Search Results (6,183)

In this study, the chemical composition of highland barley (HB), microwave fluidization HB (HB-1), extrusion and puffing HB (HB-2), and ultrafine pulverization HB (HB-3) were investigated based on untargeted metabolomics. In addition, RNA-seq transcriptomics, real-time polymerase chain reaction (qRT-PCR) and Western blot (WB) analysis were used to investigate the lipid metabolism mechanism of HB-1, induced by a high fat and cholesterol diet (HFCD). The results indicated that a total of 1292 metabolites were detected and classified into 78 distinct classes in the untargeted metabolomics analysis including fatty acyls, carboxylic acids and derivatives, glycerophospholipids, organooxygen compounds, prenol lipids, and so on. HB-1, HB-2, and HB-3 all increased the levels of amino acids and their derivatives, phenols, and carboxylic acid and its derivatives compared with HB. Furthermore, RNA-seq transcriptomic results indicated that HB-1 significantly modulated key genes of Cyp2c38, Cyp2b13, and Cyp2b9 related to steroid hormone biosynthesis and CD36, Plin4, and Fabp4 related to the PPAR signaling pathway, which played key roles in lipid metabolism. Moreover, qRT-PCR and WB results indicated that HB-1 obviously enhanced ADIPOQ expression level, while it reduced SCD-1, CD36, Fabp4, and SREBP-1c expression levels, suggesting that the alleviation of lipid metabolic dysregulation by HB-1 in hyperlipidemia mice might be mediated via participating in the PPARγ pathway. This study provided essential theoretical insights for the development and utilization of HB. Full article

This study investigated the effects of replacing soybean meal with fermented rapeseed meal (FRSM) in the diets of sika deer (Cervus nippon) during the pre-antler growth period. A single-factor experimental design was employed. A total of 24 male sika deer aged 2–3 years were randomly divided into four groups with six deer per group, including a control group (0% substitution) and three treatment groups fed diets containing 2.8%, 5.6%, and 8.4% fermented rapeseed meal (FRSM), defined as the low (L-FRSM), medium (M-FRSM), and high (H-FRSM) substitution groups, respectively. The feeding trial lasted 63 days, with measurements collected on days 30 and 63. Growth performance, nutrient digestibility, serum biochemical indices, and rectal fecal microbiota were determined. The results showed that the final body weight, total weight gain, and average daily gain L-FRSM were higher in the L-FRSM group than in the control group and other substitution groups (p < 0.05), accompanied by a reduced feed conversion ratio (p < 0.05). In addition, body height and chest circumference were improved in the L-FRSM group. Regarding nutrient digestibility, the apparent digestibility of neutral detergent fiber and dry matter at day 30, as well as calcium digestibility at day 63 were higher in the L-FRSM group compared to the control and higher-substitution groups (p < 0.05). In contrast, crude fat and dry matter digestibility were significantly lower in the H-FRSM group (p < 0.05). No statistical differences were observed among treatments in serum biochemical indices related to energy metabolism, protein metabolism, liver function, lipid metabolism, antioxidant capacity, or humoral immunity (p > 0.05). Similarly, no significant differences were detected in core microbial composition or α-diversity of rectal fecal microbiota among groups (p > 0.05). In conclusion, substituting soybean meal with 2.8% fermented rapeseed meal effectively improves growth performance and nutrient utilization without compromising health status or intestinal microbial stability in sika deer during the pre-antler growth period. The findings provide a scientific basis for optimizing dietary strategies and support the rational application of fermented rapeseed meal in sika deer production. Full article

Introduction: Oxidative stress and inflammation are major factors linked to obesity and metabolic dysfunction, leading to a significantly higher risk of related diseases. Atorvastatin and liraglutide possess lipid-lowering, antioxidant, and anti-inflammatory effects that could synergistically improve obesity-related perturbations through modulation of the Nrf2/HO-1 signaling pathway. Methodology: We assessed liraglutide’s pharmacological potential in extending atorvastatin’s benefit on obesity, hyperlipidemia, and fatty liver in rats fed a high-fat diet (HFD) for 12 weeks. We specifically evaluated the effects of liraglutide treatment on atorvastatin-induced anti-inflammatory and antioxidant mechanisms, with a particular focus on Nrf2/HO 1 modulation in adipose and hepatic tissue. In silico analyses, including molecular docking and AlphaFold- Multimer modeling, evaluated the binding affinities of atorvastatin and liraglutide to Nrf2 and HO 1. Results: Compared to ND, the HFD-fed rats had a significantly higher final body weight (362.4 ± 12.7 g vs. 245.6 ± 9.8 g in ND, p < 0.05). There was a marked increase in serum total cholesterol (178.6 ± 9.2 mg/dL vs. 98.3 ± 6.4), fasting glucose (340.1 ± 8.2 mg/dL vs. 82.3 ± 3.1), HbA1c (7.8 ± 0.3 vs. 4.5 ± 0.2), and hepatic COX-2 expression (99.9 ± 6.3 vs 19.6 ± 2.4). The oxidative stress markers were also disturbed, as indicated by SOD (42.5 ± 3.1 vs. 95.2 ± 4.6 U/mg protein), GSH (18.3 ± 1.5 vs. 42.7 ± 2.8 nmol/mg), and p62 (0.005 ± 0.001 vs. 0.125 ± 0.01). Atorvastatin lowered cholesterol (121.2 ± 7.5 mg/dL), COX-2 (61.3 ± 3.3), and body weight (301.7 ± 11.5 g) compared to HFD. Meanwhile, liraglutide caused a greater reduction in body weight (268.5 ± 10.3 g), glucose (112.5 ± 6.7 mg/dL), and COX-2 (42.2 ± 2.9) than atorvastatin. The combination therapy produced the most significant effects, returning body weight (253.6 ± 9.1 g) to baseline, normalizing glucose and lipids, reducing COX-2 to 22.9 ± 2.0, and reactivating the Nrf2/HO-1 pathway, as shown by increased HO-1 expression and the restoration of p62 levels (0.078 ± 0.004). In silico analyses suggest that atorvastatin favorably binds to Nrf2 and HO-1, while liraglutide interacts with structurally relevant interfaces on these proteins, providing a mechanistic basis for their complementary antioxidant and cytoprotective effects. Conclusions: Our findings support targeting the Nrf2/HO-1 signaling pathway as a potential therapy for reversing hyperlipidemia and preventing mediators of inflammation and oxidative stress damage in the liver tissue. The evidence of increased efficacy observed with the combined atorvastatin and liraglutide supports a potential novel understanding of the complementary effects of atorvastatin and liraglutide. This finding requires further investigation to elucidate the combination’s therapeutic advantages in treating metabolic disorder scenarios. Full article

Eating behavior requires a balance between metabolic and hedonic components. Anxiety and dietary type may influence the quantity, patterns, and other aspects of food intake. Modern diets, especially in Western societies, often contain high levels of calories from fat and simple sugars (e.g., cafeteria-style diets). This type of diet may promote overweight and/or obesity in some, although many consumers remain at a normal weight. The mechanisms underlying susceptibility or resistance to weight gain remain unclear. Here, Sprague-Dawley male rats were fed a cafeteria diet for 10 weeks and then classified into quartiles based on body mass. We evaluated locomotor activity and anxiety-like behaviors and analyzed hypothalamic proteomics in overweight (Q4) rats compared with underweight (Q1) rats. Our results showed that locomotor activity and anxiety-like behaviors did not differ across quartiles (p > 0.05). Nevertheless, the expression of several hypothalamic proteins differed between Q4 and Q1 rats. Functional enrichment analysis of these differentially expressed proteins (p ≤ 0.05) revealed changes in cytoskeleton dynamics, synaptic communication, energy production and utilization, biosynthesis of cellular components (including nucleotides and carbohydrates), and regulation of metabolism between Q1 and Q4 rats. Neuro-humoral hypothalamic output regulates metabolism and food intake. Therefore, these functional changes in the hypothalamus may be associated with rats’ susceptibility/resistance to weight gain. Full article

Background/Objectives: Chitooligosaccharide (COS) is a marine-derived natural product obtained from shrimp and crab shells. Although its anti-inflammatory and antioxidant activities are documented, its potential effects on obesity and metabolic syndrome remain largely unclear. This study aimed to investigate the efficacy of COST (MW ≈ 1000 Da) against high-fat diet (HFD)-induced obesity and metabolic syndrome in Bama pigs. Methods: Bama pigs were fed a HFD for 12 weeks to establish an obesity model, followed by 12 weeks of oral COST administration. Serum biochemical parameters, tissue indicators, histopathology, and gene/protein expression related to cholesterol metabolism were analyzed. Fecal bile acid (BA) profiles, gut microbiota composition, and short-chain fatty acid (SCFA) levels were also examined. Results: COST treatment significantly attenuated weight gain and improved multiple components of metabolic syndrome, including insulin resistance, dyslipidemia, and inflammation. Mechanistically, COST upregulated intestinal ABCG5/ABCG8 to promote cholesterol excretion, increased ABCA1 expression in intestine and liver to enhance reverse cholesterol transport (RCT), and upregulated hepatic LDL-R to facilitate LDL-C clearance from circulation while modulating hepatic cholesterol synthesis via SREBP2 downregulation and RNF145 upregulation. These transcriptional changes were confirmed at the protein level for LXR, LDL-R, and ABCA1. Additionally, COST decreased fecal secondary BA levels, reshaped gut microbiota composition, and increased SCFA production, with significant correlations among these factors. Conclusions: COST ameliorates protective effects against HFD-induced obesity and metabolic syndrome, potentially through the regulation of cholesterol metabolism and the modulation of the gut microbiota-BA-SCFA network. Full article

Background/Objectives: Carbohydrate-restricted diets (CHRs) are increasingly employed in the treatment of obesity. We aimed to investigate the effects of a CHR on hepatic lipid anabolism and its association with changes in the proinflammatory environment and insulin signaling. Methods: Forty-eight C57BL/6J female mice were used in this study. We aimed to analyze the impact of a CHR on the hepatic proinflammatory profile and its relationship with changes in insulin signaling and fatty acid anabolism in obese female mice after two months on a high-fat diet. We also examined the impact of a one-month chow diet after CHR. Blood samples were collected, and the liver was processed during all-time study periods for analyses of biochemical, hormonal, and inflammatory markers, as well as possible changes in leptin and insulin signaling pathways. Results: Compared with chow-fed mice, CHR mice showed increased interleukin (IL)-1β and IL-2 levels, as well as leptin-related signaling in the liver. There was also a decrease in the expression of fatty acid synthase and the phosphorylation of ATP-citrate lyase, which was associated with a reduction in the activation of the insulin receptor, Akt, the mammalian target of rapamycin, cAMP-response element-binding protein, and glycogen synthase kinase 3β. The subsequent reintroduction of a chow diet after CHR resulted in lower hepatic free fatty acid and triglyceride levels than in obese mice without previous CH restriction. Conclusions: This study suggests that CHR inhibits de novo hepatic lipogenesis in obese mice by attenuating insulin signaling in a low-grade proinflammatory state. Full article

Background/Objectives: People with HIV (PWH) remain at high risk for cardiovascular and metabolic complications despite effective antiretroviral therapy (ART). Diet quality is an important modifiable factor that may influence these complications. Diets high in ultra-processed foods (UPF) have been linked to adverse metabolic and inflammatory profiles in the general population, but their impact on PWH remains poorly understood. The NOVA 4 classification categorizes foods by degree of processing, from unprocessed/minimally processed (NOVA 1) to UPF (NOVA 4). Methods: We conducted a cross-sectional study of adults with virologically suppressed HIV on stable ART. Assessments included dietary intake consisting of 24 h recalls analyzed with Nutrition Data System for Research software (NDSR) and classified into NOVA categories by a registered dietitian and the following characteristics: body composition (total and regional fat by DEXA and CT scan abdomen), cardiometabolic variables (glucose, HbA1C, HOMA-IR, lipids, blood pressure), and biomarkers of inflammation, immune activation, and gut integrity quantified by ELISA. Patients were stratified into NOVA 4 groups based on the median and quartile proportions of total energy intake from NOVA 4 foods. Associations between dietary NOVA and outcomes were analyzed using generalized additive models (GAMs) adjusted for age, sex, race, and CD4 count. Results: Among 222 PWH (mean age 45.4 ± 14.2 years; 31% female; 66% non-white; BMI 30.61 ± 7.91 kg/m²), median NOVA 4 intake was 45.6% of total energy intake. Participants with higher vs. lower NOVA 4 intake showed differences in diet quality, but in GAMs, higher NOVA 4 intake was not associated with higher levels of inflammatory, cardiometabolic, gut integrity, and body composition variables. Conclusions: In PWH, UPF consumption was high but not associated with markers of cardiometabolic health, systemic inflammation, or gut integrity. This may reflect the multifactorial nature of the heightened inflammation in PWH, potentially obscuring the effect of diet. Full article

The gut microbiota plays an important role in host physiology and is highly influenced by dietary factors. This study aimed to investigate the effects of cricket powder (CP) supplementation on gut microbiota composition in high-fat diet-fed C57BL/6J mice. Male C57BL/6J mice were fed a normal diet or a high-fat diet. Mice fed the high-fat diet were administered low, medium, or high doses of CP by gavage. Serum lipid levels and liver-related biochemical indicators were measured, and gut microbiota composition was analyzed using 16S rRNA gene sequencing. We found that CP supplementation significantly (p < 0.05) altered gut microbiota diversity and community structure, with differences observed among CP doses. Alpha diversity indices were significantly reduced after the intervention (p < 0.05). Beta diversity analysis showed no significant separation among groups before the intervention, whereas a clear separation in gut microbiota structure was observed after the intervention. Correlation analysis further revealed that beneficial bacterial genera, including Lactobacillus, Bifidobacterium, and Akkermansia, were negatively associated with lipid-related parameters. Overall, these findings suggest that CP supplementation can modulate gut microbiota composition under high-fat dietary conditions, indicating its potential role in metabolic regulation. Full article

Background/Objectives: Metabolic syndrome (MS) is associated with an increased cardiovascular risk. The aim of this study was to reveal the effects of Chaenomeles japonica fruit juice (CJFJ) on energy balance and biochemical and histological parameters in rats with diet-induced MS. Methods: Fifty Wistar rats were allocated into five groups. For ten weeks, the Control group received a standard laboratory diet and tap water, while the other groups were given a high-fat high-fructose (HFHF) diet. The Control and MS groups were treated with distilled water, while the other three groups were treated with CJFJ at increasing doses. Results: Rats on an HFHF diet consumed less food and more liquids and had a higher caloric intake than the Control group. Among the CJFJ-treated animals, an increased food consumption, as well as an increased total caloric intake, and no difference in body weight gain were observed in comparison with the MS group. CJFJ did not affect glucose tolerance or the triglyceride and total cholesterol levels. CJFJ prevented an HFHF-induced decrease in superoxide dismutase and caused a decrease in thiobarbituric acid-reactive substances in serum. The medium CJFJ dose prevented an HFHF-induced increase in adipose tissue indices. Liver and adipose tissue histology revealed a protective effect of CJFJ. Conclusions: CJFJ may exert beneficial effects on visceral adiposity, oxidative status, and histopathological changes in the liver and adipose tissue in rats with diet-induced MS. Full article

Background: Probiotics and medicine food homology are known to offer gentle approaches to prevent obesity, although it is difficult with such approaches to satisfy consumers’ requirements to lose weight quickly. The probiotic strain Bifidobacterium animalis ssp. lactis 420 (B420) and Cordyceps militaris synergistically prevented obesity and related disorders in high-fat diet (HFD)-fed mice. Methods: The synergistic effects correlated with improved gut integrity, diminished systemic inflammation, and enhanced glucose homeostasis. Gut microbiota analysis revealed that the bloom of the commensal Akkermansia muciniphila contributed to the synergistic effects by inducing a profound shift in HFD-induced gut microbiota disorder. Results: The bloom of A. muciniphila was significantly correlated with a boost in mucin 2 within the colon, achieved through increased goblet cell quantity and elevated mucin 2 expression. To reveal the collaborating pathway, we found that Cordyceps militaris did not promote the propagation of B420 in vitro or in vivo. Moreover, heat-killed B420 could not enhance the preventive efficacy of Cordyceps militaris against obesity caused by the HFD. Conclusions: The metabolites of live B420 and Cordyceps militaris-derived metabolites in the gut microbiota collaboratively promoted the production of mucin 2. Thus, our results reveal a mechanism by which a combination of probiotics and medicine food homology enhance their therapeutic effects against obesity. Full article

Background: Highly lipidic tissues (e.g., adipose tissue, brain, and liver) are challenging for transcript and protein extraction and for next-generation sequencing. Lipids can clog filters, columns, and pipettes; cause autofluorescence and quenching in imaging; and interfere with centrifugation-based separation. Aim: To identify the most suitable method for extracting total RNA for RT-qPCR and an alternative method for extracting total protein for quantification in mice fed a regular or high-fat diet. Methods: We compared three total RNA extraction methods and two total protein extraction methods. Results: The highest total RNA yield and purity were obtained with TRIzol and chloroform, with optimized steps added to the original protocol to address the challenges posed by highly lipid-rich tissues. For total protein extraction, an adipose tissue-specific kit from Invent Biotechnologies yielded higher protein levels than the classical RIPA-based method. Among lipid-rich tissues, we observed that adipose tissue was more challenging to process than the brain and the liver. Conclusions: Adipose tissue, particularly under a high-fat diet, is the most challenging lipid-rich tissue, followed by the brain and then the liver. We highlight protocols that improve total RNA and protein yields and purity, which may benefit other researchers working with these tissues. Full article

This study aimed to investigate the ameliorative effects of glucuronolactone (GL) as a dietary additive on high-fat diet (HFD)-induced growth suppression and metabolic disorders in turbot. A 10-week feeding trial was conducted using juvenile turbot (16.7 ± 0.03 g). Two diets with different protein (%)/lipid (%) levels were formulated: PC (54/12) and NC (47/17). Based on the NC diet, three experimental diets were prepared by supplementing 200 (G200), 400 (G400), and 600 (G600) mg/kg of GL. The present results show that compared to the PC group, HFDs significantly inhibited the growth performance of turbot and induced severe metabolic disorders, hepatointestinal damage, and gut microbiota dysbiosis. Dietary GL supplementation effectively reversed these adverse effects. Specifically, compared to the NC group, GL supplementation significantly restored growth performance, enhanced non-specific immunity, and systematically improved metabolic health. In the liver, GL notably ameliorated tissue damage and downregulated key lipogenic genes (SREBP1, ACC, FAS, PPARγ), while upregulating genes involved in lipid oxidation and catabolism (PPARα1, CPT1, ACOX1, HSL, LPL) and lipid transport (ApoB100, MTP), thereby alleviating hepatic lipid deposition. Furthermore, GL activated the Nrf2/Keap1 antioxidant pathway, up-regulating the expression of genes such as SOD, CAT, GPX, and HO-1. It also suppressed the NF-κB-mediated inflammatory response (downregulation of IL-1β, IFN-γ and TNF-α2; upregulation of IL-10 and TGF-β2) and the mitochondrial apoptosis pathway (increased Bcl-2/Bax ratio; downregulation of Caspase3/7/9), collectively mitigating oxidative damage and cellular apoptosis. Moreover, GL restored intestinal morphology, enhanced the expression of tight junction proteins (Claudin-3, Claudin-7, ZO-1, Occludin) and MUC2, and inhibited MLCK signaling. These improvements led to a reduction in serum D-LA levels, indicating strengthened intestinal barrier function. Concurrently, GL reshaped the gut microbiota composition by enriching beneficial bacteria such as Akkermansia and suppressing potential pathogens like Listeria. In summary, GL effectively alleviated HFD-induced growth suppression and metabolic damage in turbot by improving lipid metabolism and alleviating hepatic injury, while concurrently restoring intestinal barrier integrity and microbiota homeostasis. Full article

A high-fat (HF) diet disrupts metabolic homeostasis and impairs peripheral circadian rhythms in key metabolic tissues. β-Hydroxybutyrate (BHB), a major circulating ketone body, functions not only as an energy substrate but also as a signaling metabolite regulating nutrient-sensing and inflammatory pathways. However, its role in modulating metabolic–circadian interactions under conditions of nutrient excess remains unclear. In this study, we investigated whether BHB supplementation influences metabolic signaling and circadian clock oscillations in liver, skeletal muscle and adipose tissue under chow and HF conditions. Male C57BL/6 mice were fed chow or HF with or without BHB supplementation (500 mg/kg body weight in the diet) for 7 weeks. Metabolic parameters were assessed by indirect calorimetry, and tissues were collected every 4 h across the circadian cycle. HF feeding increased body weight and adiposity (p < 0.01), reduced AMPK activation, enhanced AKT/mTOR signaling, elevated NF-κB levels and dampened clock gene rhythmicity. BHB supplementation significantly decreased food intake in HF-fed mice (p < 0.01) and partially reversed several molecular alterations in a tissue-specific manner. In skeletal muscle and adipose tissue, BHB increased AMPK activation and reduced mTOR and NF-κB signaling (p < 0.05), whereas hepatic effects were more modest. Notably, BHB modulated circadian gene expression, restoring aspects of rhythmic amplitude and/or phase, particularly in adipose tissue. These findings may indicate that BHB supplementation modulates nutrient-sensing pathways and partially restores peripheral circadian rhythms under HF conditions. While some effects may be influenced by reduced energy intake, BHB may serve as a metabolic signal linking nutrient status to circadian regulation. Full article

Background/Objectives: Non-alcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder for which there are limited pharmacotherapies. Sodium rutin (NaR), a soluble flavonoid derivative, has shown beneficial metabolic effects, but its role in NAFLD remains unclear. This study investigates whether NaR ameliorates high-fat diet (HFD)-induced NAFLD and insulin resistance through promoting hepatic lipophagy. Methods: Male mice aged 8 weeks old were fed a HFD for 12 weeks with/without NaR supplementation. Body weight was measured every week. After 12 weeks of treatment, GTT and ITT were performed to assess insulin resistance. Then, the tissues were collected and hepatic histology, serum biochemistry, and markers of autophagy and senescence were assessed. Results: NaR treatment significantly attenuated HFD-induced weight gain, reduced visceral fat and liver weights, and ameliorated hepatic steatosis and vacuolization. NaR improved serum lipid profiles; lowered alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase levels; and reduced hepatic cellular senescence. NaR enhanced hepatic autophagy, evidenced by decreased p62 levels, increased LC3-II/LC3-I ratio, and enhanced colocalization of lipid droplets with LC3 and LAMP1 in vivo and in vitro. These changes were accompanied by improved glucose tolerance and insulin sensitivity. Conclusions: NaR effectively alleviates HFD-induced NAFLD and insulin resistance by activating hepatic lipophagy. These findings support NaR as a promising multi-targeted therapeutic candidate for NAFLD. Full article

Milk fat synthesis in dairy cows is a complex process affected by ruminal fermentation, systemic metabolism, and mammary gland activity. To explore the metabolic interplay across these systems, a multi-tissue metabolomics approach (rumen fluid, plasma, and milk) using ultra-high-performance liquid chromatography–mass spectrometry was used to identify metabolic differences between Chinese Holstein cows with high (H-MF, 5.82 ± 0.41%) and low (L-MF, 3.60 ± 0.12%) milk fat content under the same diet. The bovine mammary epithelial cells (BMECs) were also cultured to evaluate the impact of a key metabolite, malic acid (MA), on lipid metabolism. Our findings reveal distinct metabolic profiles across rumen fluid, plasma, and milk, with 96, 109, and 79 differential metabolites, respectively, between the L-MF and H-MF groups. In rumen fluid, H-MF cows showed higher levels of lauric acid and succinic acid, linked to fatty acid biosynthesis, while the L-MF cows had elevated citraconic and orotic acids, associated with amino acid metabolism and liver stress. Plasma from the H-MF cows contained higher β-hydroxybutyric acid, methionine sulfoxide, and phosphatidylcholine, supporting lipogenesis, whereas L-MF plasma showed increased 3-hydroxy-L-proline, indicating tissue catabolism. In milk, the L-MF cows had higher MA, while the H-MF cows exhibited elevated L-carnitine, linked to fatty acid β-oxidation. Metabolite trend analysis during rumen fluid–plasma–milk showed that 211 metabolites were classified into 8 profiles. Profile 1 had the largest number of metabolites whose levels were down-regulated from rumen to plasma and enriched in lipid metabolism. Profile 3 (mainly related to amino acid metabolism) and profile 4 (mainly related to energy metabolism) exhibited opposite trends from plasma to milk. In vitro, 200 μM of MA reduced the triglyceride content in BMECs and down-regulated lipogenic genes and their protein expression levels (fatty acid synthase, stearoyl-CoA desaturase and sterol regulatory element binding protein 1). These results highlight how rumen fluid, plasma, and milk metabolites collectively influence milk fat synthesis, with MA acting as a key regulator of lipid metabolism in mammary epithelial cells. Full article