Species producing seeds with a water-impermeable seed coat, i.e., physical dormancy (PY), dominate the dry tropical forests. Despite increasing interest and understanding of the germination ecology of a PY species, less is known about how PY break occurs, particularly what changes lead to the opening of the \'water gap\'. Based on the moisture conent (MC) attained, two ranges of PY may exist: shallow PY, a state with higher MC and seeds could reverse to a permeable state when the relative humidity increases; and absolute PY, a completely dry state. Here, we demonstrate that this MC variation between seeds affects preconditioning and the \'water-gap\' opening stages. A conceptual model developed shows a strong relationship between temperature and duration, with high temperature breaking PY in seconds, but seasonal temperature fluctuations and constant temperatures require a longer time. The duration required at any conditions to break PY is purported to depend on the hydrophobic bonds of the lipids, which are likely weakened during the preconditioning, and the amount of water influences hydrolysis, leading to the \'water-gap\' opening. We argue that the moisture content of the seeds and its interaction with biochemical compounds are a possible explanation for why only a proportion of PY seeds become permeable to water each year. Nonetheless, empirical investigations must validate these notions.

The effects of changes in lipids on the formation of Zn-protoporphyrin (ZnPP) during the processing of Nuodeng ham were analyzed using a lipidomics approach based on UHPLC-MS/MS. The Nuodeng ham samples had a strong fluorescence emission peak at 590 nm, and the fluorescence intensity increased with the processing time. Lipid profiles were mainly affected by processing time. A total of 5 lipid classes were detected, of which glycerophospholipids (GP) and glycerolipids (GL) were the most abundant lipids. Fifty differential lipid compounds were screened, which were mainly GP and GL. Correlation analysis showed that 13 differential lipid compounds were significantly positively correlated with ZnPP content, and they contained more linoleic acid and oleic acid branch chains. Meanwhile, all triglycerides (TG) were negatively correlated with heme content, and they were enriched in stearic acid and palmitic acid branch chains. These findings can deepen the understanding of the relationship between ZnPP and lipids.

Lipidomic profiles changes of the Sanhuang chicken breast meat during cold storage (4 °C) were analyzed using ultra-high performance liquid chromatography coupled with mass spectrometry (UHPLC-MS)-based lipidomic analysis. Total lipids content decreased 16.8% after storage. Triacylglycerol (TAG), phosphatidylcholine (PC) and phosphatidylethanolamine (PE) significantly decreased, while lysophosphatidylcholine (LPC) and lysophosphatidylethanolamine (LPE) increased. Particularly, there was a trend that TAGs with fatty acids of 16:0 and 18:1, and phospholipids containing 18:1, 18:2 and 20:4 were more likely to be downregulated. The increase in the ratio of lysophospholipids/phospholipids and the degree of lipid oxidation demonstrated oxidation and enzymatic hydrolysis are potentially responsible for the lipid transformation. Moreover, 12 lipid species (P < 0.05, VIP > 1, FC < 0.8 or >1.25) were identified to be associated with the spoilage of meat. Glycerophospholipid metabolism and linoleic acid metabolism were the key metabolic pathways involved in the lipid transformations of chilled chicken.

Salted egg yolk (SEY) becomes easily \"muddy\" during storage, leading to a decrease in the quality of salted eggs. The mechanism of SEY mudding was studied in this paper. The results showed that SEY hydrogen proton binding decreased, and SEY water and lipid fluidity increased during storage. In addition, the degree of lipid oxidation and monounsaturated fatty acids in salted egg yolk lipids (SEYL) increased, and primary oxidation products and secondary oxidation products were formed. Moreover, the structure of SEY was degraded to release lipids and proteins, and these proteins and lipids were re-emulsified to form new aggregates. Finally, by PLS-DA modeling analysis, it was found that the content of ω-3 polyunsaturated fatty acids and phospholipids changed significantly after SEY became muddy. These results suggest that the muddiness of SEY can primarily be attributed to higher fluidity and protein-lipid re-emulsification, and secondarily to the oxidation of SEYL.

There is an urgent need to explore the salt penetration and water migration in the cooked salted egg yolk (CSEY) gel. The aim of this study was to investigate the effect of salt and water on the physicochemical, structural and flavor characteristics of CSEY gel stored at 25 °C. The hardness of the yolk increased significantly (608.0 g → 2730.7 g) during storage. The results of LF-NMR showed that the free water content in the yolk gel was enhanced. The microstructure of CSEY could be observed by SEM, which showed that during storage, polyhedral particles were dispersed due to the heating process. In addition, ethyl acetate (71.9 %) was completely undetectable in the CSEY-21 d. In summary, the sample at and before 14 d of storage had good processing value. Therefore, this work would provide theoretical guidance for the low-sodium pickling of SEY (salted egg yolk) and its suitable storage methods.

To investigate whether non-high-density lipoprotein cholesterol (Non-HDL-C), remnant cholesterol (RC), and the ratios of lipid indexes are more closely associated with early progression of kidney dysfunction than traditional lipid indexes; and to explore the association between changes in serum lipids during follow-up and annual decline rate in estimated glomerular filtration rate (eGFR).
In this prospective cohort study, 3909 participants with normal eGFR and age≥40 years at baseline were followed for 3.3 years. Progression of kidney dysfunction was assessed as annual decline rate in eGFR. Spearman correlation analysis, linear correlation models, and multiple logistic regression were used to assess the associations between lipid indexes at baseline/both baseline and follow-up and the annual decline rate in eGFR.
Compared with ΔLDL-C (β = 0.412), other lipid indexes such as ΔLDL-C/HDL-C (β = 0.565), ΔTC/HDL-C (β = 0.448), and ΔNon-HDL-C/HDL-C (β = 0.448) were more closely associated with annual decline rate in eGFR. High TG/HDL-C (OR = 1.699(1.177-2.454)) and TC/HDL-C (OR = 1.567(1.095-2.243)) at baseline, as well as high TC/HDL-C (OR = 1.478 (1.003-2.177)) and TG/HDL-C (OR = 1.53(1.044-2.244)) at both baseline and follow-up were associated with the annual decline rate in eGFR <0.5. High Non-HDL-C (OR = 1.633(1.025-2.602)) and LCI (OR = 1.631(1.010-2.416)) at both baseline and follow-up resulted in a 63% increase in risk of annual decline rate in eGFR >1.
High Non-HDL-C, RC and the ratios of lipid indexes were more closely associated with early progression of kidney injury than the increase of traditional lipid indexes. These lipid indexes should be monitored, even in participants with normal traditional serum lipid levels.

Background: Excess selenium has been related with adverse lipid levels in previous epidemiological studies. Meanwhile, a functional variant in SEPP1 (encodes selenoprotein P), namely rs7579, has been suggested to modulate lipid metabolism. However, the interactions between selenium status and rs7579 polymorphism on lipid changes remain unclear. Objective: To examine whether the associations between plasma selenium and 3-year lipid changes is modified by rs7579 polymorphism. Methods: A prospective cohort study was conducted among 1,621 individuals to examine the associations between baseline plasma selenium and 3-year lipid changes, as well as the interactions between plasma selenium and rs7579 polymorphism on lipid changes. Results: The median (interquartile range) concentration of plasma selenium was 91.68 (81.55-104.92) μg/L. Higher plasma selenium was associated with adverse 3-year lipid changes. Comparing the highest to the lowest quartiles of plasma selenium concentrations, 3-year lipid changes were elevated by 8.25% (95% CI: 1.54-14.96%) for triglycerides (P = 0.016), 5.88% (3.13-8.63%) for total cholesterol (P < 0.001), 7.37% (3.07-11.67%) for low-density lipoprotein cholesterol (P = 0.0008), 6.44% (2.66-10.21%) for non-high-density lipoprotein cholesterol (P = 0.0009), 4.99% (0.62-9.36%) for total cholesterol/high-density lipoprotein cholesterol ratio (P = 0.025), and 7.00% (1.55-12.46%) for low-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratio (P = 0.012). In analyses stratified by rs7579 genotypes, positive associations between plasma selenium concentrations and 3-year changes in triglycerides, TC, LDL-C, non-HDL-C, TC/HDL-C ratio, and LDL-C/HDL-C ratio were observed among CC genotype carriers, but negative associations between plasma selenium and TC/HDL-C ratio, and LDL-C/HDL-C ratio were observed among TT genotype carriers. Conclusions: Our findings suggested that plasma selenium was associated with 3-year lipid changes differentially by rs7579 genotypes, and higher plasma selenium was associated with adverse lipid changes among rs7579 CC genotype carriers, but not among T allele carriers.

Lipid profiles are influenced by both genetic and environmental factors. Genetic variants in the APOA4-APOA5-ZPR1-BUD13 gene cluster and aberrant sleep duration were independently identified to be associated with lipids in previous studies. We aimed to investigate whether sleep duration modified the genetic associations with longitudinal lipids changes.
Four single nucleotide polymorphisms (SNPs), rs17119975, rs651821, rs7396835, and rs964184 in the APOA4-APOA5-ZPR1-BUD13 gene cluster were genotyped among 8648 apparently healthy subjects from the Dongfeng-Tongji (DFTJ) cohort. Information on sleep duration was obtained by questionnaires. Changes in total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), were evaluated from baseline to 5-year follow-up.
After multivariate adjustments, we found that rs651821 and weighted genetic risk score (GRS) were significantly associated with increased triglyceride, and the genetic association with triglyceride change consistently strengthened across sleep duration categories. The differences in triglyceride changes per increment of risk allele for rs651821 were 0.028 (SE = 0.017, p = 0.112), 0.051 (SE = 0.009, p < 0.001), and 0.064 (SE = 0.016, p < 0.001) in individuals with sleep duration ≤7, >7-<9, and ≥9 h, respectively (p interaction = 0.031). The GRS also showed a significant interaction with sleep duration categories for triglyceride change (p interaction = 0.010). In addition, all of the four SNPs and GRS were inversely related to HDL-c changes.
Longer sleep duration might exacerbate the adverse effects of SNPs in APOA4-APOA5-ZPR1-BUD13 gene cluster on 5-year triglyceride changes.

Myostatin (MSTN) lacking could lead to enhanced muscle growth and lipid metabolism disorder in animals. Plenty of researches have been performed to warrant a better understanding of the mechanisms underlying the enhanced muscle growth; however, mechanisms for lipid metabolic changes are poorly understood. In this study, MSTN-depletion loaches Misgurnus anguillicaudatus (MU for short) were firstly generated by CRISPR/Cas9 technique. Based on histological observation, we found that skeletal muscle fat accumulation in MU sharply reduced compared with wild-type loaches (WT for short). To further investigate the fat change, muscle lipidomic analysis was performed. There were no significant differences in three membrane phospholipid contents between WT and MU. The contents of six other major lipid species in MU muscles were all significantly lower than those in WT muscles, indicating that MSTN deficiency could obviously decrease muscle lipid production in the loach. Meanwhile, it was also supported by results of three lipogenesis-related genes\' expressions. And then combined with muscle ATP determination and gene expression profiles of the five mitochondrial respiration chain complexes, we speculated that MSTN lacking may cause the weak of mitochondrial respiration functions in the loach muscles, leading to ATP synthesis decreasing and finally reducing the production of lipids.