Assessment of the anti-inflammatory mechanism of quercetin 3,7-dirhamnoside using an integrated pharmacology strategy.

Pouzolzia zeylanica (L.) Benn. is a Chinese herbal medicine widely used for its anti-inflammatory and pus-removal properties. To explore its potential anti-inflammatory mechanism, quercetin 3,7-dirhamnoside (QDR), the main flavonoid component of P. zeylanica (L.) Benn., was extracted and purified. The potential anti-inflammatory targets of QDR were predicted using network analysis. These potential targets were verified using molecular docking, molecular dynamics simulations, and in vitro experiments. Consequently, 342 potential anti-inflammatory QDR targets were identified. By analyzing the intersection between the protein-protein interaction and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, we identified several potential protein targets of QDR, including RAC-alpha serine/threonine-protein kinase (AKT1), Ras-related C3 botulinum toxin substrate 1 (RAC1), nitric oxide synthase 3 (NOS3), serine/threonine-protein kinase mTOR (mTOR), epidermal growth factor receptor (EGFR), growth factor receptor-bound protein 2 (GRB2), and endothelin-1 receptor (EDNRA). QDR has anti-inflammatory activity and regulates immune responses and apoptosis through chemokines, Phosphatidylinositol 3-kinase 3(PI3K)/AKT, cAMP, T-cell receptor, and Ras signaling pathways. Molecular docking analysis showed that QDR has good binding abilities with AKT1, mTOR, and NOS3. In addition, molecular dynamics simulations demonstrated that the protein-ligand complex systems formed between QDR and AKT1, mTOR, and NOS3 have high dynamic stability, and their protein-ligand complex systems possess strong binding ability. In RAW264.7 macrophages, QDR significantly inhibited lipopolysaccharides (LPS)-induced inducible nitric oxide synthase expression, nitric oxide (NO) release and the generation of proinflammatory cytokines IL-6, IL-1ß, and TNF-α. QDR downregulated the expression of p-AKT1(Ser473)/AKT1 and p-mTOR (Ser2448)/mTOR, and upregulated the expression of NOS3, Rictor, and Raptor. This indicates that the anti-inflammatory mechanisms of QDR involve regulation of AKT1 and mTOR to prevent apoptosis and of NOS3 which leads to the release of endothelial NO. Thus, our study elucidated the potential anti-inflammatory mechanism of QDR, the main flavonoid found in P. zeylanica (L.) Benn.

Effects of Dietary Protein and Lipid Levels in Practical Formulation on Growth, Feed Utilization, Body Composition, and Serum Biochemical Parameters of Growing Rockfish Sebastes schlegeli.

A 3 × 2 factorial experiment (protein levels, 42%, 46%, 50%; lipid levels, 9%, 12%) with three replicates was conducted in a circulating water system to investigate the effects of dietary protein and lipid levels on growth, feed utilization, body composition, and serum biochemical parameters of growing rockfish Sebastes schlegeli (initial weight, 29.98 ± 0.10 g). After an 8 weeks feeding trial, growth performance in terms of final body weight, percent weight gain, and specific growth rate increased with the increase of dietary protein level when fish fed diets containing a consistent level of dietary lipid. The feed conversion rate and daily feed intake were significantly affected by dietary protein and lipid levels, and decreased as dietary protein level increased from 42% to 46% or dietary lipid level increased from 9% to 12% (P < 0.05). Survival rate, viscerosomatic index, and hepatosomatic index were unaffected by dietary protein level (P > 0.05), but significantly increased with the increase of dietary lipid level (P < 0.05). On the contrary, condition factor was unaffected by dietary lipid level (P > 0.05), but significantly increased with dietary protein level increasing up to 46% (P < 0.05). The moisture contents of muscle and liver significantly decreased, but the whole-body crude lipid content, the crude protein and lipid contents of muscle increased as dietary protein or lipid level increased (P < 0.05). The contents of isoleucine, leucine, histidine, glycine, alanine of muscle, as well as the proportions of C14 : 0, C20 : 1, and C22 : 1n-9 in total fatty acids were higher in fish fed diets containing 12% lipid than those fed 9% lipid (P < 0.05), while C18 : 1n-9 and C18 : 2n-6 followed an opposite trend. The contents of phenylalanine, lysine, and tyrosine as well as the proportions of C18 : 0, C18 : 2n-6, C22 : 1n-9, and C22 : 6n-3 in total fatty acids decreased with the increase of dietary protein level (P < 0.05). Serum cholesterol and low-density lipoproteins increased significantly with dietary protein or lipid levels increasing, but TG concentration was elevated significantly in fish fed diets containing 12% lipid. Considering the present results in terms of growth and feed utilization, the suitable protein and lipid levels in diet for growing rockfish were 46% and 12%, respectively.

GB1a Activates SIRT6 to Regulate Lipid Metabolism in Mouse Primary Hepatocytes.

Lipid accumulation, oxidative stress, and inflammation in hepatocytes are features of nonalcoholic fatty liver disease (NAFLD). Garcinia biflavonoid 1a (GB1a) is a natural product capable of hepatic protection. In this study, the effect of GB1a on anti-inflammatory, antioxidant, and regulation of the accumulation in HepG2 cells and mouse primary hepatocytes (MPHs) was investigated, and its regulatory mechanism was further explored. The result showed that GB1a reduced triglyceride (TG) content and lipid accumulation by regulating the expression of SREBP-1c and PPARα; GB1a reduced reactive oxygen species (ROS) and improved cellular oxidative stress to protect mitochondrial morphology by regulating genes Nrf2, HO-1, NQO1, and Keap1; and GB1a reduced the damage of hepatocytes by inhibiting the expression of inflammatory cytokines interleukin-6 (IL-6), interleukin-1ß (IL-1ß), tumor necrosis factor-alpha (TNF-α), and nuclear factor kappa B (NF-κB) p65. The activities of GB1a were lost in liver SIRT6-specific knockout mouse primary hepatocytes (SIRT6-LKO MPHs). This indicated that activating SIRT6 was critical for GB1a to perform its activity, and GB1a acted as an agonist of SIRT6. It was speculated that GB1a may be a potential drug for NAFLD treatment.

Correction: Marginal zinc deficiency alters the heart proteome of rats.

Correction for 'Marginal zinc deficiency alters the heart proteome of rats' by Yongzhi Sun et al., Food Funct., 2023, https://doi.org/10.1039/d2fo03815c.

Marginal zinc deficiency alters the heart proteome of rats.

Zinc deficiency is closely related to cardiovascular diseases (CVDs), but the effects of marginal zinc deficiency (MZD) after birth on the heart are unknown. In this study, 4-week-old male rats were fed a low zinc diet (10 mg kg-1, 1/3 recommended nutrient intake, RNI) for 8 weeks. Echocardiography and histopathology were performed to assess the functional and morphological alterations of the heart. High-throughput proteomics was used to study the effects of MZD on cardiac protein expression. We found that MZD reduced food intake, body weight, serum zinc, and heart weight; however, the coefficient, zinc concentration, function, and histopathology of the heart were not changed. The heart proteome was altered in the marginal zinc-deficient diet group (MZG), compared with the normal zinc diet group (NZG). A total of 310 differentially expressed proteins (P < 0.05) were significantly changed by MZD, among which 163 proteins were up-regulated and 147 were down-regulated. Of these, 43 proteins are related to CVDs and 18 proteins are zinc-associated proteins. Gene Ontology and Pathway analysis revealed that 74 biological processes (BPs) and 37 pathways were significantly changed by MZD. This included six CVD-related BPs, such as regulation of heart rate, cardiac muscle contraction, regulation of ventricular cardiac muscle cell action potential, and regulation of blood pressure, and eight CVD-related pathways, such as dilated cardiomyopathy, diabetic cardiomyopathy, and hypertrophic cardiomyopathy. Our data show that marginal zinc deficiency after birth significantly alters cardiac protein expression and pathways related to CVDs.

Analyses of regulatory network and discovery of potential biomarkers for Korean rockfish (Sebastes schlegelii) in responses to starvation stress through transcriptome and metabolome.

Whether in aquaculture or in nature, starvation stress limits the growth of fish. The purpose of the study was to clarify the detailed molecular mechanisms underlying starvation stress in Korean rockfish (Sebastes schlegelii) through liver transcriptome and metabolome analysis. Transcriptome results showed that liver genes associated with cell cycle and fatty acid synthesis were down-regulated, whereas those related to fatty acid decomposition were up-regulated in the experimental group (EG; starved for 72 days) compared to the control group (CG; feeding). Metabolomic results showed that there were significant differences in the levels of metabolites related to nucleotide metabolism and energy metabolism, such as purine metabolism, histidine metabolism and oxidative phosphorylation. Five fatty acids (C22:6n-3; C22:5n-3; C20:5n-3; C20:4n-3; C18:3n-6) were selected as possible biomarkers of starvation stress from the differential metabolites of metabolome. Subsequently, correlation between these differential genes of lipid metabolism and cell cycle and differential metabolites were analyzed, and observed that these five fatty acids were significantly correlated with the differential genes. These results provide new clues for understanding the role of fatty acid metabolism and cell cycle in fish under starvation stress. It also provides a reference for promoting the biomarker identification of starvation stress and stress tolerance breeding research.

Modulated sampled-data consensus for networked Euler-Lagrange systems with differentiable pulse function.

This paper is concerned with the sampled-data consensus of networked Euler-Lagrange systems. The Euler-Lagrange system has enormous advantages in analyzing and designing dynamical systems. Yet, some problems arise in the Euler-Lagrange equation-based control laws when they contain sampled-data feedbacks. The control law differentiates the discontinuous sampled-data signals to generate its control input. In this process, infinities in the control inputs are generated inevitably. The main goal of this work is to eliminate these infinities and make the control inputs applicable. To reach this goal, a class of differentiable pulse functions is designed for the controllers. The pulse functions work as multipliers on the sampled-data signals to make them differentiable, hence avoid the infinities. A new consensus condition compatible with the pulse function is also obtained through rigorous consensus analysis. The condition is proved to be less conservative compared with that of the existing method. Finally, numerical examples are given to illustrate the findings and theoretical results.

Zinc and COVID-19: Immunity, Susceptibility, Severity and Intervention.

During the coronavirus disease 2019 (COVID-19) pandemic and continuing emergence of viral mutants, there has been a lack of effective treatment methods. Zinc maintains immune function, with direct and indirect antiviral activities. Zinc nutritional status is a critical factor in antiviral immune responses. Importantly, COVID-19 and zinc deficiency overlap in high-risk population. Hence, the potential effect of zinc as a preventive and adjunct therapy for COVID-19 is intriguing. Here, this review summarizes the immune and antiviral function of zinc, the relationship between zinc levels, susceptibility, and severity of COVID-19, and the effect of zinc supplementation on COVID-19. Existing studies have confirmed that zinc deficiency was associated with COVID-19 susceptibility and severity. Zinc supplementation plays a potentially protective role in enhancing immunity, decreasing susceptibility, shortening illness duration, and reducing the severity of COVID-19. We recommend that zinc levels should be monitored, particularly in COVID-19 patients, and zinc as a preventive and adjunct therapy for COVID-19 should be considered for groups at risk of zinc deficiency to reduce susceptibility and disease severity.

Effects of marginal zinc deficiency on learning and memory ability after birth.

Zinc deficiency during pregnancy and severe zinc deficiency after birth both impaired learning and memory ability, but the effects of marginal zinc deficiency (MZD) after birth on learning and memory are unclear. In the first experiment, 4-week-old male rats were randomly divided into three groups: the marginal zinc-deficient group (MZG, 10 mg kg-1, 1/3 RNI), normal zinc group (NZG, 30 mg kg-1, RNI), and paired zinc group (PZG, 30 mg kg-1). After a 4-week feeding period, the brain weight, brain coefficient, and serum zinc concentration were measured, and hippocampal proteomics analysis was performed. In the second experiment, 4-week-old male rats were fed the same diet for 8 weeks. In addition to the previously mentioned indicators, the Morris water maze results, brain pathology, post-translational modifications (PTMs) of hippocampal proteins, and the concentrations of indicators known to be related to learning and memory were analyzed. In both experiments, compared with those of the NZG, the food intake, body weight and serum zinc of the MZG were significantly decreased, and the brain weight was unchanged, but the brain coefficient was increased. Two hippocampal proteomics analyses and PTM screening showed that MZD did not change the expression and PTM of proteins. The brain pathology, learning, memory and the concentrations of indicators known to be related to learning and memory were not changed by MZD. Our study confirmed that marginal zinc deficiency (10 mg kg-1, 1/3 RNI) had no effect on the learning and memory abilities of rats after birth.

Qualitative and Quantitative Analysis of Six Fatty Acid Amides in 11 Edible Vegetable Oils Using Liquid Chromatography-Mass Spectrometry.

Fatty acid amides (FAAs) are endogenous lipid molecules that exhibit various physiological activities. FAAs are usually present at nanomolar levels in biological samples. In this study, a method for the qualitative and quantitative determination of six FAAs (linoleamide, linoleoyl ethanolamide, oleoyl ethanolamide, palmitic amide, oleamide, and octadecanamide) in edible vegetable oils was established. All six FAAs were detected in sesame, peanut, soybean (decolorized and non-decolorized), and blended oils; five in sunflower oil; four in rice oil; three in linseed and olive oils; and two in corn and canola oils. The total contents of FAAs were highest in sesame oil (104.88 ± 3.01 µg/mL), followed by peanut oil (34.96 ± 3.87 µg/mL), soybean oil (16.75 ± 1.27 µg/mL), and blended oil (13.33 ± 0.77 µg/mL), and the contents in the other edible vegetable oils were all <1.03 µg/mL. The concentrations of linoleoyl ethanolamide and oleoyl ethanolamide were highest in non-decolorized soybean oil, while the other four FAAs (linoleamide, palmitic amide, oleamide, and octadecanamide) showed the highest concentrations in sesame oil. The total contents of these FAAs in eight different oils were higher than those in biological fluids and tissue. Our study confirmed that edible vegetable oils are rich in FAAs, and provides reliable data for evaluating the nutritive value of vegetable oils.

Garcinia Biflavonoid 1 Improves Lipid Metabolism in HepG2 Cells via Regulating PPARα.

Garcinia biflavonoid 1 (GB1) is one of the active chemical components of Garcinia kola and is reported to be capable of reducing the intracellular lipid deposition, which is the most significant characteristic of non-alcoholic fatty liver disease. However, its bioactive mechanism remains elusive. In the current study, the lipid deposition was induced in HepG2 cells by exposure to oleic acid and palmitic acid (OA&PA), then the effect of GB1 on lipid metabolism and oxidative stress and the role of regulating PPARα in these cells was investigated. We found that GB1 could ameliorate the lipid deposition by reducing triglycerides (TGs) and upregulate the expression of PPARα and SIRT6, suppressing the cell apoptosis by reducing the oxidative stress and the inflammatory factors of ROS, IL10, and TNFα. The mechanism study showed that GB1 had bioactivity in a PPARα-dependent manner based on its failing to improve the lipid deposition and oxidative stress in PPARα-deficient cells. The result revealed that GB1 had significant bioactivity on improving the lipid metabolism, and its potential primary action mechanism suggested that GB1 could be a potential candidate for management of non-alcoholic fatty liver disease.

Integrated multi-omics uncovers reliable potential biomarkers and adverse effects of zinc deficiency.

BACKGROUND: Zinc deficiency is a worldwide public health problem. Currently, there are no established biomarkers available for the accurate diagnosis of zinc-deficiency in individuals. Additionally, a comprehensive view of the adverse effects of zinc deficiency is lacking. Our aim was to identify superior biomarkers of zinc deficiency and uncover the adverse effects of zinc deficiency. METHODS: We performed multi-omics analysis using serum proteomics-metabolomics and liver proteomics on zinc-deficient rats to identify candidate biomarkers and reveal the associated adverse effects of zinc deficiency. Secondly, the candidate biomarkers were validated in two zinc-deficient populations and an RCT zinc supplementation trial on a zinc-deficient population. RESULTS: Our integrated multi-omics approach revealed numerous biomarkers (>2000) and glutathione metabolism as the most important changed pathway in zinc deficiency. Three candidate biomarkers from glutathione metabolism were validated in repeated zinc-deficient rats by quantitative analysis. Only glutathione sulfotransferase omega-1 (GSTO1) (among 3 candidate biomarkers) was validated in the two zinc-deficient populations and zinc-supplemented population. Compared with serum zinc, serum GSTO1 yielded a better response to zinc supplementation and a higher correlation coefficient with zinc intake and the AUC value and has the potential for diagnosing zinc deficiency. By integrated multi-omics, we identified both established and novel adverse effects of zinc deficiency. CONCLUSIONS: Our integrated multi-omics analysis revealed more complete information about zinc deficiency; GSTO1 was found to be a reliable potential biomarker for diagnosis of zinc deficiency. This trial is registered at http://www.chictr.org.cn/registry.aspx as ChiCTR1900028162.

Discrimination of heating and frying vegetable oils based on UPLC/Q-TOF MSMS and chemometrics.

Fried foods have potential adverse effects on health. However, the compounds produced during the process of frying in different vegetable oils are unknown. In this work, ultra performance liquid chromatography (UPLC), quadrupole time-of-flight mass spectrometry (Q-TOF MSMS) and chemical pattern recognition analysis was first conducted to analyze the changes in compounds in 8 different vegetable oils before and after thin-layer heating (without food) and to reveal the potential markers of oil used for deep-frying food. Then, these markers were validated in used frying oil. Our results of principal component analysis (PCA), partial least-squares discriminant analysis (PLS-DA) indicated that both thin-layer heating and deep-frying significantly change the compounds of vegetable oils. Thirty-six of the markers associated with thin-layer heating from the 8 different oils were identified in used frying oils and can be used as common markers of oil used for deep-frying. Additionally, 22 markers detected in individual vegetable oils provided unique markers of used frying oils. These markers can be used to distinguish used frying oil and have the potential to reveal the associated physiological harm.

Fecal g. Streptococcus and g. Eubacterium_coprostanoligenes_group combined with sphingosine to modulate the serum dyslipidemia in high-fat diet mice.

BACKGROUND & AIMS: Although high-fat diet (HFD) could impact the composition of fecal microbiome and their metabolites, it is still largely unknown which fecal bacteria and metabolites are relatively important in responding to the HFD. This study aimed to identify the crucial fecal bacteria and metabolites in the HFD mice using a microbial-metabolite network, and to investigate the synergistic mediation effect of the crucial fecal bacteria and metabolites on serum dyslipidemia induced by the HFD. METHODS: The 16srDNA sequencing and the ultra-performance liquid chromatography (UPLC/TOF MSMS) platform were performed to characterize the composition and function of fecal microbiome, and metabolites in the HFD. The microbial-metabolite network, correlation and mediation analyses were performed to examine the relationships among fecal microbiome, metabolites, and serum dyslipidemia indicators. Mice models were conducted to evaluate the effect of fecal metabolite on dyslipidemia. RESULTS: Compared to the control, 32 genera were altered in the HFD, including 26 up-regulated and 6 down-regulated. A total of 42 altered pathways were observed between the control and HFD, and the "Glycosphingolipid biosynthesis" was identified as the most significant pathway (fold change = 0.64; p < 0.001). Meanwhile, 49 fecal metabolites were altered in the HFD, and the fecal microbiome was associated with the fecal metabolism (M2 = 0.776, p = 0.008). Based on the microbial-metabolite network, two major hub genera were screened (HUB1: g. Streptococcus, HUB2: g. Eubacterium_coprostanoligenes_group), and one bacterial metabolite, sphingosine, was found in this study. Further, the HUB2 was positively associated with fecal sphingosine (r = 0.646, p = 0.001), and its downstream metabolic pathway, "Glycosphingolipid biosynthesis" pathway (r = 0.544, p = 0.009). The regulatory relationship between the HUB2 and sphingosine synergistically mediated the effect of HFD on TCHO (33.7%), HDL-C (37.3%), and bodyweight (36.7%). Besides, compared to the HFD, the HFD with sphingosine supplementation had lower bodyweight (35.12 ± 1.23 vs. 39.42 ± 1.25, p < 0.001), TG (0.44 ± 0.08 vs. 0.52 ± 0.05, p = 0.002), TCHO (3.81 ± 0.34 vs. 4.51 ± 0.38, p = 0.002), and LDL-c (0.82 ± 0.09 vs. 0.97 ± 0.15, p = 0.016). CONCLUSIONS: The g. Streptococcus and g. Eubacterium_coprostanoligenes are two hub genera in the fecal micro-ecosystem of the HFD, and the g. Eubacterium_coprostanoligenes mediates the effect of HFD on dyslipidemia through sphingosine. Sphingosine supplementation can improve dyslipidemia induced by HFD.

Assessment of the efficacy of using taurine supplements to improve growth and feed utilization of juvenile starry flounder (Platichthys stellatus) given diets based on soy-protein.

A feeding trial was conducted to assess the feasibility of supplementing taurine in soy-based diets for juvenile starry flounder Platichthys stellatus. The basal diet (Crude protein 66.5%, crude lipid 8.5%) was supplemented with 0 (control), 0.5%, 1.0%, 1.5%, 2.0% and 2.5% taurine to formulate six test diets. Each diet was fed to 40 juvenile fish (22.25 g) in triplicate tanks (120 L) attached to a sea water circulation-system. Fish were fed twice daily by hand to apparent satiation during the 56-d trial. At the end of the trial, fish were counted and weighed for the analyses of growth performance, diet utilization and survival after a 24-h fast. Blood, intestines and muscles were collected for the analyses of serum oxidation resistance, digestive enzymes and body compostion. Livers were collected from the remaining fish at 4 h post-feeding for metabolic enzymes analyses. The results showed that fish fed diets supplemented with 1.0-2.5% taurine grew from 22.25-22.26 g to 47.88-50.40 g with higher average weight gain (25.62-28.12 vs 23.07 g ), specific growth rate (1.37-1.46 vs 1.27%/d ), feed intake (1.04-1.06 vs 1.00%/d), protein efficiency (2.50-2.61 vs 2.44) and lower feed conversion rate (0.84-0.83 vs 0.89) than the control treatment. Diets supplemented with 1.5-2.5% taurine significantly elevated the activities of pepsin (2.47-2.55 vs 2.22, U mg-1 prot), trypsin of distal intestine(14.55-15.24 vs 11.94, U mg-1 prot), hepatic glucokinase (126.62-129.42 vs 105.56, U mg-1 prot) and fatty acid synthetase (125.56-136.89 vs 108.45, U mg-1 prot). All diets supplemented with taurine increased the activities of lipase (32.23-36.67 vs 29.53, U g-1 prot) and trypsin (35.85-37.89 vs 33.54, U mg-1 prot) of proximal intestine, hepatic aspartate transaminase (736.990-832.38 vs 699.24, U mg-1 prot), alanine aminotransferase (477.40-551.86 vs 373.97, U mg-1 prot) and glycogen synthase (2.16-2.59 vs 1.97, U mg-1 prot), as well as serum superoxide dismutase (4.33-4.59 vs 4.07, U mg-1 prot ) and glutathione peroxidase (42.23-50.25 vs 39.17, mol mg-1 prot). Therefore, taurine supplementation benefits juvenile starry flounder growth, digestion, nutrients metabolism and oxidation resistance. The optimal taurine requirement for starry flounder is 1.75%, and the recommended supplementation level is at least 1.6% for maximizing growth of fish fed a low-fishmeal diet (13.6%).

HPHT Synthesis: Effects of the Synergy of Pressure Regulation and Atom Filling on the Microstructure and Thermoelectric Properties of Yb x Ba8-x Ga16Ge30.

Type-I clathrate compounds Yb x Ba8-x Ga16Ge30 have been synthesized by the high-pressure and high-temperature (HPHT) method rapidly. The effects of the synergy of atom filling and pressure regulation on the microstructure and thermal and electrical properties have been investigated. With the content of Yb atom increasing, the carrier concentration is improved, the electrical resistivity and the absolute Seebeck coefficient are decreased, while the thermal conductivity is reduced significantly. A series of extremely low lattice thermal conductivities are achieved, attributed to the enhancement of multiscale phonon scattering for the "rattling" of the filled guest atoms, the heterogeneous distribution of nano- and microstructures, grain boundaries, abundant lattice distortions, lattice deformations, and dislocations. As a result, a maximum ZT of about 1.07 at 873 K has achieved for the Yb0.5Ba7.5Ga16Ge30 sample.

The effects of zinc deficiency on homeostasis of twelve minerals and trace elements in the serum, feces, urine and liver of rats.

BACKGROUND: Zinc deficiency can change the concentrations of minerals and trace elements in the body. However, previous studies still had many limitations. OBJECTIVE: To reveal the effects of zinc deficiency on homeostasis of 16 minerals and trace elements. METHODS: Forty-five rats were divided randomly into three groups: normal zinc diet (30 mg/kg), low zinc diet (10 mg/kg), and pair-fed diet(30 mg/kg). The concentrations of 16 minerals and trace elements in serum, feces, urine, and liver were measured by inductively coupled plasma mass spectrometry. The excretion of 16 elements in urine and feces were calculated and compared. RESULTS: Zinc-deficient rats exhibited significant changes in up to 12 minerals and trace elements. The low zinc diet induced decreased excretion of zinc and concentrations of zinc in serum, feces, urine, and liver. Zinc deficiency increased feces concentrations of Mg, Cu, Se, K, Ag, Fe and Mn; decreased the concentrations of Mg, Cu, Se, K in liver and urine, and a diminished amount of Ag was observed in serum. Decreased urinary concentrations of Zn Ca, Mg, Cu, Se, K, Na, As and Cr, suggested that zinc-deficient rats increased the 9 elements' renal reabsorption. Decreased concentrations of Ca in liver, urine, and feces, decreased excretion in urine and feces and increased serum total Ca suggested that zinc deficiency increased the redistribution of Ca in serum or other tissues. Zinc deficiency increased excretion of Cu, Se, Fe; and decreased the excretion of other 8 elements except for Ag. CONCLUSIONS: Zinc deficiency changed the excretion, reabsorption and redistribution of 12 minerals and trace elements in rats. Our findings are the first to show that zinc deficiency alters the concentrations of Ag, Cr, and As. SUPPLEMENTARY INFORMATION: Supplementary information accompanies this paper at 10.1186/s12986-019-0395-y.