Objective To describe the trends and epidemiological characteristics of the disease burden of nutritional deficiencies in China from 1990 to 2021 and to project the incidence from 2022 to 2040. Methods Using data from the Global Burden of Disease Study 2019 on the incidence, mortality, and Disability-Adjusted Life Years (DALY) rates of nutritional deficiencies in China from 1990 to 2021, we analyzed the Annual Percentage Change (APC) and Average Annual Percentage Change (AAPC) via Joinpoint regression models. A Bayesian age-period-cohort model was employed to project incidence rates from 2022 to 2040. Results From 1990 to 2021, the overall incidence rate of nutritional deficiencies in China showed a continuous declining trend, with an AAPC of −4.25%. The age-standardized incidence rate also exhibited a continuous decline, with an AAPC of −3.96%. The mortality rate initially decreased and then increased, but showed an overall downward trend with an AAPC of −3.45%. The age-standardized mortality rate declined overall, with an AAPC of −4.97%. The DALY rate displayed a general downward trend (AAPC = −3.78%), as did the age-standardized DALY rate (AAPC = −4.07%). In 2021, the DALY rate for females was three times that of males, and the age-standardized DALY rate for females was 2.5 times that of males. The disease burden declined most rapidly in the 0-4 age group, with AAPCs for incidence, mortality, and DALY rates of −5.66%, −10.80%, and −7.89%, respectively. Projections from the Bayesian age-period-cohort model indicated that the age-standardized incidence rate in China would decrease from 3205.11 per 100 000 in 2022 to 2331.78 per 100 000 in 2040, representing a reduction of 27.22%. Conclusion The disease burden of nutritional deficiencies in China showed a downward trend from 1990 to 2021. Projections suggest that the age-standardized incidence rates for the overall population, females, and males will continue to decline from 2022 to 2040.

Objective To investigate the potential association between maternal total fluid intake at 3 months of infant age and breastfeeding practices and duration. Methods The study was embedded in the Tongji Maternal and Child Health Cohort. Information on total fluid intake for postpartum women was collected via telephone interviews at 3 months of infant age. Total fluid intake was categorized by quartiles. Information on breastfeeding practices and duration was collected via telephone interviews at 3, 6, 12, and 24 months of infant age. Breastfeeding practice was divided into full breastfeeding (FBF) and any breastfeeding (ABF). Logistic and multivariable linear regression models were used to investigate the association of total fluid intake with breastfeeding practices and duration. Results Among 2483 postpartum women-infants, 1350 (54.4%) and 966 (38.9%) received FBF at 3 and 6 months of infant age, respectively, and 2056 (82.8%), 1774 (71.4%), and 646 (36.8%) received ABF at 3, 6, and 12 months of infant age, respectively. The medium (interquartile range) of total fluid intake was 1600 ml (1250-2000 ml). About 2352 (94.7%) did not meet the recommended intake (2600ml). Compared to the mothers with the highest quartile of total fluid intake, those with the lowest quartile of total fluid intake were more likely to cease FBF at 3 months (OR=3.87; 95% CI = 3.03–4.96) and at 6 months (OR=3.05; 95% CI=2.38–3.92) of infant age, and to cease ABF at 12 months of infant age (OR=1.67; 95% CI=1.28–2.17). However, among mother-infants who received FBF at 3 months of infant age, fluid intake at 3 months of infant age was not significantly associated with breastfeeding practices at 6 and 12 months of infant age. Additionally, compared to the mothers with the highest quartile of total fluid intake, those with the lowest quartile of total fluid intake were more likely to cease breastfeeding early (adjusted β=－1.22; 95% CI=－1.85–0.58). Conclusion The postpartum women with lower total fluid intake were more likely to cease breastfeeding. Short duration of breastfeeding was positively associated with limited total fluid intake in postpartum women.

Objective To apply a precision nutrition buffet mode and test its nutritional effects in pilots. Methods A total of 149 pilots were selected as the study subjects. They were served by traditional buffet mode upon admission. A 3-day dietary survey and blood lipids and uric acid measurements were conducted. Then, a precise nutrition buffet mode was adopted. Twenty days later, a 3-day dietary survey was conducted and blood lipids and uric acid were rechecked. Food supply standards, dietary reference intakes and Chinese Diet Balance Index (DBI 22) were used to evaluate the quality of dietary nutrition. The differences in blood lipids and uric acid before and after the intervention were analyzed. Results In traditional buffet mode, the intakes of salt, oil, poultry and livestock meat far exceeded the recommended intake. The intakes of many nutrients were excessive. In the precision nutrition buffet mode, the intakes of salt, oil, poultry and livestock meat, as well as many nutrients decreased significantly. High bound score (HBS) of the traditional buffetmode was 14, indicating excessive low-level dietary intake. The HBS of the precision nutrition buffet mode was 7, indicating a more appropriate intake. After the intervention by precision nutrition buffet mode, blood uric acid, triglyceride and cholesterol levels were significantly delined. Conclusion Compared to the traditional buffet mode, precision nutrition buffet mode is better in securiong a balance dietary intake. The precision nutrition buffet mode is worthy of promotion and application.

Objective To investigate the effects of high-protein diet on urinary metabolome in rats with food restriction. Methods Twenty-four male Wistar rats were randomly divided into three groups (8 per group). The normal control group received 15% casein diet and water ad-libitum. The food restriction group was pair-fed the 15% casein diet with 30% food intake of the normal control. The protein supplemented group was pair-fed 30% casein diet with the 30% food intake of the normal control. Urine samples were collected 2 weeks after pair feeding. Nuclear magnetic resonance spectrometer was used to investigate the changes of urinary metabolite profiles. Results Both food restriction and protein supplemented groups significantly altered the urinary metabolites. Food restriction led to a decrease in the levels of citric acid, α-ketoglutaric acid, N-acetyl glycoprotein and an increase in the level of taurine in the urine, while the levels of citric acid, α-ketoglutaric acid, and N-acetyl glycoprotein were higher in the protein supplemented group than in the food restriction group, and the level of taurine was also higher than in the food restriction group. Conclusion A high-protein diet is helpful in improving metabolic disorders in the food restricted rats.

Objective To explore the mechanism by which maternal vitamin D deficiency during pregnancy impairs placental development and leads to fetal growth restriction by regulating PAR1 expression. Methods Female Sprague-Dawley (SD) rats aged four weeks were randomly allocated into two groups according to their body weight, with 10 rats in each group: the control group (Ctrl), fed a standard diet, and the vitamin D deficiency group (VDD), fed a vitamin D-deficient diet. After 8 weeks of feeding, the rats were mated with normal male SD rats. On day 18 of gestation, both groups of female rats were euthanized under anesthesia, and samples were collected for detection of relevant indicators via ELISA and Western blot analysis. Results Before pregnancy and on gestational day 18 (GD18), the serum 25(OH)D concentrations in the Ctrl group were (20.37 ± 5.03) ng/ml and (9.09 ± 2.96) ng/ml, respectively, while in the VDD group, they were (13.62 ± 4.55) ng/ml and (5.34 ± 1.63) ng/ml, respectively. The serum 25(OH)D levels in the VDD group were significantly lower than those in the Ctrl group both before pregnancy and on GD18 (P<0.01 or P<0.05). On GD18, the weight gain during pregnancy in the VDD group was significantly lower than that in the Ctrl group (P<0.01). Compared to the Ctrl group, the protein expression levels of VDR, DBP, and CYP27B1 in the placental tissue of the VDD group were significantly downregulated (P<0.01), and the levels of 25(OH)D and 1,25(OH)₂D were significantly reduced (P<0.05). The placental diameter and weight in the VDD group were significantly lower than those in the Ctrl group (P<0.01). The expression levelof MMP2 protein was significantly downregulated (P<0.05), while the expression level of E-cadherin protein was significantly upregulated (P<0.05). The number of embryo implantations, live fetuses, embryo weight, and crown-rump length in the VDD group were significantly lower than those in the Ctrl group (P<0.01), and the number of resorbed fetuses was significantly increased (P<0.01). Compared to the Ctrl group, the expression level of PAR1 protein in the placenta of the VDD group was significantly downregulated (P<0.01). Conclusion Maternal vitamin D deficiency during gestation significantly downregulates placental PAR1 expression, leading to placental developmental disorders and fetal growth retardation.

Objective To explore the effects of manganese supplementation on lung inflammation in obese asthmatic mice exposed to ovalbumin (OVA) and to provide new insights for clinical treatment. Methods Sixty male Kunming mice were randomly divided into five groups: control group (CON), obesity group (HF), asthma group (OVA), obese asthma group (HF+OVA), and obese asthmatic manganese intervention group (Mn, hereinafter referred to as the Mn intervention group), with 12 mice in each group. Groups HF, HF+OVA, and Mn were fed a high-fat diet for 12 weeks, and the other two groups were fed a control diet. Mice in the OVA, HF+OVA, and Mn intervention groups were sensitized by intraperitoneal injection of 200 μl of 0.05 mg/ml OVA sensitization solution on the first day of the 9th, 10th, and 11th weeks. On the 12th week, mice were treated by nasal drip 50 μl of 0.05 mg/ml OVA saline solution for 3 consecutive days to induce asthma. During the feeding period of high-fat diet, the Mn intervention group received 1 mg/kg MnCl2 intranasally every two days to induce asthma. After the last nasal drip exposure, asthmatic behavioral changes were observed and airway hyperresponsiveness was measured. Body weight was measured every fortnight during the modeling period, body composition was measured after 12 weeks. Hematoxylin-eosin staining was performed to observe the pathological changes in lung tissues. White blood cells in mouse bronchoalveolar lavage fluid (BALF) were counted and classified. The Mn contents in the serum and lung tissues were detected, and the levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in BALF were analyzed. Results Compared with the CON group, the mice in the HF group gained 12.4% in body weight, while the HF+OVA group gained 23.2%. The body fat ratios increased by 46.1% and 67.7% in the HF and HF+OVA groups, indicating the obesity model was successfully constructed. The mice in the OVA and HF+OVA groups showed symptoms such as nose scratching and nodding breathing, with increased airway hyperresponsiveness, indicating that the asthma model was established. Significant pathological changes were observed in the lung tissue of asthma mice, with an increased number of inflammatory cells and elevated levels of IL-6 and TNF-α. These symptoms were more pronounced in HF+OVA mice (P0.05). Compared with the HF+OVA group, mice in the Mn intervention group showed a 17.9% reduction in body weight and a 27.4% reduction in body fat ratio. Meanwhile, asthma symptoms were mitigated, airway hyperresponsiveness decreased, and pathological damages to lung tissues reduced. The number of inflammatory cells was decreased, and the levels of IL-6 and TNF-α levels declined (P0.05). Conclusion Mn supplementation protects against inflammatory responses in the lungs of obese asthmatic mice, and its mechanism is related to inhibited inflammatory responses.

Objective To investigate the mechanism of action of vanillic acid (VA) in regulating osteoclast differentiation and its effect on osteoporosis in ovariectomized (OVX) mice. Methods In vitro experiment: receptor activator for nuclear factor-κB ligand (RANKL)-treated RAW264.7 cells were used to establish an osteoclast differentiation model. The cells were divided into negative control (NC), RANKL- differentiated (Diff), and RANKL plus VA at 50, 100, and 200 μmol/L groups. Cell viability was assessed using the cell counting kit-8(CCK8) assay. The osteoclast differentiation was detected by tartrate resistant acid phosphatase (TRAP) staining and immunoblot analysis of osteoclast differentiation-related proteins. Cellular reactive oxygen species (ROS) levels were measured using a 2',7'-Dichlorodihydrofluorescein diacetate（DCFH-DA）probe, and Western blotting was performed to detect nuclear factor erythroid2-related factor 2(Nrf2), Kelch like epichlorohydrin related protein 1(Keap1), glutamate-cysteine ligase catalytic subunit (GCLC), superoxide dismutase (SOD), and catalase (CAT) protein expressions. Additionally, ML385 was used to inhibit Nrf2 expression to evaluate its role in osteoclast differentiation and oxidative stress. In vivo experiment: an osteoporosis model was established in OVX mice. The mice were divided into sham, OVX, OVX+estradiol (E2), OVX+VA50 mg/kg, and OVX+VA100 mg/kg (n= 6 per group) groups. Femoral bone structure was analyzed using micro computed tomography（Micro-CT）. Serum RANKL and osteoprotegerin (OPG) levels were assessed by enzyme linked immunosorbent assay (ELISA), and serum oxidative stress markers (SOD, CAT, and malondialdehyde (MDA)) were also quantified. Nrf2 expression in femur sections was evaluated immunofluorescently. Results In vitro: VA at concentrations of 1-500 μmol/L was non-toxic to RAW264.7 cells. Osteoclast differentiation, protein expression, and ROS levels were significantly elevated in the Diff group compared to the NC group (P<0.05). VA (200 μmol/L) significantly inhibited osteoclast differentiation, decreased protein expression and ROS levels, promoted Nrf2 nuclear translocation, and increased antioxidant enzyme (GCLC, SOD, CAT) expression (P<0.05). These changes were reversed after the inhibition of Nrf2 by ML385 (P<0.05). In vivo: compared to the sham group, OVX mice exhibited significantly reduced femoral structural mass, increased serum RANKL and MDA levels, and decreased serum OPG, SOD, and CAT levels, along with reduced Nrf2 expression (P<0.05). VA (100 mg/kg) treatment significantly improved bone structure, reduced serum RANKL and MDA levels, increased serum OPG, SOD, and CAT levels, and elevated Nrf2 expression compared to the OVX group (P<0.05). Conclusion VA mitigates osteoporosis in OVX mice by activating the Nrf2 signaling pathway, and thereby inhibiting osteoclast differentiation and oxidative stress.

Objective To investigate the protective effects and mechanism of sodium butyrate (NaB) on dextran sulfate sodium salt (DSS) induced inflammatory bowel disease in mice. Methods Thirty-eight 7-week-old C57BL/6J mice were randomly divided into control group, model group, NaB (500 mg/(kg·d) ig) group and 5-aminosalicylic acid (5-ASA) group (150mg/(kg·d )ig). NaB administration commenced 3 days before DSS induction and continued throughout the experimental period. During molding with DSS, the control group received sterile water, while the other three groups were given 2.5% DSS for 6 days and followed by sterile water until sacrifice. On day 7, mice were euthanized for colon length measurement and tissue weight analysis. The body weight, disease activity index (DAI) and colon length among different groups were compared. Colon pathology was evaluated via HE staining, and the number of goblet cells in the colon was observed after AB-PAS staining. To assess the degrees of ferroptosis, GSH, Fe2+, MDA levels and SOD activity were measured. The WB method was used to detect the expression of GPX4 and SLC7A11 and the phosphorylation levels of ERK and STAT3. IHC was used to detect the expression level of GPX4. Results Compared to the control group, the model group exhibited significant weight loss (P<0.001), elevated DAI (P<0.001), and shortened colon length (P<0.001). HE staining showed colon cell infiltration, shallow crypt, disappeared villi structure. The AB-PAS staining showed that the number of goblet cells was decreased. Meanwhile, both decreased expression of GPX4 and SLC7A11(P<0.05, P<0.05) and suppressed phosphorylation of ERK and STAT3 (P<0.05, P<0.05) indicated that ERK and STAT3 phosphorylation were inhibited and ferroptosis occured. Compared to the model group, the NaB group displayed reduced DAI (P<0.01), increased colon length (P<0.001). HE staining showed that colon structure was recoved AB-PAS staining indicated increased goblet cells. GSH level and SOD activity were increased (P<0.01, P<0.01), while MDA and Fe2+ levels decreased significantly (P<0.01, P<0.01). GPX4 and SLC7A11 protein expressions were increased (P<0.01, P<0.05), and the phosphorylation of ERK and STAT3 was significantly enhanced (P<0.05, P<0.05). Conclusion Sodium butyrate may play a protective role in inflammatory bowel disease through ERK and STAT3 phosphorylation and ferroptosis inhibition.

Objective To investigate the protective action and molecular mechanisms of fucoxanthin (Fx) on cisplatin-induced kidney injury in mice. Methods Fifty mice were divided into a control group (n = 10) and an experimental group (n = 40). The experimental group received an intraperitoneal injection of cisplatin (7 mg/kg) once per week for four consecutive weeks to induce kidney injury. The experimental group was then further divided into four subgroups: model group, positive drug amifostine group (10 mg/kg), low-dose Fx group (50 mg/(kg·d)), and high-dose Fx group [100 mg/(kg·d)]. The normal and model groups received a standard diet, while the other three groups underwent respective interventions for another four weeks. At the end of the experiment, the mice were sacrificed to measure serum levels of creatinine (CRE), blood urea nitrogen (BUN), and uric acid (UA). Oxidative enzyme activity, inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), as well as kidney injury markers kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL), were assessed in kidney tissues. Histopathological changes in the kidney were evaluated using hematoxylin and eosin (HE) staining. Western blot analysis was performed to detect the expressions of oxidative stress-related nuclear factor erythroid 2-related factor 2 (Nrf2) family members and ferroptosis-related glutathione peroxidase 4 (GPX4) proteins. Immunohistochemistry was also used to observe Nrf2 and GPX4 protein levels in kidney tissues. Results Fx intervention reduced serum CRE, BUN, and UA levels in mice, decreased TNF-α, IL-1β, and IL-6 levels in the kidney, increased antioxidant enzyme activity, and lowered KIM-1 and NGAL levels. Renal histopathological changes were also improved. Additionally, Fx increased the expressions of Nrf2, heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), and GPX4 proteins. Immunohistochemical analysis showed that Fx treatment led to increased Nrf2 and GPX4 protein expression in kidney tissues. Conclusion Fx protests against cisplatin-induced kidney injury in mice. The mechanism may involve alleviation of inflammation and oxidative stress, and inhibition of ferroptosis via activation of the Nrf2/GPX4 signaling pathway.

Objective To explore the effect of different acute high-altitude exposure durations on appetite and intestinal flora in mice. Methods Thiry SPF C57BL/6J male mice aged 7-8 weeks were randomly divided into 3 groups, with 10 mice in each group: plain control group (group P), acute plateaus 1 day group (group G1), and acute plateaus 7 days group (group G7). Among them, Group G7 was transferred to the plateau environment simulation cabin (simulated altitude of 5 000 m) immediately after the experiment began until the experiment ended. Group P was fed in the plain animal house. Group G1 was fed in the plain animal house for 3 days, and then transferred to the simulated cabin of plateau environment (simulated altitude of 5 000 m) for 1 day. During the experiment, the body weight and food intake were recorded every day. At the end of the environmental simulation, feces samples were collected into freezing tube, and blood samples were collected from orbital vein and serum was separated. The contents of NPY and PYY in the serum were determined by ELISA kits. After DNA extraction from mouse feces samples, the V3-V4 region in the variable region of 16S rDNA was selected for PCR amplification, DNA sequencing analysis and functional classification annotation. Results The acute plateaus exposure obviously inhibited the appetite of mice, and at the same time caused the weight loss. After entering the plateau, serum content of PYY increased and the NPY decreased. Among them, there was a significant difference between the group G1 and the group P (P<0.05). The low-pressure hypoxia exposure affected the composition of intestinal flora diversity in mice. The relative abundance of probiotics such as Bifidobacterium decreased, while the relative abundance of Enterococcus increased. The functional annotation results of COG gene showed that the functional characteristics of carbohydrates, amino acids and energy metabolism in the intestinal flora were increased. Rapid entry into the plateau environment adversely affected the generation and transformation of energy in intestinal flora and the expression of related genes such as biosynthesis, transport and catabolism of secondary metabolites. Conclusion Acute high-altitude exposure significantly suppresses the appetite and affected the composition of intestinal flora diversity.

With the accelerating global population aging and the growing burden of chronic diseases, unhealthy lifestyle habits further increase the risk of age-related diseases such as diabetes, cardiovascular diseases, and neurodegenerative disorders. Time-restricted eating, a dietary pattern that limits the eating time window without restricting total caloric intake, food variety, and quantities, has been shown to have significant potential for promoting healthy aging. Accumulating evidences indicate that time-restricted eating helps regulate circadian rhythm disturbances caused by long-term unhealthy habits (such as sleep deprivation and irregular eating patterns) and has positive effects on weight management, blood glucose levels, lipid metabolism, cardiovascular health, and cognitive function with high compliance. Although the health benefits of time-restricted eating are widely recognized, further research is needed to evaluate its long-term effects and applicability, so as to provide a solid scientific foundation and practical guidance for promoting healthy aging.

Depression is one of the most common mental disorders. Zinc is the only identified endogenous ligand for G protein-coupled receptor 39 (GPR39) to date. GPR39 is widely distributed in the nervous system. Recent studies have shown a close association between zinc and its receptor GPR39 and depression. Abnormal expression and functional changes of GPR39 can affect neurotransmitter balance and neural plasticity, thereby influencing the development of depression. Agonists of GPR39 have shown certain potential application value in the prevention and treatment of depression.

As the aging of the population intensifies, the attention paid to elderly diabetic patients is increasing. The physiological changes brought about by aging are closely related to the onset and progression of diabetes. The clinical manifestations and nutritional needs of elderly diabetic patients differ from those of younger patients. Targeted dietary therapy is of great importance for the management of diabetes in the elderly. We outlines the mechanisms linking aging and diabetes development, elucidates the nutritional and metabolic changes in elderly diabetic patients and focuses on the nutritional therapy for elderly diabetic patients, so as to provide new insights into the prevention and treatment of diabetes in the elderly.