This study elucidated the impacts of coenzyme Q10 (COQ10) supplementation in a high-fat diet (HFD) on growth, lipid metabolism and mitochondrial function in spotted seabass (Lateolabrax maculatus). Totally five diets were formulated: a diet with normal fat content (11 % lipid, NFD), a HFD (17 % lipid) and three additional diets by supplementing 5, 20 or 80 mg/kg of COQ10 to the HFD. After an 8-week culture period, samples were collected and analysed. The results demonstrated that COQ10 inclusion prevented the HFD-induced deterioration of growth performance and feed utilisation. COQ10 alleviated the deposition of saturated fatty acids following HFD intake and promoted the assimilation of n-3 and n-6 PUFA. Moreover, COQ10 administration inhibited the surge in serum transaminase activity and reduced hepatic lipid content following HFD ingestion, which was consistent with the results of oil red O staining. In addition, HFD feeding led to reduced hepatic citrate synthase and succinate dehydrogenase activities and decreased ATP content. Notably, COQ10 administration improved these indices and up-regulated the expression of mitochondrial biogenesis-related genes (pgc-1α, pgc-1β, nrf-1, tfam) and autophagy-related genes (pink1, mul1, atg5). In summary, supplementing 20–80 mg/kg of COQ10 in the HFD promoted growth performance, alleviated hepatic fat accumulation and enhanced liver mitochondrial function in spotted seabass.

The study of polyphenols’ effects on health has been gaining attention lately. In addition to reacting with important enzymes, altering the cell metabolism, these substances can present either positive or negative metabolic alterations depending on their consumption levels. Naringenin, a citrus flavonoid, already presents diverse metabolic effects. The objective of this work was to evaluate the effect of maternal naringenin supplementation during pregnancy on the tricarboxylic acid cycle activity in offspring’s cerebellum. Adult female Wistar rats were divided into two groups: (1) vehicle (1 ml/kg by oral administration (p.o.)) or (2) naringenin (50 mg/kg p.o.). The offspring were euthanised at 7th day of life, and the cerebellum was dissected to analyse citrate synthase, isocitrate dehydrogenase (IDH), α-ketoglutarate dehydrogenase (α-KGDH) and malate dehydrogenase (MDH) activities. Molecular docking used SwissDock web server and FORECASTER Suite, and the proposed binding pose image was created on UCSF Chimera. Data were analysed by Student’s t test. Naringenin supplementation during pregnancy significantly inhibited IDH, α-KGDH and MDH activities in offspring’s cerebellum. A similar reduction was observed in vitro, using purified α-KGDH and MDH, subjected to pre-incubation with naringenin. Docking simulations demonstrated that naringenin possibly interacts with dehydrogenases in the substrate and cofactor binding sites, inhibiting their function. Naringenin administration during pregnancy may affect cerebellar development and must be evaluated with caution by pregnant women and their physicians.

Suboptimal vitamin B2 status is encountered globally. Riboflavin deficiency depresses growth and results in a fatty liver. The underlying mechanisms remain to be established and an overview of molecular alterations is lacking. We investigated hepatic proteome changes induced by riboflavin deficiency to explain its effects on growth and hepatic lipid metabolism. In all, 360 1-d-old Pekin ducks were divided into three groups of 120 birds each, with twelve replicates and ten birds per replicate. For 21 d, the ducks were fed ad libitum a control diet (CAL), a riboflavin-deficient diet (RD) or were pair-fed with the control diet to the mean daily intake of the RD group (CPF). When comparing RD with CAL and CPF, growth depression, liver enlargement, liver lipid accumulation and enhanced liver SFA (C6 : 0, C12 : 0, C16 : 0, C18 : 0) were observed. In RD, thirty-two proteins were enhanced and thirty-one diminished (>1·5-fold) compared with CAL and CPF. Selected proteins were confirmed by Western blotting. The diminished proteins are mainly involved in fatty acid β-oxidation and the mitochondrial electron transport chain (ETC), whereas the enhanced proteins are mainly involved in TAG and cholesterol biosynthesis. RD causes liver lipid accumulation and growth depression probably by impairing fatty acid β-oxidation and ETC. These findings contribute to our understanding of the mechanisms of liver lipid metabolic disorders due to RD.

The effect of accelerated aging (AA) and seed priming on specific seed enzymes was studied in soybeans. Aging seeds for 48 and 96 h at 41°C and 100% humidity reduced germination from 92% to 68% and 0%, respectively. Malate dehydrogenase (MDH) glutamate dehydrogenase (GDH), and esterase were assayed in extracts from dry and imbibing seeds. Malate dehydrogenase activity was the least affected by AA treatments. Certain GDH isozyme activity was reduced by 17% after 48 h of AA and almost completely lost after 96 h. Imbibing for 24 h increased GDH activity in 48 h-accelerated-aged seeds but not the 96 h-aged seeds. Two esterase isozymes in dry seeds showed a 77% loss of activity after 48 h of AA. This treatment increased the total esterase activity, with the greatest activity observed after 96 h of AA. This was due to the appearance of a diffuse high molecular weight (HMW) region of activity observed on native polyacrylamide gels and specifically induced in the embryonic axes. Imbibing 48-h-accelerated-aged seeds for 48 h caused a reappearance of the two esterase enzymes lost during aging. The HMW esterase staining region also appeared after imbibing unaged seeds for 24 h. Seed priming, caused a response similar to imbibition for each enzyme except the HMW esterase activity. Priming 48-h-accelerated-aged seeds reduced the HMW esterase activity. This was not observed during imbibition of aged seeds and indicates the first identification of a specific enzymatic response unique to a seed priming treatment.

This work presents a cooperative effort to integrate new molecular (isozyme and SSU analyses) characters into the morphological taxonomy of the genus Gigaspora (Glomales). Previous analyses of published Gigaspora SSU sequences indicated the presence of a few polymorphic nucleotides in the region delimited by primers NS71-SSU 1492′. In our study, the SSU of 24 isolates of arbuscular mycorrhizal (AM) fungi from the Gigasporaceae were amplified and the NS71-SSU 1492′ region was directly sequenced. The corresponding sequences of four more isolates of AM fungi from Gigasporaceae, already published, were also included in our analyses. Three Gigaspora groups were identified on the basis of a 6 nucleotide-long ‘molecular signature’: Gigaspora rosea group (G. rosea+G. albida), Gigaspora margarita group (G. margarita+G. decipiens) and Gigaspora gigantea, which constituted a group by itself. The isozyme profiles (malate dehydrogenase, MDH) of 12 of these 28 isolates, and seven other isolates not sequenced, were compared. The results obtained further supported the grouping of isolates provided by the SSU analysis. Both SSU and MDH analysis indicated that two out of the 35 isolates had been misidentified, which was confirmed when their morphology was reassessed. The use of the Gigaspora intrageneric molecular signature as a quick, unambiguous and objective method to recognize Gigaspora isolates under any (field or laboratory) experimental conditions is suggested.