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Introduction Visceral (VAT), subcutaneous (SFT), and total body fat (FM) contribute to hepatic steatosis, yet their relative and sex-specific effects across total, regional, and site-specific levels remain unclear. We investigated associations between fat depots, standardized skinfold sites, and liver fat (LF) while adjusting for key metabolic covariates. Methods In this secondary data analysis of a cross-sectional study, 48 adults (50% women; 49.6 ± 20.9 y; BMI 25.7 ± 3.7 kg/m²) underwent quantitative MRI to assess VAT and LF and ultrasound-based body mapping to quantify total and regional SFT as well as standardized skinfold sites. Bioelectrical impedance analysis determined FM. Regression analyses were conducted with LF as the dependent variable, identifying and controlling for significant covariates (diabetes mellitus [DM], arterial hypertension [aHT], hypercholesterolemia [HC], physical activity, age) (partial r). The Lindeman–Merenda–Gold (LMG) method decomposed total R² into fat-specific contributions. Total fat depots were adjusted for body surface area (BSA). Results All regression models examining associations with LF showed total r values ranging from 0.63 to 0.79. In men, DM was the only significant covariate (p = 0.002). Values are given as: partial r, LMG share (% of R 2 ). LF correlated with VAT/BSA (0.40, 51%), total SFT/BSA (0.38, 42%), and FM/BSA (0.36, 51%). Regionally, upper-body SFT (0.40, 45%) and SFT_arms (0.37, 47%) contributed most, whereas lower-body SFT (0.35, 13%) showed minimal impact. The triceps skinfold was the most influential site among skinfolds (0.45, 50%). In women, HC was the only significant covariate (p = 0.02). LF correlated with VAT/BSA (0.40, 49%), total SFT/BSA (0.51, 27%), and FM/BSA (0.47, 36%). Regional models yielded upper-body SFT (0.43, 36%), SFT_arms (0.38, 23%), and lower-body SFT (0.41, 9%). Among single sites, the umbilical skinfold was most relevant (0.43, 36%), followed by the biceps (0.42, 33%). Conclusion VAT remains pivotal for LF in both sexes, yet SFT exhibits clear sex- and region-specific relevance. Only subcutaneous fat of the upper-body and arms contributed meaningfully to liver fat. Simple skinfold assessments—particularly triceps in men—may serve as practical indicator for early risk stratification. Larger, prospective cohorts are needed to confirm these findings. Trial registration Not applicable this study did not involve any health care intervention.

Background Maintaining a proper balance between saturated and unsaturated fatty acids in membrane phospholipids is essential for normal cellular function. The evolutionarily conserved transmembrane protein AdipoR2 plays a central role in this homeostatic process. While the detrimental effects of saturated fatty acids on cells have been previously documented, the associated ultrastructural changes remain less investigated. Methods Here, we used transmission electron microscopy to study the consequences of silencing AdipoR2 in the presence or absence of fatty acid supplements. Results We found that exposure of human cells to palmitic acid (PA)—the most abundant saturated fatty acid in the human body—disrupts the ultrastructure of cytoplasmic membranes and mitochondrial cristae. PA exposure also induces distinctive blebbing between the inner and outer membranes of the nuclear envelope. These membrane abnormalities are exacerbated by AdipoR2 silencing and are partially prevented by supplementation with oleic acid (OA), an unsaturated fatty acid. Furthermore, we observed ectopic localization of the mitophagy marker PINK1 and the fatty acid metabolism enzyme ACSL1 to closely apposed ER membranes, a structure that forms exclusively in PA-treated cells. Conclusions Together, these findings reveal that exogenous PA triggers significant membrane defects, worsened in the absence of AdipoR2, and alters protein distribution within the cell.

Brain is a vital organ of the human body which performs very important functions such as analysis, processing, coordination, and execution of electrical signals. For this purpose, it depends on a complex network of nerves which are ensheathed in lipids tailored myelin; an abundant source of lipids in the body. The nervous system is enriched with important classes of lipids; sphingolipids and cholesterol which compose the major portion of the brain particularly in the form of myelin. Both cholesterol and sphingolipids are embedded in the microdomains of membrane rafts and are functional units of the neuronal cell membrane. These molecules serve as the signaling molecules; hold important roles in the neuronal differentiation, synaptogenesis, and many others. Thus, their adequate provision and active metabolism are of crucial importance in the maintenance of physiological functions of brain and body of an individual. In the present review, we have highlighted the physiological roles of cholesterol and sphingolipids in the development of the nervous system as well as the association of their altered metabolism to neurological and neurodegenerative diseases.

Metabolic dysfunction-associated steatotic liver disease (MASLD) has garnered considerable attention globally. Changing lifestyles, over-nutrition, and physical inactivity have promoted its development. MASLD is typically accompanied by obesity and is strongly linked to metabolic syndromes. Given that MASLD prevalence is on the rise, there is an urgent need to elucidate its pathogenesis. Hepatic lipid accumulation generally triggers lipotoxicity and induces MASLD or progress to metabolic dysfunction-associated steatohepatitis (MASH) by mediating endoplasmic reticulum stress, oxidative stress, organelle dysfunction, and ferroptosis. Recently, significant attention has been directed towards exploring the role of gut microbial dysbiosis in the development of MASLD, offering a novel therapeutic target for MASLD. Considering that there are no recognized pharmacological therapies due to the diversity of mechanisms involved in MASLD and the difficulty associated with undertaking clinical trials, potential targets in MASLD remain elusive. Thus, this article aimed to summarize and evaluate the prominent roles of lipotoxicity, ferroptosis, and gut microbes in the development of MASLD and the mechanisms underlying their effects. Furthermore, existing advances and challenges in the treatment of MASLD were outlined.