Search Results (905)

Background/Objectives: Promoting white adipose tissue (WAT) browning into thermogenic beige adipocytes is a promising anti-obesity strategy. Yanggyeoksanhwa-tang (YST) has been used traditionally to alleviate obesity-related conditions. Catalpol and rhoifolin are major bioactive components of Rehmannia glutinosa (Gaertn.) and Lonicera japonica (Thunb.) with known metabolic or anti-inflammatory effects. However, their direct roles in adipocyte browning and the mechanisms via β3-adrenergic receptor (β3-AR) signaling are not well defined, and this study addresses this gap. Methods: To evaluate browning potential, 3T3-L1 adipocytes were treated with catalpol and rhoifolin during differentiation. The expression of browning markers and lipid metabolism or catabolism transcription factors was analyzed using Western blotting and quantitative real-time polymerase chain reaction. The involvement of the β3-AR and adenosine monophosphate–activated protein kinase (AMPK) signaling pathways was further validated using specific agonists and antagonists. Results: Both compound treatments significantly upregulated beige-specific (Cd137, Cited, Tbx1, Cidea, Fgf21, Tmem26) and mitochondrial biogenesis markers (Cox4, Nrf1, Tfam), accompanied by a marked increase in thermogenic markers (UCP1, PGC-1α, Prdm16). Concurrently, lipolysis-related genes such as Atgl, Hsl, and Plin1 were elevated, while lipogenesis targets (Fasn, Lpl, Srebf1, Acaca) were downregulated through activation of the β3-AR signaling pathway. Conclusions: These findings suggest that catalpol and rhoifolin, key phytochemicals of YST, promote WAT browning and lipolysis. Our findings indicate that these compounds induce browning and modulate metabolism via the β3-AR pathway. These results serve as a cornerstone for natural anti-obesity therapy, pending further validation in vivo and clinical studies. Full article

Lymphoplasmacytic gastritis (LPG) is one of the most prevalent chronic diseases affecting cheetahs (Acinonyx jubatus) under human care, yet its underlying cause remains unresolved. Gastric inflammation occurs in the majority of adult captive cheetahs but is uncommon in free-ranging populations, suggesting that management-related factors contribute to disease pathogenesis. This review proposes that LPG represents a bile acid-driven gastroenteropathy arising from disruption of the natural feeding ecology of the cheetah. In free-ranging systems, cheetahs consume large episodic meals separated by prolonged fasting intervals and ingest whole-prey containing substantial connective tissue and collagen. In captivity, feeding patterns are typically characterized by smaller, more frequent meals and diets dominated by lean skeletal muscle with reduced structural complexity. I hypothesize that this mismatch alters gastric emptying kinetics, disrupts coordinated pancreatic and biliary secretion, and destabilizes fat digestion. Inefficient lipolysis may impair micelle formation and promote bile acid mislocalization within the gastrointestinal tract, increasing mucosal exposure to hydrophobic bile acids capable of inducing chemical epithelial injury. Within this framework, lymphoplasmacytic gastritis is interpreted as a secondary inflammatory reaction to chronic bile acid-mediated mucosal stress rather than a primary immune-mediated disorder. The model also provides a mechanistic explanation for the frequent coexistence of gastritis with fat and protein maldigestion in captive cheetahs. Differential responses to antimicrobial therapy, glucocorticoids, sulfasalazine, pancreatic enzyme supplementation, and bile acid-modifying agents are broadly consistent with this proposed mechanism. Recognition of LPG as a physiologically driven gastroenteropathy has important implications for management, emphasizing restoration of feast–fast feeding patterns, inclusion of collagen-rich carcass components, and targeted modulation of bile acid composition and signaling. Full article

The increasing demand for premium-quality meat has intensified interest in the molecular regulators that govern lipid deposition and sensory quality. Lipid metabolism, encompassing synthesis, oxidation, and storage, represents a key biological process affecting intramuscular fat content, tenderness, and flavor. G0/G1 Switch Gene 2 (G0S2) is widely recognized as an endogenous, non-competitive inhibitor of adipose triglyceride lipase. By inhibiting this key lipase, G0S2 restrains triglyceride hydrolysis and helps preserve lipid storage. Recent studies further suggest that G0S2 participates in adipocyte differentiation, mitochondrial regulation, apoptosis, and inflammatory signaling. Together, these findings indicate that G0S2 functions not only in lipolysis control but also as a multifunctional regulator of energy metabolism and cellular homeostasis. Despite its pleiotropic roles, which position G0S2 as a key integrator of lipid metabolism and cellular signaling networks, the specific roles and regulatory mechanisms by which G0S2 influences lipid metabolism and meat quality remain incompletely understood. This review summarized recent advances in G0S2-mediated lipid metabolism with emphasis on its regulatory network in livestock species. The physiological mechanisms by which G0S2 modulated lipolysis, lipid deposition, and intramuscular adipogenesis were discussed, along with nutritional, hormonal, and epigenetic factors controlling its expression. Moreover, its functional implications for meat quality improvement, marbling formation, and feed efficiency were highlighted. Understanding the molecular and regulatory features of G0S2 provided a foundation for developing genetic and nutritional strategies to optimize lipid utilization and enhance meat quality in modern animal production systems. Full article

Background: Supplementing aquafeeds with emulsifiers can enhance lipid utilization, yet the physiological effects of lysolecithin, derived from enzymatic lecithin conversion, remain under-explored. Objectives: This study examined the effects of lysolecithin supplementation on hepatopancreatic transcriptome and gut microbiota in largemouth bass (Micropterus salmoides) fed stearin-based high-lipid diets. Methods: Two diets were formulated: a control containing 130 g kg⁻¹ stearin fish oil (SO), and in the experimental diet (SL), 3.1 g kg⁻¹ rapeseed oil was replaced with 3.1 g kg⁻¹ lysolecithin oil. Each diet was fed to three replicate groups for 56 days. Hepatopancreas and distal intestine were sampled for transcriptome profiling, and gut microbiota were characterized at 28 and 56 days. Results: Lysolecithin supplementation resulted in 424 differentially expressed genes compared with the control (322 up- and 102 downregulated). KEGG enrichment indicated major effects on lipid metabolic processes, notably activation of the PI3K-AKT signaling pathway, enhanced adipocyte lipolysis, and modulation of adipocytokine signaling, suggesting improved insulin sensitivity and lipid mobilization. Histological analysis showed mild distal intestinal inflammation in the SO group. Gut microbiota composition shifted over time; lysolecithin increased the relative abundance of Cetobacterium and reduced potential opportunistic taxa compared with the control. Conclusions: Overall, dietary inclusion of lysolecithin improved lipid utilization in largemouth bass, likely by enhancing lipid metabolism and promoting beneficial gut microbial profiles. These findings support lysolecithin as a promising feed additive for optimizing high-lipid aquafeeds. Full article

The most common complication of active brucellosis in humans is osteoarticular injury. In the bone marrow microenvironment, mesenchymal stem cells (MSCs) can differentiate into either adipocytes or osteoblasts, and this balance is tightly regulated because an increase in adipogenesis may negatively affect bone formation and favor bone loss. The differentiation of MSCs into adipocytes or osteoblasts is tightly regulated by mechanisms that promote cell fate toward one lineage while repressing the other. Our study demonstrated that Brucella abortus infects MSCs but does not affect the deposition of organic and mineral matrix during osteoblast differentiation. However, the infection upregulates Receptor Activator of Nuclear Factor Kappa-B Ligand (RANKL) expression in osteoblasts, which may contribute to osteoclast activation and bone resorption. Conversely, B. abortus infection significantly influences adipocyte differentiation by modulating lipolysis, lipogenesis, and interactions between lipid droplets and mitochondria. This leads to increased cellular cholesterol levels and reduced intracellular triglycerides, accompanied by glycerol release. These changes result in more differentiated adipocytes and larger lipid droplets. Consequently, we observed increased IL-6 secretion and a higher leptin/adiponectin ratio. Importantly, these effects were independent of a functional type IV secretion system (T4SS), as purified Brucella DNA fully reproduced the adipogenic phenotype. Moreover, inhibition of TLR9—the primary sensor of bacterial DNA—significantly reduced the DNA-induced adipogenic response, demonstrating that adipocyte modulation is at least in part mediated through TLR9 signaling. In summary, B. abortus promotes MSC differentiation toward an inflammatory adipocyte phenotype. It involves a TLR-9-mediated DNA detection. It may contribute to osteoarticular injury and infection-associated bone resorption. Full article

Lipolysis is an interfacial reaction. Lecithins are natural emulsifiers containing a mixture of phospholipids (PL). Lecithin composition can be modified via enzymatic hydrolysis of PLs to produce lysophospholipids (LPL). The quantities of PL and LPL and the PL/LPL ratio are related to the emulsifying properties and interfacial activity of digestive lipases. This study aims to: (i) produce oil-in-water nanoemulsions of rapeseed oil (RSO) with soybean lecithin (SBL) and hydrolyzed lecithin (HL) at different concentrations and homogenization pressures and measure the mean droplet diameter (MDD) and polydispersity index (PdI) by dynamic light scattering; (ii) hydrolyze the emulsions in vitro with intestinal extracts of rainbow trout and estimate the degree of hydrolysis of lipids (DH) by the pH-stat method; and (iii) model the results on MDD, PdI, and DH through the response surface methodology (RSM). When HL was used as an emulsifier, DH, MDD, and PdI were fitted to polynomial quadratic, two-factor interaction, and linear models, respectively. MDD, PdI, and DH were fitted to polynomial quadratic SBL models. The optimal conditions were emulsifier concentrations of 0.45% and 0.76% w/w and homogenization pressures of 10,790 and 10,781 psi for HL and SBL, respectively. Under these conditions, DH = 34.9% and 33.08%, MDD = 241.9 and 543.6 nm, and PdI = 0.29 and 0.52 for HL and SBL, respectively. Full article

Due to its high efficiency and safety, oocyte vitrification finds broad application in many fields of life sciences, such as clinical assisted reproduction and conservation of animal genetic resources. However, vitrification may cause cellular damage and reduce the quality of oocytes and their cumulus cells (CCs), which could be closely related to disorders in lipid metabolism. At present, the impact of vitrification upon the lipid profile of oocytes and CCs has not been systematically elucidated. In this study, we used porcine germinal vesicle cumulus–oocyte complexes (COCs) as a model to analyze their lipid characteristics after vitrification and in vitro maturation (IVM), utilizing untargeted lipid metabolomics. Our results showed that an overall count of 37 down-regulated and 8 up-regulated differential lipids was identified in the vitrified oocytes. Pathway analysis confirmed the enrichment in glycerophospholipid metabolism and fat digestion and absorption, etc. Combined with transcriptomic analysis, three enriched pathways were revealed, including the AMPK signaling pathway, metabolic pathways, and fatty acid elongation. On the other hand, a total of four down-regulated and eight up-regulated differential lipids were detected in the vitrified CCs. Pathway enrichment implicated autophagy, glycerophospholipid metabolism, etc. A joint analysis of metabolomic and transcriptomic data revealed four enrichment pathways, including cholesterol metabolism, fat digestion and absorption, regulation of lipolysis in adipocytes, and metabolic pathways. Notably, the supplementation of lysophosphatidylcholine during IVM attenuated oxidative stress, enhanced mitochondrial activity, and enhanced the viability and embryonic development of cryopreserved porcine oocytes. The results indicate that vitrification alters lipids in oocytes and CCs, and the supplementation of lipids plays a role in improving the quality of vitrified oocytes. Full article

Background/Objectives: Recent studies have shown that the solubilisation of poorly water-soluble drugs can be enhanced by using infant formula as a lipid-based formulation. In those studies, digestion of the triglycerides in infant formula to produce more polar lipids, namely fatty acids and monoglycerides, produced a high-capacity solubilisation environment for weakly basic drugs such as clofazimine, driven mainly by ion-pairing of the fatty acid with the drug. However, digestion of lipid-based formulations is not expected to provide the same effect for nonionised or acidic drugs and in fact may present a reduced solubilisation capacity for weakly acidic drugs. Methods: In this study, a weakly acidic drug, tolfenamic acid, was dispersed in reconstituted infant formula, and the infant formula was digested under in vitro simulated intestinal conditions. The quantity of tolfenamic acid that was solubilised in the infant formula during digestion was determined by high-performance liquid chromatography and small-angle X-ray scattering. Results: Unexpectedly, digestion of the infant formula increased the solubilisation capacity for tolfenamic acid. Reconstituting infant formula at a higher fat content also increased the rate and extent of solubilisation of tolfenamic acid during digestion. The quantity of tolfenamic acid that was solubilised during digestion correlated approximately linearly with the quantity of free fatty acids produced during digestion. Conclusions: These results show that a weakly acidic drug can also exhibit digestion-driven solubilisation in a lipid-based formulation in the absence of ion-pairing and highlights the need to better understand drug response to digestion of lipid-based foods and formulations, and their versatility as a formulation option even for poorly water-soluble acidic drugs. Full article

Bone formation requires a substantial energy supply to sustain extracellular matrix production and mineralization, yet the temporal contribution of lipid metabolism during osteoblast maturation remains incompletely characterized. This study investigated the molecular and transcriptional remodeling of lipid metabolism. Intracellular lipid distribution was analyzed by confocal microscopy using Nile Red staining. Transcriptional modulation of lipid synthesis, storage, lipolysis, genes associated with mitochondrial fatty acid oxidation, and osteogenic markers were assessed by quantitative real-time PCR, and the biochemical composition was evaluated by Raman spectroscopy. Early stages of spheroid development showed higher expression of genes involved in lipid synthesis and storage (FASN, DGAT2, and PLIN2) together with intracellular lipid accumulation, whereas later stages displayed increased expression of lipolytic and β-oxidation markers (PNPLA2/ATGL, CPT1A, and HADHA), accompanied by the redistribution of lipid droplets. The Raman analysis revealed a time-dependent variation of lipid-associated CH₂/CH₃ bands and modulation of protein-related Amide I–III signals, consistent with biochemical remodeling during maturation. Overall, the data indicate a coordinated transcriptional shift from lipid accumulation-associated pathways toward lipid mobilization during osteogenic progression in a 3D culture. This model provides a controlled experimental platform for investigating metabolic regulation during bone formation and for studying metabolic alterations associated with skeletal disorders. Full article

Bitter taste receptors (TAS2Rs) are G protein-coupled receptors best known for detecting bitter compounds in the oral cavity. However, their expression patterns and physiological roles in the liver remain largely unexplored. Here, we employed molecular and immunohistochemical approaches to demonstrate that multiple TAS2Rs are expressed in human Hep3B cells and mouse primary hepatocytes (MPHs) and co-localized with β-adrenergic receptors (βARs) at the bile canaliculi. Bioluminescence resonance energy transfer (BRET), cAMP assays, and Western blot analyses revealed that certain TAS2Rs exhibit ligand-dependent coupling preferences for the G protein subunits Gαi1, Gαi2, and Gαi3. This coupling leads to inhibition of cAMP production and a reduction in protein kinase A (PKA) substrate phosphorylation. Biochemical assays further showed that TAS2R activation significantly attenuates βAR-mediated lipolysis, as well as the production of glycerol and free fatty acid in both Hep3B cells and MPHs. These effects were partially reversed by small interfering RNA (siRNA)-mediated knockdown of TAS2Rs. Moreover, studies using a steatotic mouse model demonstrated that bitter compounds inhibit lipid droplet degradation, resulting in hepatic triacylglycerol accumulation. Collectively, these findings reveal a role for TAS2Rs in modulating hepatic lipid metabolism and highlight their potential as therapeutic targets for the prevention and treatment of liver diseases. Full article

Although blackberries are associated with health benefits, their impact on adipocyte biology remains poorly understood. Here, we investigated the effect of a blackberry extract (Rubus fruticosus fruit extract, RFE) on adipogenesis and lipolysis in the 3T3-L1 cell model and characterized its transcriptomic response. Adipogenesis and lipolysis were assessed by Oil Red O and AdipoRed™ staining and glycerol release, respectively. RNA-Seq analysis was processed with the PIGx pipeline, and differential gene expression was evaluated with edgeR. RFE strongly promoted adipogenesis, increasing Oil Red O staining by 29% (n = 3, p < 0.01), and showed anti-lipolytic activity, reducing glycerol release by 51% (n = 3, p < 0.05). Whole-transcriptome analysis revealed that RFE significantly regulated 4904 genes, enhancing the adipogenic program. Functional profiling identified metabolic pathways influenced by RFE, including those related to lipid biosynthesis. Notably, RFE also modulated extracellular matrix (ECM) pathways, suggesting a shift toward a less fibrotic microenvironment. These findings indicate that RFE promotes subcutaneous adipose tissue expansion while supporting ECM remodeling, favoring healthy adipose growth and reduced fibrosis. To our knowledge, this is the first evidence that RFE simultaneously stimulates adipocyte differentiation and ECM remodeling. Overall, RFE emerges as a promising active ingredient for lipofilling cosmetic applications aimed at improving adipose tissue volume and quality. Full article

In this study, a novel combination strategy of sodium trimetaphosphate (STMP) phosphorylation and dextran (DX) glycosylation was employed to modify soy protein isolate (SPI). The phosphorylated protein–dextran conjugate (TSPI-DX) was successfully prepared and then was used as an emulsifier to prepare the astaxanthin emulsion, with the aim to enhance the emulsion delivery performance. Structural analysis revealed that phosphorylation and glycosylation altered the microenvironment of the side chains, leading to changes in protein secondary structure, which consequently loosened the protein architecture and enhanced molecular flexibility. The functional properties of TSPI-DX, including its solubility, emulsifying activity (EAI) and emulsifying stability (ESI), were markedly enhanced. Furthermore, the concurrent modification through phosphorylation and the Maillard reaction yielded a synergistic effect, boosting the DPPH radical scavenging rate by 86.5% and increasing the ferric-ion reducing power nearly fourfold. The astaxanthin emulsion prepared by modified SPI also exhibited several advantages. The TSPI-DX emulsion exhibited a markedly smaller mean particle size and a larger absolute Zeta-potential value. Consequently, with the higher electrostatic repulsion and steric hindrance among the droplets, the astaxanthin emulsion prepared by TSPI-DX demonstrated superior encapsulation efficiency and stability across various conditions, including storage, oxidation, thermal, and pH challenges. Moreover, in vitro digestion experiments revealed that the modified SPI emulsion facilitated a higher extent of lipolysis and astaxanthin bioaccessibility. Therefore, this work proposes a novel strategy for constructing plant-protein emulsion systems with enhanced delivery and release capabilities. Full article

Lipids are the major energy reservoir, but excessive fat accumulation drives immune cell trapping, chronic inflammation, autoimmunity, and cancer. Lipid synthesis, secretion, degradation, and the shuttling to cellular organelles and compartments are still poorly investigated in all cell types of the mammalian body. The major routes of FA uptake are dietary uptake, lipolysis, and de novo synthesis. We highlight disease associations zooming in on the Signal Transducer and Activator of Transcription 1/3/5 (STAT1/3/5) molecules in association with cytokine, growth factors, and hormone action, steering lipid metabolism. We compare STAT-lipid crosstalk from nuclear and mitochondrial perspectives, highlighting roles in immunity, metabolic diseases, and cancer, and providing insights into key regulatory mechanisms of lipid metabolism. A high degree of cellular flexibility in metabolic adaptation explains the need for fine-tuning, in which STAT molecules can function as rheostats to maintain energy equilibrium within cellular compartments. This concept bridges, e.g., high-energy flux or the Warburg effect, with the Hydride Transfer Complex upon low-energy provision. Another interesting STAT1/3/5 aspect is their Lipid droplet (LD) association and LD formation. LDs play key roles in disease initiation or progression, including autoimmunity or cancer, as well as chronic inflammatory diseases due to their role in (1) lipotoxicity, (2) cell death regulation, (3) immune system amelioration, and (4) energy provision. Finally, the therapeutic consequences of the angles are outlined, along with future research directions. Full article

Reducing cake fat while maintaining aeration, crumb softness, and consumer acceptance remains challenging because fat crystals contribute to interfacial stabilization and structure development. This study evaluated an interfacial processing strategy in which oil dispersion is refined by pre-emulsification to evaluate whether refining oil dispersion by pre-emulsification modulates the functional impact of lipase (via in situ formation of surface-active lipolysis products). A D-optimal design (16 formulations) quantified the effects of fat type (shortening vs. sunflower oil), fat level (100% vs. 50%), pre-emulsification (absent/present), and lipase dose (0, 50, 100 ppm; flour basis) on batter and baked-cake quality. Responses included moisture, color, volume/visual structure, texture and hedonic sensory evaluation for selected formulations. Lipase improved structure and texture, with the strongest benefits in reduced-fat samples, where hardness-related parameters decreased and volume/crumb refinement improved. Pre-emulsification modulated lipase performance in a formulation-dependent manner, indicating significant interactions. In sensory tests, the combined approach improved low-fat acceptance compared with the low-fat control. Overall, pre-emulsification-enabled lipase action offers a route to recover key quality attributes in low-fat cakes without conventional emulsifiers. Full article

Background: Propionate, a gut microbiota-derived metabolite, has previously been shown to alleviate chronic alcoholic liver disease (ALD) by preserving intestinal barrier integrity. However, its direct hepatoprotective mechanisms remain unclear. Methods: In this study, employing an acute ALD model to minimize the interference from gut–liver axis effects, we investigated the direct hepatic protection of propionate. Results: Our results demonstrated that propionate administration significantly attenuated hepatic steatosis and oxidative stress. Consistently, in EtOH/OA (oleic acid)-exposed AML-12 hepatocytes, propionate enhanced cell viability and reduced lipid accumulation. Integrated proteomic and metabolomic analyses revealed that propionate altered hepatic proteins and metabolites profiles to stimulate lipolysis, promote fatty acid oxidation, and strengthen antioxidant defenses, consequently restoring lipid homeostasis in ALD mice. Mechanistically, we identified that these beneficial effects may be driven by the upregulation of regucalcin (RGN) following propionate treatments, which, in turn, may activate downstream PPARα signaling via increased levels of p-AMPK, PPARα, ACOX1 and CPT1A. Conclusions: These findings provide novel insight into the liver-centric mechanism through which propionate ameliorates ALD and further support its therapeutic potential in ALD treatment. Full article