Obesity in women of reproductive age is often associated with low-grade inflammation and functional iron deficiency. Epigallocatechin gallate (EGCG), a major green tea catechin, has antioxidant, anti-inflammatory, and metabolic-regulating properties but may also interfere with iron absorption. This randomized, double-blind, placebo-controlled pilot study evaluated the effects of EGCG on lipid profile, inflammation, iron status, and plasma metabolomics in women with obesity. Seventeen participants (BMI ≥30 kg/m2; age 20-44 years) received 400 mg/day EGCG (green tea extract: 98% polyphenols, 60% catechins, ∼50% EGCG) or placebo for eight weeks. Outcomes included serum lipids, inflammatory markers (CRP, IL-6, TNF-α, IL-10), iron indices (ferritin, hepcidin, serum iron, transferrin saturation), glucose, and metabolomics. No between-group difference remained significant after correction for multiple comparisons. Total cholesterol (β = -10.9 mg/dL; p  = 0.16) and LDL-C (β = -9.7 mg/dL; p  = 0.16) showed decreases, and IL-6 the largest, though nonsignificant, reduction (p  = 0.09); other cytokines and glucose were unchanged. Metabolomics identified 29 nominally differential metabolites enriched in lipid metabolism, plasmalogen biosynthesis, and mitochondrial β-oxidation, none surviving FDR correction. Iron status was stable. These findings suggest metabolic effects of EGCG and support short-term safety at 400 mg/day. Larger, longer trials with targeted metabolomics are warranted.

Fractionated low dose ionizing radiation (LDIR) can induce various biological effects, which are key potential triggers for the development of radiation-induced lung injury (RILI). This study aims to investigate the effects of fractionated LDIR on early-stage cellular senescence, as well as on the levels of oxidation-antioxidation and DNA damage repair, in mouse lung tissue. C57BL/6J mice were exposed to fractionated LDIR, and subsequent assays were performed to evaluate the biological effects. Compared with the control group, mice in all dose groups showed the following changes: varying degrees of pathological alterations in lung tissue; elevated SA-β-Gal activity and upregulated expression of senescence-related genes in lung tissue; increased serum levels of urea, blood glucose (BG), and triglycerides (TG), along with reduced high-density lipoprotein cholesterol (HDL-C) levels; increased levels of oxidative damage markers in lung tissue, accompanied by elevated total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) activity, but decreased reduced glutathione (GSH) levels; upregulated expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream genes; and increased DNA damage markers in lung tissue, as well as elevated mRNA and protein levels of the DNA repair gene O6-methylguanine-DNA methyltransferase (MGMT). The oxidative damage and DNA damage potentially induced by fractionated LDIR exceeded the compensatory capacity of the repair systems, probably leading to a dual dynamic imbalance in both oxidation-antioxidation and DNA damage repair. These may contribute to the progression of cellular senescence in lung tissue and the initiation of early-stage RILI.

Microbial bile salt hydrolase (BSH) plays a central role in shaping bile acid composition and gut-liver metabolic signaling, yet its therapeutic potential in metabolic dysfunction-associated steatohepatitis (MASH) remains incompletely defined. Here, we evaluated the efficacy of the non-absorbable BSH inhibitor GR-7 in a diet induced mouse model of steatohepatitis using early and late intervention strategies with different dosing regimens. GR-7 reduced food intake and exerted stage- and dose-dependent therapeutic effects, with early intervention robustly suppressing hepatic fibrosis even at low dose, whereas late-stage administration of high-dose GR-7 markedly reduced hepatic steatosis and inflammation, as evidenced by decreased liver weight, hepatic triglyceride and cholesterol levels, and plasma ALT. Although late intervention did not result in statistically significant histological reversal of fibrosis, a trend toward improvement was observed, together with suppression of fibrogenic gene expression, suggesting that prolonged treatment may further enhance antifibrotic efficacy. Mechanistically, GR-7 effectively inhibited microbial BSH activity in vivo, leading to reduced cecal unconjugated primary and secondary bile acids-including deoxycholic acid and lithocholic acid, which was associated with improved gut barrier integrity and reduced hepatic inflammation. In parallel, BSH inhibition reprogrammed hepatic bile acid metabolism toward activation of the alternative CYP27A1-mediated synthesis pathway, accompanied by reduced food intake, thereby contributing to improved hepatic lipid accumulation. Furthermore, late-stage high-dose treatment selectively remodeled the hepatic immune landscape rather than fully restoring homeostasis, highlighting immune recalibration as a key component of therapeutic response. Together, these findings identify microbial BSH inhibition as a promising microbiome-targeted therapeutic strategy for MASH.

A common concern during thyroid hormone replacement therapy is over-substitution leading to increased risk of primarily osteoporotic fracture, and adverse cardiac outcomes in particular. The addition of synthetic triiodothyronine (T3) to treatment regimens for hypothyroidism has been singled out as being associated with a higher risk of such adverse effects. While thyroid-stimulating hormone (TSH) has been a universally accepted, useful parameter for monitoring treatment responses in thyroid diseases, it is not perfect. This is highlighted by the fact, that 5-10% of patients with hypothyroidism continue to exhibit hypothyroid symptoms, despite normal circulating TSH levels.

Dietary oils are energy sources for the growth and reproduction of poultry. Soybean oil (SO) is widely used but competes with the human food supply. In this study, black soldier fly maggot oil (BSFMO) was used as a sustainable alternative to SO for improving breeder hen productivity, chick quality, and immunity. A total of 360 39-week-old Black Yao Chicken 2A breeding hens with an average body weight of 2567 ± 66 g and an egg-laying rate of 70% were randomly allocated to three dietary treatments (n = 120 per group): 2% SO, 2% SO-BSFMO blend (SMO), and 2% BSFMO. After a 5-week feeding trial, 200 eggs per group were incubated, and 120 hatched chicks per group were randomly chosen and reared for 6 weeks. Compared with the SO group, BSFMO significantly increased laying rate, egg weight, egg size, yolk weight, yolk color, and feed conversion efficiency (P < 0.05). The concentrations of follicle‑stimulating hormone, estradiol, triglyceride, and high‑density lipoprotein cholesterol in plasma were increased, while low‑density lipoprotein cholesterol was decreased (P < 0.05). BSFMO also enhanced plasma immunoglobulin A, G, M; interleukin‑2; total antioxidant capacity; superoxide dismutase; and glutathione peroxidase and decreased malondialdehyde (P < 0.05). Chicks from the BSFMO group showed higher quality, growth performance, immune status, hepatic mRNA expression of insulin‑like growth factors (IGF1, IGF2), and epigenetic regulatory genes (DNMT1, DNMT3A) (P < 0.05). In conclusion, maternal feeding with BSFMO improved the productivity and immunity of breeder hens, chick quality, and representative epigenetic gene mRNA expressions of offspring. As an alternative lipid source to soybean oil in animal nutrition, BSFMO can be used in poultry farming for safe and sustainable poultry production and can reduce food competition.

Reducing dietary nutrient density may lower the feed cost but compromise the growth performance in piglets. Given the ability of lysolecithin (LPI) to enhance nutrient utilization, its supplementation may help piglets adapt to a low-nutrient (LN) diet. This study aimed to investigate the effects of dietary LPI supplementation on growth performance, nutrient utilization, metabolism, and muscle development in piglets fed a LN diet. A total of 96 nursery piglets (17.0 ± 0.2 kg in initial body weight [BW] and 50 d of age) were randomly assigned to three groups in a randomized complete block design and received either the normal-nutrient diet (CON), a LN diet, or the LN diet supplemented with 400 mg/kg lysolecithin (LN-LPI) for 28 d. Each dietary treatment included 8 replicates of 4 piglets each. Results showed that the LN-LPI diet improved the average daily gain (ADG; P = 0.040) during the first two weeks, feed-to-gain ratio (F:G; P = 0.032), and BW (P = 0.065) throughout the experimental period, reaching levels comparable to those of piglets in the CON group. Compared with the LN diet, the growth-promoting effect of LPI may be attributed to its role in increasing the digestibility of ether extract (EE; P < 0.001) and gross energy (GE; P = 0.022) in diets, as well as increasing the relative weight of psoas major muscles (PMM) and the EE (P = 0.049) and crude protein (CP) content (P = 0.007) in muscle. Accordingly, compared with the LN diet, LPI supplementation decreased the blood urea nitrogen (P = 0.003) and total cholesterol (TC) concentrations (P = 0.017), and increased total superoxide dismutase (T-SOD) levels in plasma (P = 0.005) and liver (P = 0.006), along with the lower malondialdehyde (MDA) levels in blood (P < 0.001) and liver (P = 0.003). In addition, microarray analysis indicated that dietary LPI supplementation promoted expression of lipid synthesis and transport-related genes in the liver (FAS, P = 0.040; FABP5, P = 0.001; and SLC27A6, P = 0.025), and amino acid (AA) transport and synthesis-related genes (LAT, P = 0.021; LAMC3, P = 0.004), compared with the LN diet in muscle. In conclusion, this study demonstrated that the LN-LPI diet mitigated the compromised growth performance commonly observed under nutrient restriction, potentially mediated by improving nutrient utilization and redox status, and modulating lipid and protein metabolism.

Obesity is known to be associated with dyslipidaemia, cardiovascular disorders, oxidative stress, adipogenic and adipokine responses. The anti-obesity effect of Coula edulis nut extract (CEE) was investigated in high-fat-diet (HFD) fed obese Wistar rats. After a four-week HFD feeding, the rats received the nut extract p.o. for 5 weeks in a two-batch design. Batch I: Normal Control (ND only) Obese Control (HFD only), Standard Control (HFD + 0.03 g/kg b.w. Orlistat) and extract-treated groups 1 and 2 (HFD + CEE1g/kg b.w. and HFD + CEE2g/kg b.w., respectively). Batch II: Normal Control (ND only), Obese Control (ND only), Standard Control (ND + 0.03 g/kg b.w. Orlistat) and extract-treated groups 1 & 2 (ND + CEE1g/kg b.w. and ND + CEE2g/kg b.w., respectively). During the 5-week extract treatment, Batch I rats were fed HFD alongside, whereas the Batch II rats were fed normal diet (ND) instead. Weight gain, feed intake, anthropometric indicators, blood lipids, cardiovascular risk indices, pancreatic lipase activity, tissue lipid content, hepatic cholesterol biosynthesis, oxidative stress indices, expression of adipogenic/lipogenic genes and adipose histology were determined. Coula edulis extract was found to decrease weight gain, obesity indicators, lipogenesis, pancreatic lipase activity, cardiovascular risk factors, oxidative stress, and PPAR-γ, C/EBP-α and SREBP-1c mRNA levels (p < 0). Together, the results indicate that Coula edulis nut extract could attenuate obesity by modulating lipid digestion, cholesterol synthesis, oxidative stress and adipogenic/lipogenic transcription factors.

Exposure to per- and polyfluoroalkyl substances (PFAS) has been linked to renal impairment, but evidence on mixed PFAS exposure in the general Chinese population and the underlying mechanisms remains limited. This study therefore investigated the associations between PFAS exposure and renal function and evaluated the potential mediating role of blood lipids. Serum levels of legacy and emerging PFAS, renal function parameters, and blood lipid profiles were measured in 1,370 adult residents from Zhejiang Province, China; additionally, 452 lipid metabolites were quantified in a subset of 316 participants. Using multiple linear regression, restricted cubic splines (RCS), and mixture exposure models, we found that PFAS mixture exposure was associated with reduced renal function, with eGFR decreases ranging from 2.2% to 2.9% per quartile increase across models, and PFOA as a predominant contributor. Mediation analyses further revealed that elevated total cholesterol, low-density lipoprotein cholesterol, and disturbances in fatty acids and phospholipids mediated 6.3% to 65.9% of the association between PFAS exposure and renal function decline. Collectively, these findings suggest that mixed PFAS exposure, particularly to PFOA and PFHpA, may induce impaired renal function, with increased blood lipids playing an important mediating role.