The effect of previous frozen storage (-18 °C for 6 months) and different coating media (aqueous: water and brine; oily: sunflower, refined olive, and extra-virgin olive oils) on the essential macroelement and trace element content of canned Atlantic mackerel (Scomber scombrus) was studied. Previous frozen storage led to an increased (p < 0.05) content of canned samples of K (oil-coated samples) and Ca (all coating conditions) and to a decreased (p < 0.05) content of P (aqueous-coating samples) and S (water- and oil-coated samples). For trace elements, a content increase (p < 0.05) in Cu and Se (brine-canned samples) and Mn (water- and refined-olive-oil-coated samples) was detected in canned fish muscle with frozen storage. Concerning the coating effect, aqueous-coating samples showed lower (p < 0.05) Mg, P, S, K, and Ca contents than their corresponding oil-coated samples. For trace elements, lower average contents were found for Co, Cu, Mn, Se, and Fe in aqueous-coating fish muscle when compared to their counterparts coated in oily media. Content changes in the different elements in canned fish muscle are discussed based on interactions with other tissue constituents and modifications that such constituents undergo during processing (i.e., protein denaturation, liquor losses from the muscle, lipid changes).

Fatty acid oxidation disorders (FAODs) are inborn errors of metabolism (IEMs) caused by defects in the fatty acid (FA) mitochondrial β-oxidation. The most common FAODs are characterized by the accumulation of medium-chain FAs and long-chain (3-hydroxy) FAs (and their carnitine derivatives), respectively. These deregulations are associated with lipotoxicity which affects several organs and potentially leads to life-threatening complications and comorbidities. Changes in the lipidome have been associated with several diseases, including some IEMs. In FAODs, the alteration of acylcarnitines (CARs) and FA profiles have been reported in patients and animal models, but changes in polar and neutral lipid profile are still scarcely studied. In this review, we present the main findings on FA and CAR profile changes associated with FAOD pathogenesis, their correlation with oxidative damage, and the consequent disturbance of mitochondrial homeostasis. Moreover, alterations in polar and neutral lipid classes and lipid species identified so far and their possible role in FAODs are discussed. We highlight the need of mass-spectrometry-based lipidomic studies to understand (epi)lipidome remodelling in FAODs, thus allowing to elucidate the pathophysiology and the identification of possible biomarkers for disease prognosis and an evaluation of therapeutic efficacy.

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.

Phenylketonuria (PKU) is the most prevalent inborn error of amino acid metabolism. The disease is due to the deficiency of phenylalanine (Phe) hydroxylase activity, which causes the accumulation of Phe. Early diagnosis through neonatal screening is essential for early treatment implementation, avoiding cognitive impairment and other irreversible sequelae. Treatment is based on Phe restriction in the diet that should be maintained throughout life. High dietary restrictions can lead to imbalances in specific nutrients, notably lipids. Previous studies in PKU patients revealed changes in levels of plasma/serum lipoprotein lipids, as well as in fatty acid profile of plasma and red blood cells. Most studies showed a decrease in important polyunsaturated fatty acids, namely DHA (22:6n-3), AA (20:4n-6) and EPA (20:5n-6). Increased oxidative stress and subsequent lipid peroxidation have also been observed in PKU. Despite the evidences that the lipid profile is changed in PKU patients, more studies are needed to understand in detail how lipidome is affected. As highlighted in this review, mass spectrometry-based lipidomics is a promising approach to evaluate the effect of the diet restrictions on lipid metabolism in PKU patients, monitor their outcome, namely concerning the risk for other chronic diseases, and find possible prognosis biomarkers.

Several diseases and disorders have been suggested to be associated with zinc deficiency, especially learning and memory impairment. To have better understanding about the connection between lipid changes and cognitive impairments, we investigated the effects of a zinc-chelated diet on certain brain lipids of Drosophila melanogaster by using time-of-flight secondary ion mass spectrometry (ToF-SIMS). The data revealed that there are increases in the levels of phosphatidylcholine and phosphatidylinositol in the central brains of the zinc-deficient flies compared to the control flies. In contrast, the abundance of phosphatidylethanolamine in the brains of the zinc-deficient flies is lower. These data are consistent with that of cognitive-diminishing drugs, thus providing insight into the biological and molecular effects of zinc deficiency on the major brain lipids and opening a new treatment target for cognitive deficit in zinc deficiency.

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.

BACKGROUND: Galangin, a natural flavonoid, is found in honey and Alpinia officinarum Hance (Zingiberaceae). Galangin has antiviral, antimicrobial, antidiabetic and anticancer properties, without side effects. The effects of galangin on hyperglycaemia and lipid abnormalities are not known.
OBJECTIVE: To elucidate the effectiveness of galangin on hyperglycaemia-associated complications and lipid changes in rats with streptozotocin (STZ)-induced hyperglycaemia.
METHODS: Diabetes was induced in adult Wistar rats by administering 40 mg/kg of STZ. In our previous study, galangin had no toxicity at concentrations up to 320 mg/kg. Therefore three doses of galangin (4, 8 or 16 mg/kg BW) or glibenclamide (600 µg/kg BW) were administered daily to diabetic rats orally for 45 days.
RESULTS: Diabetic rats showed a significant (p < 0.05) increased levels of plasma glucose (281.10 mg/dL) and decreased levels of insulin (6.01 μU/mL). Additionally, diabetic rats showed a significant (p < 0.05) increased levels of plasma lipid profiles such as total cholesterol (149.05 mg/dL), triglycerides (143.28 mg/dL), free fatty acids (139.37 mg/dL), phospholipids (127.53 mg/dL), plasma low-density lipoprotein-cholesterol (98.72 mg/dL), plasma very low-density lipoprotein-cholesterol (28.65 mg/dL), and significant (p < 0.05) decreased in plasma high-density lipoprotein-cholesterol (21.68 mg/dL). When galangin was administered to the hyperglycaemic rats, plasma glucose and insulin levels and lipid profiles reverted to levels similar to those in healthy control rats.
CONCLUSIONS: Administration of galangin reduced hyperlipidaemia related to the risk of diabetic complications and could be beneficial for diabetic hyperlipidaemic patients. Further work detailing its mechanism-of-action for improving hyperglycaemic-associated lipid abnormalities is needed.

Etiolated seedlings of Avena sativa L. were illuminated under fluorescent light of 1,500 lux at 25°C and the lipid changes in their first leaves and isolated plastids were followed during 24 hr of greening. Lipid changes were divided into a degradation phase [0 hr of illumination (hr-L) to 3 hr-L] and a synthetic phase (3 hr-L to 24 hr-L). In the degradation phase, which paralleled prolamellar body transformation in the plastids, both plastidic lipids, monogalactosyldiglyceride (MGDG), digalactosyldiglyceride (DGDG), sulfoquinovosyldiglyceride (SQDG) and phosphatidylglycerol (PG), and extraplastidic lipids, phosphatidylcholine (PC), phosphatidylethanolamine (PE) and phosphatidylinositol (PI), were partially degraded. Plastidic lipids (except DGDG) began to increase at 1.5 hr-L without the de novo synthesis of fatty acids, at the same time that there was a temporary accumulation of diglyceride, whose fatty acids were similar to the fatty acids of phospholipids such as PC, PE and PI, but different from the fatty acids of DGDG. This suggests that there is conversion of phospholipids to plastidic lipids during the later degradation phase. During the later degradation phase and the early synthetic phase (until 6 hr-L), plastid division occurred, resulting in a 30% increase in the plastid number per cell. Plastidic lipids were synthesized rapidly during the synthetic phase, in accordance with the beginning of light-enhanced fatty acid synthesis and thylakoid proliferation. In addition, the fatty acid composition of the plastidic lipids changed markedly throughout the synthetic phase : in MGDG, DGDG and SQDG, α-linolenate increased as linoleate decreased at both the C-1 and C-2 positions of sn-glycerol; in PG, α-linolenate increased in compensation for the decrease in linoleate at C-1 and hexadecenoate (3t) appeared and increased in compensation for the decrease in palmitate at C-2. This is evidence of the parallel desaturation of linoleate to linolenate at both C-1 and C-2 of MGDG, DGDG and SQDG, and also of the position-specific desaturation of linoleate to linolenate at C-1 of PG and of palmitate to hexadecenoate at C-2 of PG. The formation of hexadecenoate was entirely light-dependent. Extraplastidic lipids increased slightly in the early synthetic phase (3 hr-L to 6 hr-L), but declined later.