Search Results (197)

Background/Objectives: Colon adenocarcinoma is a heterogeneous disease, and tumours of similar pathological stage may differ in their metabolic and proliferative characteristics. Stearoyl-CoA desaturase (SCD) is involved in lipid metabolic reprogramming and may reflect aspects of tumour biology. The main goal of this study was to analyse SCD expression and its associations with clinicopathological factors, particularly focusing on histological grade. The relationship between SCD and proliferating cell nuclear antigen (PCNA) was evaluated as a secondary objective. Methods: Public TCGA/UALCAN and CPTAC/UALCAN data were examined as supportive transcriptomic and proteomic observations. Immunohistochemical SCD and PCNA expression was assessed in 113 patients with colon adenocarcinoma, and SCD localisation was additionally examined by qualitative immunogold electron microscopy. Standardised SCD and PCNA scores were combined with equal weighting to generate a secondary exploratory z-score. Associations with clinicopathological characteristics were assessed using appropriate univariable analyses, while the relationship between SCD and PCNA and the potential incremental contribution of SCD beyond PCNA were examined using correlation and exploratory regression-based analyses. ROC analyses were used only as exploratory descriptions of statistical separation between predefined clinicopathological groups. Results: Observations from supportive public databases indicated that SCD expression was higher in tumour tissue compared to normal tissue at both the transcriptomic and proteomic levels. In the institutional cohort, SCD expression was elevated in tumour tissue relative to matched non-neoplastic mucosa and was associated primarily with histological grade but not with nodal status or pathological stage. SCD showed a modest positive correlation with PCNA. The secondary exploratory combined SCD–PCNA score was associated with histological grade and with nodal status but did not outperform PCNA alone. Adding SCD to PCNA provided only limited incremental information for G3 histology and no incremental value for nodal involvement. Conclusions: SCD is a tumour-associated metabolic marker in colon adenocarcinoma, with its strongest association observed for histological grade. The combined score should not be interpreted as a biological entity or superior biomarker. Full article

Background: Kidney disorders are strongly related to metabolic disturbances, including obesity and type 2 diabetes. Excessive intake of sugar and saturated fats promotes lipid accumulation, cellular energy issues and inflammatory responses. Cannabigerol (CBG), a non-psychotropic phytocannabinoid, has recently gained attention for its metabolic, anti-inflammatory and potential protective properties. Methods: The present study investigated the effect of two weeks of CBG administration (last 14 days of the experiment) on fatty acid (FA) composition, FA metabolic pathways and FA transporters in rats subjected to a high-fat high-sucrose diet (HFHS) for 6 weeks. Male Wistar rats were divided into four groups: Control, CBG, HFHS, and HFHS+CBG. Kidney tissue and urine samples were analyzed by gas–liquid chromatography (GLC) for lipid fractions and FA profiles, while protein expression of FA transporters and metabolic enzymes was assessed by immunoblotting. Polysaccharides and collagen fibers were visualized using Periodic Acid-Schiff (PAS) and AZAN staining, respectively. ELISA and colorimetric kits were used to measure urinary albumin and creatinine contents. Results: HFHS feeding altered renal lipid homeostasis, increasing saturated and monounsaturated fatty acids (SFA and MUFA, respectively) levels and affecting desaturation and elongation ratios. CBG supplementation affected renal lipid metabolism by lowering triacylglycerol (TAG) accumulation, restoring polyunsaturated fatty acids (PUFA) in phospholipid (PL) and altering FA ratios, suggesting an improvement in lipid balance. CBG also increased the expression of carnitine palmitoyltransferase 1 (CPT1) and lipoprotein lipase (LPL) and decreased the expression of stearoyl-CoA desaturase 1 (SCD1) and fatty acid synthase (FAS), suggesting a shift toward enhanced FA oxidation and reduced lipogenesis. Conclusions: Overall, CBG exerted good effects on renal lipid metabolism and may mitigate early lipid-mediated injury associated with metabolic kidney disorders. Full article

Clear cell renal cell carcinoma (ccRCC) is increasingly recognized as a lipid-addicted malignancy in which de novo lipogenesis (DNL) supports tumor growth, survival, and treatment resistance. ccRCC-specific genetic alterations, particularly loss of VHL and activation of hypoxia-inducible factor (HIF) signaling, promote SREBP-mediated upregulation of key lipogenic enzymes, including ATP-citrate lyase (ACLY), acetyl-CoA carboxylase (ACC), fatty acid synthase (FASN), and stearoyl-CoA desaturase 1 (SCD1). These pathways support membrane biogenesis and redox balance while also promoting metabolic flexibility, enabling adaptation to therapeutic and microenvironmental stresses. Emerging preclinical studies suggest that pharmacological inhibition of lipogenic enzymes, either alone or in combination with tyrosine kinase inhibitors, mTOR inhibitors, HIF-2α antagonists, or immune checkpoint blockade, may suppress ccRCC progression. However, most therapeutic data remain limited to preclinical models, and clinical validation is still lacking. This review synthesizes recent advances in molecular regulation and therapeutic targeting of DNL in ccRCC and discusses the challenges and future opportunities to improve mechanistic understanding and explore potential therapeutic applications. Full article

This study demonstrated the effects of dietary supplementation with 1% raspberry (RO) or 1% strawberry (SO) seed oil from 5 to 12 weeks of age (n = 6/group) on folliculogenesis, hormonal parameters, the ovarian fatty acid profile, and the expression of related genes in juvenile rabbits. After slaughter, ovaries and blood were collected. Ovaries were used for histology, fatty acid profiling, and gene expression analysis, while plasma was used to measure progesterone (P4), testosterone (T), estradiol-17β (E2), follicle-stimulating hormone (FSH), and anti-Müllerian hormone (AMH) concentrations. Both RO and SO reduced the number of primary follicles (p = 0.04), whereas RO increased the number of antral follicles (p = 0.04) compared with the control. In both supplemented groups, FSH (p = 0.04 and p = 0.035) and AMH (p = 0.04) concentrations were higher. RO increased P4 and E2 (p = 0.03 and p = 0.013) concentrations, while SO only increased P4 (p = 0.02) levels. SO altered the ovarian fatty acid profile, increasing selected monounsaturated fatty acids and reducing polyunsaturated fatty acids, likely by increasing the expression of the converting enzyme, stearoyl-CoA desaturase 5 (p = 0.038). Overall, both oils influenced folliculogenesis through hormonal changes, and SO modified ovarian fatty acid composition, which may affect ovarian function in juvenile rabbits. 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

This experiment investigated the effects of dietary Artemisia ordosica Krasch. (AOK) supplementation on the n3-polyunsaturated fatty acid (n3-PUFA) profile of subcutaneous adipose tissue (SADT) in Arbas cashmere goats and explored the underlying transcriptional mechanisms. Forty healthy, weaned kids (120 ± 10 days of age; similar body weight) were randomly allocated to two groups (n = 20): a control group (CON, basal diet) and an AOK group (AOK, basal diet with 3% of the roughage replaced by AOK). The feeding trial spanned 104 days, consisting of a 14-day adaptation period and 90 days of data acquisition. Compared with the CON group, AOK significantly reduced the content of saturated fatty acids (SFAs) and n6-polyunsaturated fatty acids (n6-PUFAs)/n3-PUFAs (n6/n3). In contrast, the levels of n3-PUFAs in the SADT of cashmere goats increased markedly (p < 0.05). Compared with the CON group, AOK exhibited significantly higher activities of hormone-sensitive lipase (HSL) (p = 0.027), adenylyl cyclase 2 (ADCY2) (p = 0.010), adenylyl cyclase 5 (ADCY5) (p = 0.046), cluster of differentiation 36 (CD36) (p = 0.013), solute carrier family 27 member 4 (SLC27A4) (p = 0.021), and fatty acid binding protein 4 (FABP4) (p = 0.040), along with significantly lower activities of fatty acid synthase (FAS) (p = 0.002), lipoprotein lipase (LPL) (p = 0.048), and stearoyl-coa desaturase (SCD) (p = 0.026) in SADT. Compared with the CON group, the activities of superoxide dismutase (SOD) (p = 0.032), catalase (CAT) (p = 0.010), glutathione peroxidase (GSH-PX) (p = 0.029), and total antioxidant capacity (T-AOC) (p = 0.002) were significantly increased in the AOK group. Transcriptomic profiling revealed that AOK supplementation downregulated mRNA levels of ADCY2, ADCY5, LPL, FAS, SCD, stearoyl-CoA desaturase 1 (SCD1), stearoyl-CoA desaturase 2 (SCD2), glycogen synthase 1 (GYS1), acyl-CoA oxidase 1 (ACOX1), acetyl-CoA carboxylase (ACC), diacylglycerol acyltransferase 1 (DGAT1), fatty acid desaturase 1 (FADS1), solute carrier family 27 member 2 (SLC27A2), erythroblastic leukemia viral oncogene homolog 4 (ERBB4), and carnitine palmitoyltransferase 1B (CPT1B) (p < 0.05). It also markedly induced acyl-CoA synthetase long-chain family member 4 (ACSL4) (p < 0.01) in SADT. Genes significantly enriched in the adenosine-monophosphate-activated protein kinase (AMPK) signaling pathway included LPL, SCD1, CPT1B, and GYS1 (p = 0.010). Genes significantly enriched in the phosphatidylinositol 3-kinase-akt (PI3K-Akt) signaling pathway included GYS1 and ERBB4 (p = 0.015). CPT1B, ADCY2, and GYS1 were identified as the genes significantly enriched in the insulin resistance signaling pathway (p = 0.048). LPL was the only gene significantly enriched in the cholesterol metabolism pathway (p = 0.049). Genes showing a tendency toward significant enrichment in the peroxisome-proliferator-activated receptor (PPAR) signaling pathway included ACSL4, CPT1B, SCD1, and LPL (p = 0.051). These interconnected cascades improve insulin sensitivity, stimulate triglyceride (TG) hydrolysis, and modulate n3-PUFA levels. Supplementation with AOK enhances n3-PUFA content by accelerating TG breakdown while simultaneously restraining FA oxidation in SADT. Consequently, AOK supplementation can be effectively used to enhance the nutritional value of cashmere goat meat through improved n3-PUFA deposition in SADT. Full article

Background/Objectives: Altered lipid metabolism is a key feature of type 2 diabetes mellitus (T2DM), yet its impact on early spinal cord involvement remains poorly understood. Distinguishing between pathological lipid accumulation and adaptive metabolic responses is essential for interpreting initial stages of neural alteration in T2DM. This study aimed to characterize spinal cord lipid composition and ATPase activities in a rat model of T2DM. Methods: Zucker diabetic fatty (ZDF) rats were used as a model of T2DM and divided into diabetic and obese groups, with lean Zucker rats as controls. ATPase activities in spinal cord tissue were measured spectrophotometrically, and lipid profiling was performed using gas chromatography with flame-ionization detection. Indices of stearoyl-CoA desaturase-1 (SCD1) and delta-5 desaturase activity (D5D) were calculated from specific fatty acid ratios as estimates of enzyme-related activity. Results: Diabetic rats exhibited significantly higher levels of free monounsaturated fatty acids (MUFAs) compared with controls, while the obese group showed a moderate increase. Elevated SCD1 indices were indicative of increased estimated MUFA synthesis. Levels of free polyunsaturated fatty acids (PUFAs), including those crucial for myelin stability, as well as ATPase activities, remained unchanged, suggesting preserved basal membrane-associated enzyme function. Conclusions: This study identifies lipid alterations in the spinal cord preceding overt neurodegenerative changes in T2DM, characterized by increased free MUFA abundance, without evidence of altered ATPase activities. These findings support the interpretation that lipid changes observed at this stage are more consistent with adaptive metabolic remodeling than with overt structural or functional neural impairment. Full article

The accumulation dynamics and regulatory mechanisms of the alkylamides, the key pungent compounds in the fruits of Sichuan peppers, remain poorly understood. Using fruits of the Zanthoxylum planispinum var. dintanensis (Dintan) harvested at five key developmental stages, we comprehensively mapped the accumulation of numbering compounds and their underlying molecular drivers by integrating HPLC-based metabolite profiling and de novo transcriptomics. Total alkylamide content increased during development, with hydroxyl-α-sanshool (HαSS) being predominant. The contributions of hydroxyl-β-sanshool (HβSS) and hydroxyl-ε-sanshool (HεSS) increased in later stages. Cluster and correlation analyses identified 51 candidate genes strongly correlated (|r| ≥ 0.6) with HαSS accumulation, predominantly enriched in fatty acid and branched-chain amino acid metabolism pathways. The expression patterns of five stearoyl-CoA desaturase (SCD) genes, one long-chain acyl-CoA synthetase (ACSL/fadD), and one S-(hydroxymethyl)glutathione dehydrogenase/alcohol dehydrogenase (frmA) gene closely mirrored HαSS accumulation. In contrast, 3-oxoacyl-[acyl-carrier-protein] synthase II (fabF) and one β-ketoacyl-CoA synthase (KCS) gene exhibited a negative correlation. Accordingly, a positive regulatory network was constructed for HαSS accumulation. These findings revealed key candidate targets for deciphering the molecular basis of its unique flavor and for breeding high-pungency cultivars. Full article

The prevalence of metabolic dysfunction-associated steatohepatitis (MASH) is rising worldwide. hFGF1^ΔHBS, a variant of human fibroblast growth factor 1 with three substitutions in its heparin-binding sites, was previously shown by our group to ameliorate fatty liver. However, hFGF1^ΔHBS also significantly modulates systemic metabolism, making it unclear whether its hepatic benefits arise from direct liver-specific actions. Additionally, its poor pharmacokinetic profile underscores the need for alternative delivery strategies. Here, we employed adeno-associated virus serotype 8 under the thyroxine-binding globulin promoter (AAV8-TBG) to achieve sustained, hepatocyte-specific expression of hFGF1^ΔHBS. In high-fat-, high-cholesterol-diet-fed apolipoprotein E knockout mice, liver-directed hFGF1^ΔHBS expression markedly reduced hepatic steatosis, inflammation, and fibrosis, independent of changes in body weight, blood glucose, insulin sensitivity, body composition, or circulating triglyceride and cholesterol levels. Mechanistically, hFGF1^ΔHBS gene transfer normalized fatty acid synthesis and suppressed fatty acid uptake by downregulation of stearoyl-CoA desaturase-1 and cluster of differentiation 36. Importantly, these therapeutic effects were achieved without inducing hepatic hyperproliferation, as evidenced by unchanged expression of proliferating cell nuclear antigen and antigen Kiel 67. Collectively, our findings demonstrate that hFGF1^ΔHBS exerts direct hepatoprotective effects and that AAV8-TBG-mediated liver-directed hFGF1^ΔHBS delivery represents a safe and effective strategy for treating MASH. Full article

Metabolic reprogramming is a fundamental hallmark and a key driver of malignant tumors. By reshaping glucose, lipid, and amino acid metabolism, as well as mitochondrial function, it sustains the abnormal proliferation and survival of tumor cells, making it a crucial target for anti-tumor therapy. Curcumin, a natural multi-target compound, exhibits unique advantages in intervening in tumor metabolic reprogramming due to its low toxicity and broad-spectrum regulatory properties. In various tumor models, it can directly modulate the activity of key glycolytic enzymes, such as hexokinase 2, lactate dehydrogenase A, and pyruvate kinase M2, as well as transporters like glucose transporter 1. Furthermore, it inhibits the expression of proteins related to lipid metabolism, including fatty acid synthase and stearoyl-CoA desaturase 1, while also intervening in amino acid metabolic networks, such as glutaminase and branched-chain amino acid transaminase. Additionally, curcumin targets mitochondrial function and reactive oxygen species balance, creating multi-dimensional intervention effects through various pathways, including the induction of ferroptosis by regulating the SLC7A11/GPX4 axis and modulating gut microbiota metabolism. Its mechanism of action involves the synergistic regulation of key signaling pathways, including phosphoinositide 3-kinase/Akt, NF-κB, AMP-activated protein kinase, and hypoxia-inducible factor-1alpha. Furthermore, its specific effect profile demonstrates significant dependency on cell type and tumor model. This article systematically reviews the regulatory effects of curcumin on these critical metabolic processes and pathways in tumor metabolic reprogramming, revealing its molecular mechanisms in disrupting tumor growth and progression by targeting energy and biosynthetic metabolism. These findings provide a significant theoretical foundation and a preclinical research perspective for the development of natural antitumor drugs based on metabolic regulation, as well as for optimizing combination therapy strategies. Full article

Boll abscission in cotton (Gossypium spp.) is a key factor that limits yield; however, the molecular mechanisms underlying this process remain poorly understood. In this study, boll abscission characteristics were uncovered in four cotton varieties that exhibited extreme differences in boll abscission rates via tissue sectioning. Transcriptome analysis was performed on the four cotton varieties. Using weighted gene co-expression network analysis (WGCNA) of the transcriptome data, we identified a stearoyl-(acyl-carrier-protein) desaturase (SACPD) as a potential key regulator of boll abscission. We also performed evolutionary analyses on the SACPD gene family across five cotton species and identified 63 members that were classified into four evolutionary clades, with duplication-polyploidization events being a major driver of gene expansion. Tissue-specific expression profiling revealed that Gossypium hirsutum GhSACPD19 is highly expressed in the abscission zone. Our findings suggest a role of GhSACPD19 in regulating boll abscission, likely through metabolism of jasmonate, a well-known positive regulator of abscission. Our work offers new insights into the regulation of organ abscission at cellular and molecular levels and presents a valuable resource for cotton yield improvement. Full article

This study examined the effect of long-term physical activity during the finishing period on meat and fat quality, and metabolic gene expression in obese Alentejano (AL) pigs. From 87.3 to 161.6 kg BW and for 130 days, eighteen pigs were assigned to either individual pens without an exercise area (NE, n = 9) or an outdoor park with an exercise area (WE, n = 9). Both groups received identical commercial diets at 85% ad libitum intake. Loin (Longissimus lumborum—LL), tenderloin (Psoas major—PM), and dorsal subcutaneous fat samples were obtained at slaughter, and analyzed for fatty acid composition and gene expression. Physical activity modulated the fatty acid profile and key metabolic genes in muscle and fat tissues. WE pigs showed higher palmitoleic (p = 0.031) and linolenic (p = 0.022) acids in LL, while Fatty acid synthase and Leptin in LL were downregulated (p = 0.071 and p = 0.018, respectively); Fatty acid binding protein 4 was downregulated (p = 0.003) and Stearoyl-CoA desaturase upregulated (p = 0.020) in the PM of WE pigs, indicating changes in lipid metabolism. Also, Myosin heavy chain 7 was upregulated (p = 0.016) in LL, suggesting oxidative muscle remodeling. These findings suggest that moderate, long-term physical activity during finishing induces modest but favorable metabolic adaptations in muscle and fat tissues without compromising meat quality in AL pigs, supporting its use in traditional rearing systems aimed at balancing animal welfare and product quality in local breeds. Full article

The development of hepatic steatosis in geese is a complex, multistage process involving genes related to lipid synthesis, transport, storage, and metabolism. Key genes activated during this process include ME1 (malic enzyme 1), SCD1 (stearoyl-CoA desaturase), ACSL1 (acyl-CoA synthetase long-chain family member 1), and ELOVL6 (elongation of very-long-chain fatty acids protein 6). The expression of these genes varies depending on the tissue, breed, and metabolic context. Geese possess a unique ability to develop hepatic steatosis (fatty liver) without accompanying inflammation or liver damage. This condition typically arises from overfeeding, either through carbohydrates or fats, leading to significant triglyceride accumulation in hepatocytes. Importantly, this state remains reversible and is considered non-pathological. The physiological and molecular changes observed in overfed geese, particularly regarding liver lipid accumulation and serum enzyme activity, closely resemble those found in human non-alcoholic fatty liver disease (NAFLD). This similarity makes geese an excellent biomedical model for studying NAFLD. Overfeeding initiates a cascade of enzymatic reactions that regulate lipid metabolism at the genetic level. These reactions decrease circulating free fatty acids and glucose while promoting triglyceride storage in the liver. The aim of this study is to synthesize current knowledge on the genetic regulation of fatty acid metabolism in geese, highlighting how these genes coordinate the processes of activation, desaturation, synthesis, and elongation during induced steatosis. Moreover, the summarized effects of different diet supplements will enhance goose feeding strategies for foie gras production. Full article

In this study, we aimed to characterize intramuscular fat (IMF) tissue in fattening steers through a comparison with subcutaneous fat (SCF) tissue. The IMF of the longissimus thoracis et lumborum and the SCF of the back fat from three fattening steers (mean body weight of 703.50 ± 11.45 kg) were collected, and the muscle tissue, connective tissue, and fascia were carefully removed. Gene and protein expressions and the lipid contents were assessed via transcriptomic, proteomic, and lipidomic analyses, respectively. Subsequently, tissue-specific factors were identified using integrated analysis. The results revealed that the expressions of sarcoplasmic/endoplasmic reticulum Ca²⁺ transporting 2 (ATP2A2), enolase 3 (ENO3), fructose-bisphosphatase 2 (FBP2), myosin heavy chain 7 (MYH7), myosin light chain 3 (MYL3), myosin light chain kinase (MYLK), glycogen phosphorylase (PYGM), troponin C1 (TNNC1), and tropomyosin 2 (TPM2) significantly increased in IMF at both the mRNA and protein levels, whereas those of fatty acid-binding protein 4 (FABP4), stearoyl-CoA desaturase (SCD), and apolipoprotein E (APOE) were reduced. The abundances of both phosphatidylinositol (PI) (18:1/20:4) and phosphatidylcholine (PC) (15:0/18:2) were positively correlated with APOE. Conversely, that of PI (18:1/20:4) was negatively correlated with ENO3 and PYGM, whereas PC (15:0/18:2) was negatively correlated with TNNC1 and MYLK. In conclusion, we identified calcium signaling and glycolysis as key IMF-regulating pathways. ATP2A2, ENO3, FBP2, MYH7, MYL3, MYLK, PYGM, TNNC1, TPM2, and LPE 18:0 were negatively associated with IMF deposition, whereas FABP4, SCD, APOE, PI (18:1/20:4), and PC (15:0/18:2) were positively associated with it. These findings offer underlying IMF-related targets to promote IMF deposition in cattle. Full article

Background: Obesity is a complex metabolic disease associated with several health complications, including insulin resistance, hypertension, and type 2 diabetes mellitus. Growing evidence indicates that fatty acid profiles and the activity of desaturating enzymes—stearoyl-CoA desaturase-1 (SCD1), delta-5 desaturase (D5D), and delta-6 desaturase (D6D)—are important factors in the pathophysiology of obesity. This review aims to summarise the current understanding of the alterations in lipid metabolism and desaturase activity in obesity, its complications, and potential therapeutic interventions. Methods: A literature review was performed using the PubMed, Scopus, and Web of Science databases. Systematic reviews, meta-analyses, clinical studies, cross-sectional studies, and animal studies that assessed fatty acid profiles and desaturase activity in the context of obesity were included. Results: Obesity is associated with significant changes in the profiles of saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (PUFAs), as well as altered desaturase activity. Increased activity of SCD1 and D6D and decreased activity of D5D are observed even in childhood and correlate with metabolic risk markers. Genetic variation in genes encoding fatty acid desaturases, such as fatty acid desaturase 1 (FADS1), fatty acid desaturase 2 (FADS2), and SCD1, influences lipid metabolism and susceptibility to metabolic disorders. Nutritional interventions, supplementation (e.g., omega-3 fatty acids, L-carnitine, and crocin), physical activity, and bariatric surgery positively influence the fatty acid profile and enzymatic activity, modifying the risk of obesity-related diseases. Conclusions: Fatty acid profile and desaturase activity are significantly altered in obesity and represent potential biomarkers and therapeutic targets for its treatment and the prevention of related complications. Their assessment may contribute to a more personalised approach to treating obesity and associated metabolic diseases. Full article