The challenges related to this deficiency need to be addressed on national and international levels. This review aims to summarize briefly the disease burden caused by Fe deficiency in the context of global public health and aspires to offer some hands-on guidelines.

Taurine amino acid supplementation impacts performance, blood hematology, oxidative stress, and jejunum morphology in broiler chickens.

Excess levels of free radicals cause oxidative damage to cells. Taurine is a rare amino acid with antioxidant effects whose dietary deficiency increases oxidative damage to the cell membrane. To investigate the effects of dietary taurine supplementation on performance, blood hematology, oxidative stress, and jejunum morphology in broilers, 300 broilers (Ras 308, 1D of age) were randomly allocated into 4 groups with 5 replicates of 15 birds. The experimental treatments included basic diet (control treatment) and basic diet with 1, 3, and 6g/kg taurine amino acid. During 1 to 45 days, the inclusion of taurine supplementation in diets improved the body weight gain (BWG), feed consumption (FC), and feed conversion ratio (FCR) of broilers (P < 0.05). In CBC tests, the experimental treatments were significantly different concerning the red blood cell (RBC) count, the average hemoglobin in the cell, the RBC width in the curve, and the hematocrit (P < 0.05). Despite the significance of oxidative stress among the treatments, the control and fourth treatments showed the highest and the lowest oxidative stress, respectively (P < 0.05). Also, in jejunum morphology, the fourth treatment showed the best performance in terms of villus length and width and the villus length to crypt depth (V/C) ratio (P < 0.05). Overall, 6g/kg taurine addition to the diet reduced oxidative stress and positive features in the jejunum morphology while improving the functional traits of broilers.

Dietary zinc deficiency increases damage rate and copy number of mitochondrial DNA in the mouse liver

Zinc is an essential trace element involved in many physiological processes, ranging from cellular growth and immune functions to enzymatic activity and gene expression. Inadequate dietary zinc levels can disrupt the functioning of numerous organs, including the liver. Given the pivotal role played by the liver, in-depth understanding of the mechanisms driving disorders in this organ caused by zinc deficiency is of great importance. In the present study, the effects of a four-week low-zinc diet on the integrity and copy number of mitochondrial DNA (mtDNA) in the liver was assessed using a mouse model. The research revealed a significantly elevated damage rate and an increased copy number of mtDNA in the livers of mice subjected to a low-zinc diet when compared to control animals. These findings indicate that a zinc deficiency, by promoting DNA damage in mitochondrial genomes, increases a potential risk of harmful mutations that could compromise ATP production in the liver. The rise in the mtDNA copy number suggests an initial compensatory response to the detrimental effects of the zinc deficiency, which is likely to diminish with a chronic insufficiency of this element. The study confirmed the significant role of mitochondria in the processes leading to liver dysfunction induced by a zinc deficiency. It showed additionally that mtDNA is a very sensitive indicator of the liver's condition that is responsive to environmental changes such as a micronutrient deficiency in the diet.