Search Results (240)

Lipedema is a chronic adipose tissue disorder characterized by disproportionate and often painful enlargement of the extremities, occurring predominantly in women. Despite increasing clinical recognition, the underlying pathophysiology remains incompletely understood and is likely multifactorial. Existing evidence suggests contributions from vascular alterations, adipose tissue remodeling, inflammatory activation, hormonal influences, and lymphatic dysfunction. This review proposes a hypothesis-generating integrative framework in which lipedema may reflect a regenerative imbalance of subcutaneous adipose tissue. Within this model, genetically and hormonally modulated endothelial permeability could promote activation of perivascular adipose-derived stromal/stem-cell niches and stromal vascular fraction signaling pathways, thereby facilitating coupled angiogenesis and adipogenesis. Progressive adipocyte hyperplasia and hypertrophy may subsequently contribute to inflammatory remodeling, pain generation, and secondary impairment of dermal and subdermal lymphatic drainage. The proposed framework attempts to integrate clinical, histological, imaging, molecular, and endocrine observations into a biologically coherent conceptual model. At the same time, the review emphasizes the current limitations of the available evidence, the heterogeneity of lipedema phenotypes, and the ongoing controversies regarding disease progression, obesity overlap, and the relative role of lymphatic dysfunction. Finally, the potential mechanistic rationale of lymphatic-sparing liposuction is discussed in the context of tissue decompression, restoration of lymphatic transport, and interruption of persistent adipose remodeling. The model presented here should be interpreted as a hypothesis-generating conceptual scaffold requiring prospective validation. Importantly, the present framework should be interpreted as a biologically plausible and hypothesis-generating conceptual model rather than a definitive mechanistic doctrine. Several proposed interactions remain associative and require prospective biological validation. Full article

Background/Objectives: A high-fat diet (HFD) promotes hepatic steatosis, inflammation, and systemic metabolic imbalance. Notably, HFDs can affect the gut–liver axis and adipose tissue homeostasis. Galectin-3 (Gal-3) binds to β-galactosides and plays regulatory roles in the gut–liver axis, connecting metabolic stress with inflammation and tissue remodelling. The objective of this study was to investigate whether Gal-3 affects the gut–liver axis and adipose tissue biology after HFD supplementation. Methods: Six-week-old C57BL/6 mice were randomly divided into either wild-type (Lgals3^+/+) or knockout (Lgals3^−/−) groups. Both groups received an HFD orally for 12 weeks, along with their respective control groups. Physiological measurements and microscopic examination of the gut, liver, and fat tissue were conducted using optical microscopy. Results: The HFD induced obesity in Lgals3^+/+ mice, but not in Lgals3^−/− mice, which exhibited lower weight gain, food intake, daily energy intake, and energy efficiency than Lgals3^+/+ mice. Moreover, Lgals3^−/− HFD mice had hyperglycaemia and hyperinsulinemia. Histological analysis revealed hypertrophied adipose tissue in Lgals3^+/+ HFD mice with abundant Gal-3⁺ crown-like structures, rarely observed in Lgals3^−/− HFD mice. In the jejunum, Lgals3^+/+ HFD mice showed a significant reduction in Gal-3 expression in intestinal epithelial cells, whereas inflammatory signals were increased in Lgals3^−/− HFD mice. In the liver, Lgals3^+/+ HFD mice showed significant steatosis and macrophages expressing Gal-3. In contrast, Lgals3^−/− HFD mice showed pronounced hepatocyte ballooning, suggesting a more progressive stage of metabolic dysfunction-associated steatotic liver disease (MASLD). Conclusions: Together, these data suggest that Gal-3 protects the gut–liver axis and adipose tissue against cytotoxic effects caused by HFD. Full article

Visceral adipose tissue (VAT) is a metabolically active organ that undergoes structural and functional remodeling under obesogenic conditions. Early-life stress, such as maternal separation (MS), may modulate these processes, but its depot-specific effects remain poorly characterized. This study aimed to determine whether MS modulates VAT remodeling in response to post-weaning high-fat diet (HFD) exposure in male C57BL/6 mice. Animals underwent MS during the early postnatal period (PND2–16) or remained unmanipulated (UM), and were subsequently fed either a control diet (CD) or an HFD for 16 weeks (groups: UM-CD, UM-HFD, MS-CD, MS-HFD). Visceral adipose tissue was collected and analyzed at PND133. Perigonadal (PGAT), retroperitoneal (RPAT), and mesenteric (MSAT) visceral adipose tissue deposits were analyzed by histology, Picrosirius Red staining, and immunohistochemistry for leptin and UCP-1; apoptosis was assessed by TUNEL assay. HFD induced adipocyte hypertrophy and early inflammatory changes, while MS predominantly affected stromal organization. Collagen remodeling was depot-specific: PGAT showed an adaptive pattern, RPAT exhibited a significant MS×HFD interaction, and MSAT was primarily affected by MS regardless of diet. Leptin immunoreactivity increased with HFD in UM animals but was attenuated in MS mice, particularly in MSAT. UCP-1 signal was low and heterogeneous, without clear morphological browning. Apoptosis increased in MSAT under MS-HFD conditions. These findings indicate that early-life stress programs depot-specific VAT remodeling, with MSAT emerging as particularly susceptible to obesogenic challenge. Full article

Background/Objectives: Obesity is a complex disease involving the accumulation of an excessive amount of body fat. It is a condition that develops when energy intake and expenditure are out of balance. Inflammation and hypertrophy are caused by the storage of too much white adipose tissue, resulting in adiposity, which also secretes several pro-inflammatory cytokines. Several marketed drugs used to treat obesity have many side effects from long-term ingestion. Other therapeutic compounds from marine sources have already been established for treating obesity. In this paper, the main aim is to establish the anti-obesity effect of derived omega-3 fatty acids, i.e., 20:3(n-3)11-14-17 Icosa Trienoic Acid from Setipinna phasa oil. Methods: In the present investigation, inbred male Swiss albino mice were segregated into six categories as Control, Positive Control, Obese Control, and 20:3(n-3)11-14-17 Icosa Trienoic Acid treated groups with three different doses: Treatment 1, Treatment 2 and Treatment 3. To establish the potentiality of extracted fatty acid, different parameters would be considered, such as body weight, lipid composition and different obesity and obesity-associated inflammation markers. Results: After the isolated compound from Setipinna phasa oil was applied to the treated mice group, it decreased their body weight and serum lipid profile by 39.05%, 62.69%, 62.72%, and 78.46% compared to obese mice. They also had lower levels of uric acid, Serum Glutamic-Oxaloacetic Transaminase, Serum Glutamic Pyruvic Transaminase, and Alkaline Phosphatase, at 67.52%, 57.09%, 64.80%, and 43.99%, than the obese group. Accordingly, the treated group’s expression of genes linked to obesity and pro-inflammatory cytokines was downregulated. The isolated compound affected both anti-inflammatory and anti-obesity markers’ increased expression. Conclusions: After the experiments, it was found that the possibility of using fatty acids might be helpful as an anti-inflammatory and anti-obesity therapeutic strategy. This therapeutic strategy will be cheap and cost-effective. Full article

Pregnancy is characterized by progressive maternal hyperlipidemia, including increased triglycerides, total cholesterol, and low-density lipoprotein, with dynamic fluctuations in high-density lipoprotein. Excess maternal free fatty acids induce oxidative stress through reactive oxygen species, causing mitochondrial dysfunction, lipid peroxidation, activation of inflammatory pathways, and epigenetic remodeling in the placenta and fetal tissues. These molecular alterations impair placental lipid transport and nutrient sensing, leading to hypertrophy of fetal liver, myocardium, and adipose tissue, while disrupting neonatal glucose and lipid homeostasis and increasing susceptibility to perinatal complications and long-term metabolic disorders. This review aims to evaluate mechanistic pathways linking maternal lipid metabolism, oxidative stress, placental function, and fetal organ remodeling. Mechanistic and translational studies were identified through searches of PubMed, Scopus, the Cochrane Library, and Web of Science (2000–2025) using predefined keywords including lipid metabolism, free fatty acids, oxidative stress, placental lipid transport, epigenetics, DNA methylation, fetal programming, and perinatal outcomes. Evidence indicates that maternal lipid imbalance drives placental oxidative and epigenetic modifications, directly contributing to fetal organ hypertrophy and neonatal metabolic dysregulation. In conclusion, maternal dyslipidemia represents a modifiable determinant of fetal organ hypertrophy and long-term metabolic risk, supporting the clinical relevance of maternal lipid monitoring and targeted metabolic interventions during pregnancy. Full article

Background: Unhealthy expansion of adipose tissue (AT) due to excessive dietary intake of omega-6 or overnutrition stimulates the overaccumulation of the extracellular matrix (ECM), resulting in AT metabolic dysregulation. Hypertrophic conditions, excessive adipose depots, and hypoxia stimulate the overproduction of collagenous and non-collagenous proteins, which pathophysiologically initiate the pro-fibrotic signaling pathway associated with fibrosis progression, resulting in atherosclerosis and cardiovascular diseases. Methods: We aimed to investigate adipocyte plasticity in response to a varying ratio of omega-3 (ω3) to omega-6 (ω6) supplementation during the chemically induced adipogenic differentiation of human mesenchymal stem cells. Additionally, changes in lipid accumulation, adipocyte hypertrophy and hyperplasia, active lipid metabolites, and inflammatory cytokine profiles were evaluated. Furthermore, conditioned media from adipocytes treated with different ω3/ω6 ratios were applied to platelets to assess inflammatory responses through prostaglandin and thromboxane measurements. Results: A 1:3 ratio of ω3/ω6 (20:60 µM) significantly reduced lipid accumulation, promoted brown-like adipocyte morphology, and decreased apoptosis and reactive oxygen species (ROS) generation, as confirmed via FACS analysis. Transcriptional control of adipose tissue expansion was confirmed by the downregulation of LIPIN1 and COL1A1 mRNA expression and p-prostaglandin12-R protein levels in a 1:3 ratio when compared with 1:1, 1:2, 1:4, or 2:6 ratios of ω3/ω6. Notably, a 1:3 ratio of fatty-acid-treated adipocyte-conditioned media-treated platelets significantly reduced platelet activation and aggregation, as evidenced by lower p-thromboxane A2 protein levels. Conclusions: Supplementation with a 1:3 (20:60 µM) ω3/ω6 ratio favored the development of lean adipocytes, evidenced by the decreased lipid storage achieved by mitochondrial thermogenesis, which attenuated minimal adipocyte expansion and metabolic inflammation. Full article

Obesity is a chronic, highly prevalent disease affecting nearly one-third of the global population and represents a major independent risk factor for heart failure (HF), particularly heart failure with preserved ejection fraction (HFpEF). Excess adiposity—especially visceral and epicardial adipose tissue (EAT)—acts as an active endocrine and immune organ, promoting chronic low-grade inflammation, oxidative stress, endothelial dysfunction, and adverse myocardial remodeling. Expanded EAT exerts both paracrine inflammatory effects and mechanical constraint on the myocardium, contributing to diastolic dysfunction, microvascular impairment, atrial arrhythmogenesis, and elevated filling pressures despite preserved systolic function. Evidence demonstrates a dose–response relationship between increasing body mass index and incident HF. Clinically, obesity-related HFpEF is characterized by concentric left ventricular hypertrophy, impaired relaxation, increased plasma volume, reduced exercise tolerance, and relatively low natriuretic peptide levels, complicating diagnosis. HF management includes traditional treatment with diuretics, renin-angiotensin system inhibitors, β-blockers, mineralocorticoid receptor antagonists, and angiotensin receptor-neprilysin inhibitors. These agents widely remain foundational as they primarily target hemodynamic and neurohormonal pathways in HF. In contrast, sodium–glucose cotransporter 2 inhibitors consistently reduce HF hospitalizations across the ejection fraction spectrum, while glucagon-like peptide-1 receptor agonists and dual incretin therapies (e.g., tirzepatide) promote substantial weight loss, improve symptoms, and demonstrate promising anti-remodeling effects in obesity-related HFpEF. Recognizing obesity-driven HF as a distinct cardiometabolic entity supports an integrated therapeutic strategy combining structured weight reduction with guideline-directed HF polypharmacotherapy to address both hemodynamic burden and upstream adiposity-related mechanisms. Full article

The increasing prevalence of obesity and metabolic disorders poses a major global health challenge. In the present study, purple sweet potato Tainung No. 73 was fermented using Lactobacillus amylovorus OFMLa-73 and Levilactobacillus brevis OFMLb-143 to enrich the specific bioactive metabolite indolelactic acid. Furthermore, supplementation with fermented sweet potato (FSPE) ethanol extract resulted in a significant reduction in body weight gain, adipocyte hypertrophy, and hepatic lipid accumulation, while also improving serum lipid profiles in high-fat diet-induced obesity mice. These physiological improvements were associated with the downregulated expression of adipogenic and inflammatory genes in both liver and adipose tissues. Furthermore, lipidomic analysis revealed that FSPE modulated key lipid species, including ceramides and acylcarnitines, which are implicated in metabolic dysfunction. Collectively, these findings demonstrated that lactic acid fermentation enhanced purple sweet potato’s functional potential, positioning FSPE as a promising candidate for dietary intervention in obesity management. Full article

Obesity, an escalating global health crisis, is characterized by adipose tissue hypertrophy and chronic low-grade inflammation. Although anti-obesity drugs can induce weight loss, their use is limited by adverse effects, underscoring the need for safer therapeutic strategies. In this study, we generated a recombinant form of Trichinella spiralis-derived macrophage migration inhibitory factor (rTs-MIF) and investigated its anti-inflammatory and anti-obesity effects via immunometabolic regulation. Male C57BL/6 mice fed a 45% high-fat diet were orally administered rTs-MIF, and its effects were evaluated by measuring fat mass, glucose metabolism, serum cytokines, liver histology, and adipose tissue parameters. In 3T3-L1 cells, we examined the effects of rTs-MIF on adipocyte differentiation, obesity-related gene expression, and intracellular signaling pathways. Oral rTs-MIF suppressed body weight gain, reduced fat mass, improved glucose levels, and decreased the food efficiency ratio. It also lowered pro-inflammatory cytokines and increased markers associated with M2 macrophages. In 3T3-L1 cells, rTs-MIF inhibited adipocyte differentiation and reduced the expression of lipogenic transcription factors and mouse Mif while modulating AKT and p44/42 MAPK signaling. These findings identify rTs-MIF as a potential bioactive candidate that ameliorates obesity by regulating the immune–metabolic axis. Full article

Background/Objectives: Itaconic acid (ITA) is an immunometabolite with anti-inflammatory and metabolic regulatory functions, but its cellular source and role in brown adipose tissue (BAT) remain unclear. This study aims to reveal the expression patterns of the key ITA synthesis gene Irg1 in BAT at different developmental stages and to investigate the effects of cold exposure and exogenous ITA on BAT metabolic function and cardioprotection. Methods: Single-cell RNA sequencing was used to analyze the gene expression profiles of stromal vascular fraction (SVF) cells in BAT from P7 neonatal and adult mice. Bioinformatic methods were applied to identify cell types expressing Irg1. Cold exposure (4 °C) and exogenous ITA treatment were employed to evaluate BAT morphology, and the ITA content in BAT was detected using gas chromatography–triple quadrupole mass spectrometry, UCP1 protein expression, and body temperature changes. A transverse aortic constriction (TAC) surgery model was established to induce cardiac dysfunction, and BAT excision was performed to explore the BAT-dependent effects of ITA on myocardial hypertrophy, fibrosis, and cardiac function. Results: In P7 neonatal mouse BAT, Irg1 was predominantly expressed in a subset of interferon-responsive activated macrophages (macrophage27), while in adult mice, it was mainly expressed in neutrophils and a functionally similar macrophage subset (macrophage25). Cold exposure significantly suppressed Irg1 expression in neutrophils but did not affect its expression in macrophages, also resulting in a significant decrease in ITA content in BAT. Exogenous ITA significantly enhanced BAT thermogenesis under cold conditions, which manifested as reduced lipid droplets, upregulated UCP1 expression, and increased body temperature. In the TAC model, ITA treatment markedly improved cardiac function, attenuated myocardial hypertrophy and fibrosis, and these protective effects were significantly diminished after BAT excision. Conclusions: ITA promotes cold adaptation and ameliorates cardiac injury by enhancing BAT metabolic function, and its effects depend on the presence of BAT. This study provides new insights for the treatment of metabolic cardiovascular diseases. Full article

Background/Objectives: Numerous studies have documented cardioprotective effects of adiponectin in animal models of cardiometabolic disease (CMD). Adiponectin receptor agonist ALY688 has demonstrated functional significance against pressure overload-induced cardiac remodeling events in a mouse model of heart failure with reduced ejection fraction (HFrEF), potentially through modulation of the systemic metabolome. However, the specific metabolites and their pathophysiological contribution to cardioprotection in cardiac hypertrophy or heart failure remain unclear. This study aimed to characterize systemic metabolic alterations across five tissues in HFrEF and determine how ALY688 modifies these pathways to mediate cardioprotection in the transverse aortic constriction (TAC) model. Methods: Targeted metabolic profiling was performed on heart, liver, muscle, epididymal white adipose tissue (eWAT), and serum collected five weeks post-surgery from wild-type male C57BL/6 mice. Mice underwent either Sham or TAC-induced left ventricular pressure overload, with or without daily subcutaneous ALY688 administration. Metabolites were quantified using liquid chromatography–tandem mass spectrometry (LC–MS/MS) and statistically analyzed at the tissue level. Results: Consistent with pathological cardiac remodeling, the comprehensive metabolomic analysis revealed that TAC induced widespread disruption of systemic metabolic homeostasis. ALY688 treatment significantly modified several key metabolite classes, including triglycerides (TGs) and glycosylceramides (HexCer). Notably, ALY688 also altered multiple gut-derived metabolites, including trimethylamine N-oxide (TMAO), 5-aminovaleric acid (5-AVA), and glycodeoxycholic acid (GDCA), highlighting a potential gut–liver–heart axis mediating its cardioprotective effects. Conclusions: These findings demonstrate that ALY688 mitigates TAC-induced metabolic dysregulation across multiple tissues. The identified metabolic signatures suggest that ALY688 exerts cardioprotective effects, at least in part, through restoration of systemic metabolic homeostasis and engagement of a gut–liver–heart metabolic axis. These results provide mechanistic insight into adiponectin receptor agonism and support further exploration of ALY688 as a potential therapeutic strategy for HFrEF. Full article

It is now widely recognized that adipocytes have the ability to produce a myriad of bioactive compounds released into the circulation and affecting distal organs, including the heart. These factors, termed adipokines, are also produced by various tissues in addition to adipocytes, including cardiac tissue, and have the ability to modulate cardiac function and the response to pathology. Among the processes greatly affected by adipokines is myocardial remodelling due to hypertrophy and fibrosis, two processes that contribute to the development of heart failure. This is particularly relevant under conditions of obesity, and the accompanying increased adiposity, in general, results in increased adipokine production. The effects of adipokines on cardiac remodelling can be both beneficial or adverse, depending on the adipokine type, such as adiponectin and leptin, respectively. The molecular bases underlying the effects of adipokines on myocardial remodelling have been extensively studied and likely involve a multiplicity of cell signalling processes, thus demonstrating substantial complexity. Emerging evidence suggests that these proteins play an important role in cardiac pathology. Their precise contribution is yet to be determined with certainty, as this likely reflects a balance between pro-remodelling and anti-remodelling factors. Full article

Background: Long pulse width stimulation (LPWS; 120–150 ms) has the potential to stimulate denervated muscles in persons with spinal cord injury (SCI). We examined whether testosterone treatment (TT) + LPWS would increase skeletal muscle size, leg lean mass and improve overall metabolic health in SCI persons with denervation. We hypothesized that one year of combined TT + LPWS would downregulate gene expression of muscle atrophy and upregulate gene expression of muscle hypertrophy and increase mitochondrial health in SCI persons with lower motor neuron (LMN) injury. Methods: Ten SCI participants with chronic LMN injury were randomized into either 12 months, twice weekly, of TT + LPWS (n = 5) or a TT+ standard neuromuscular electrical stimulation (NMES; n = 5). Measurements were conducted at baseline (week 0), 6 months following training (post-intervention 1), and one week following 12 months of training (post-intervention 2). Measurements included body composition assessment using magnetic resonance imaging (MRI) and dual x-ray absorptiometry (DXA). Metabolic profile assessment encompassed measurements of resting metabolic rate, carbohydrate and lipid profiles. Finally, muscle biopsy was captured to measure RNA signaling pathways and mitochondrial oxidative phosphorylation. Results: Compliance and adherence were greater in the TT + NMES compared to the TT + LPWS group. There was a 25% increase in the RF muscle CSA following P1 measurement in the TT + LPWS group. There was a recognizable non-significant decrease in intramuscular fat in both groups. There was a trend (p = 0.07) of decrease in trunk fat mass following TT + LPWS, with an interaction (p = 0.037) in android lean mass between groups. There was a trend (p = 0.08) in mean differences in DXA-visceral adipose tissue (VAT) between groups at P1 measurements. For genes targeting muscle atrophy, TT + LPWS showed a trending decline in MURF1 and FOXO3 genes returning to similar levels as TT + NMES before 12 months. Conclusions: These pilot data demonstrated the safety of applying LPWS in persons with SCI. Six months of TT + LPWS demonstrated increases in rectus femoris muscle CSA. The effects on muscle size were modest between groups. Signaling pathway analysis suggested downregulation of genes involved in muscle atrophy pathways. Future clinical trials may consider a home-based approach with more frequent applications of LPWS. Full article

Background/Objectives: The increase in the global prevalence of obesity has created a need for safe and effective preventive strategies. Probiotics have gained attention for their potential to modulate the gut microbiota and improve metabolic health. In this study, we examined the anti-obesity effects of Lactiplantibacillus plantarum strain 06CC2 (LP06CC2) in a mouse model of mild diet-induced obesity that mimics early-stage metabolic imbalance without significant body weight gain. Methods: Mice were fed a high-fat diet for 8 weeks, with or without LP06CC2 supplementation. Biochemical assays were used to determine the metabolic effects of LP06CC2, and 16S rRNA sequencing was performed to analyze the gut microbiota. Results: LP06CC2 attenuated epididymal fat accumulation and adipocyte hypertrophy, improved the gene expression profiles related to lipid metabolism and inflammation in adipose tissue, and reduced early hepatic steatosis. 16S rRNA sequencing revealed that LP06CC2 modulated the diversity and composition of the gut microbiota, notably suppressing HFD-induced increases in Mucispirillum schaedleri and other taxa associated with inflammation. LP06CC2-treated mice exhibited higher alpha diversity and partial restoration of their microbial profiles toward those of the normal diet-fed animals. LP06CC2 also downregulated pro-inflammatory cytokines and genes related to lipid uptake while modulating markers of thermogenesis and lipolysis. Conclusions: These findings indicate that LP06CC2 can prevent fat accumulation and gut dysbiosis in the pre-obese state, supporting its potential as a functional food ingredient for early intervention in obesity. Further human trials and studies using advanced obesity models are warranted to confirm its efficacy and elucidate its underlying mechanisms of action. Full article

Background/Objectives: Increased fat intake and high content of saturated fatty acids in the diet are associated with higher body weight and an increased risk of obesity. This study aimed to determine the impact of a high-fat diet (HFD) on white adipose tissue (WAT) metabolism and to verify whether this effect depends on the sources of lipids in HFD. Methods: Male C57BL/6J mice, 7 weeks old, received a control (Ctrl.) or high-fat diet (HFD) with 10% and 45% energy from fat, respectively, for 15 weeks. Lard was used as the main dietary fat in the HFD group. Next, the HFD group was subdivided into HFD-L, HFD-CO, HFD-OO and HFD-FO groups differing in the lipid sources (lard, coconut oil, olive oil, fish oil, respectively). The experiment was continued for 12 consecutive weeks. The study analyzed the concentration of different fatty acids in visceral (VAT) and subcutaneous (ScAT) adipose tissue; the levels of autophagy markers: beclin1, Atg5, LC3, p62, AMPK; ER stress markers: phos-PERK, CHOP, XBP-1 and oxidative stress parameters: TAS and TBARS in VAT and ScAT. Results: Mice in all HFD groups showed increased body mass and adipose tissue hypertrophy. Blood glucose concentration remained elevated in the HFD-L group but normalized in other HFD groups by the end of the dietary intervention. Fatty acid content in VAT and ScAT reflected the dietary sources in HFD. The HFD-L, HFD-CO, HFD-OO groups showed increased beclin1, ATG5, and p62 levels in VAT but the LC3-II/LC3-I ratio was similar to the control, suggesting impaired autophagic flux. In the HFD-FO group, the LC-II/LC-I ratio was elevated, along with decreased p62 levels, indicating active autophagic degradation. Changes in autophagy activity were insignificant in ScAT. ER stress markers were also mostly unaffected by HFD in both adipose tissue depots. TAS and TBARS values in VAT and ScAT were similar in the HFD-L and HFD-CO groups, and the HFD-OO group showed increased TAS and decreased TBARS, while the HFD-FO reduced TBARS. Conclusions: Antioxidant capacity and autophagy activity in WAT depended on fat content and lipid source, especially in the visceral depot. Fish oil induced changes in cellular metabolism, especially in VAT, diminishing the detrimental effects of HFD. Full article