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Metabolic-associated steatohepatitis liver disease (MASLD) currently impacts a quarter of the global population, and its incidence is expected to increase in the future. As a result, hepatocellular carcinoma associated with MASLD is also on the rise. Notably, this carcinoma does not always develop alongside liver cirrhosis, often leading to a more advanced stage at diagnosis. The challenge lies in accurately identifying patients who are at a higher risk to tailor screening processes effectively. Additionally, several therapeutic approaches are being explored to prevent hepatocellular carcinoma, although there are no universally accepted guidelines yet. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) is a progressive liver disease characterized by the build-up of fat in the liver of individuals in the absence of alcohol consumption. This condition has become a burden in modern societies aggravated by the lack of appropriate predictive biomarkers (other than liver biopsy). To better understand this disease and to find appropriate biomarkers, a new technology has emerged in the last two decades with the ability to explore the unmapped role of lipids in this disease: lipidomics. This technology, based on the combination of chromatography and mass spectrometry, has been extensively used to explore the lipid metabolism of NAFLD. In this review, we aim to summarize the knowledge gained through lipidomics assays exploring tissues, plasma, and lipoproteins from individuals with NAFLD. Our goal is to identify common features and active pathways that could facilitate the finding of a reliable biomarker from this field. The most frequent observation was a variable decrease (1–9%) in polyunsaturated fatty acids in phospholipids and non-esterified fatty acids in NAFLD patients, both in plasma and liver. Additionally, a reduction in phosphatidylcholines is a common feature in the liver. Due to the scarcity of studies, further research is needed to properly detect lipoprotein, plasma, and tissue lipid signatures of NAFLD etiologies, and NAFLD subtypes, and to define the relevance of this technology in disease management strategies in the push toward personalized medicine. [ABSTRACT FROM AUTHOR]

Adipose tissue (AT), once considered a mere fat storage organ, is now recognized as a dynamic and complex entity crucial for regulating human physiology, including metabolic processes, energy balance, and immune responses. It comprises mainly two types: white adipose tissue (WAT) for energy storage and brown adipose tissue (BAT) for thermogenesis, with beige adipocytes demonstrating the plasticity of these cells. WAT, beyond lipid storage, is involved in various metabolic activities, notably lipogenesis and lipolysis, critical for maintaining energy homeostasis. It also functions as an endocrine organ, secreting adipokines that influence metabolic, inflammatory, and immune processes. However, dysfunction in WAT, especially related to obesity, leads to metabolic disturbances, including the inability to properly store excess lipids, resulting in ectopic fat deposition in organs like the liver, contributing to non-alcoholic fatty liver disease (NAFLD). This narrative review delves into the multifaceted roles of WAT, its composition, metabolic functions, and the pathophysiology of WAT dysfunction. It also explores diagnostic approaches for adipose-related disorders, emphasizing the importance of accurately assessing AT distribution and understanding the complex relationships between fat compartments and metabolic health. Furthermore, it discusses various therapeutic strategies, including innovative therapeutics like adipose-derived mesenchymal stem cells (ADMSCs)-based treatments and gene therapy, highlighting the potential of precision medicine in targeting obesity and its associated complications. [ABSTRACT FROM AUTHOR]

Trans-10, cis-12-conjugated linoleic acid (CLA)-enriched diets promote atherosclerosis in mice despite increasing blood concentrations of HDL cholesterol. This suggests that under these conditions, the HDL apolipoproteins (apo) produced are abnormal. To test this hypothesis, apoE-deficient mice were fed a Western-type diet enriched with linoleic acid (control), cis-9, trans-11-CLA or trans-10, cis-12-CLA (1.0% wt/wt) for 12 wk, and the effects on HDL metabolism and apoC-III levels recorded. Compared with the control and cis-9, trans-11-CLA mice, those fed the trans-10, cis-12-CLA diet had significantly higher HDL cholesterol concentrations, and had a higher incidence of hypertriglyceridemia and hepatic steatosis. Plasma apoA-I and paraoxonase concentrations were significantly lower in the trans-10, cis-12-CLA group than in the cis-9, trans-11-CLA group. These reductions were associated with decreased hepatic expression of these proteins and a shift toward lipid-poor apolipoprotein particles. The plasma apoA-II concentration increased with its corresponding mRNA concentration in the liver, and was preferentially bound to HDL in the trans-10, cis-12-CLA mice, thus explaining the increased HDL cholesterol concentrations in this group. Significant, positive associations were found between apoA-II and C-III (r = 0.883, P < 0.001) and between apoA-II and atherosclerosis (r = 0.68, P < 0.001). These results indicate that trans-10, cis-12-CLA intake modifies HDL to form a proatherogenic apoA-II containing particle and promotes phenotypic changes compatible with metabolic syndrome. Cis-9, trans-11-CLA does not promote this detrimental effect. KEY WORDS: * conjugated linoleic acid * apolipoprotein * high density lipoproteins * atherosclerosis * paraoxonase

Background: The Global Leadership Initiative on Malnutrition (GLIM) provided a new approach for the diagnosis of malnutrition based on a number of phenotypic and etiologic criteria. However, different diagnostic criteria could potentially lead to heterogeneity in the diagnosis. We identified different subsets of criteria to define malnutrition in a cohort of elder nursing‐home residents and investigated their clinical utility in terms of 1‐year survival. Methods: Our study included all residents (n = 485) from 3 nursing homes. We proposed 12 GLIM models based on different phenotypic and etiologic criteria. The main outcome was 1‐year all‐cause mortality. We also assessed the sensitivity and specificity for different phenotypic criteria using time‐dependent receiver operating characteristic curves, and cutoff values were calculated. Results: During 1 year of follow‐ups, 94 deaths occurred. The prevalence of malnutrition was 13.5% for models based on reduced food intake (RFI) and 10.45% for models based on inflammation associated with acute disease (IAD). Unadjusted Cox regression analyses showed that malnutrition was associated with a 2.31‐ to 4.64‐fold increase in mortality when diagnosed using IAD‐dependent models or with a 1.37‐ to 1.78‐fold increase in mortality using RFI‐dependent models. Cutoffs associated with mortality for the phenotypic criteria were lower than those recommended in the GLIM criteria. Conclusion: This study describes the association of several variations of the GLIM model with 1‐year mortality in nursing‐home residents. However, our data suggest a high heterogeneity to fulfill the GLIM criteria and the necessity of finding specific, tailored cutoff points for the studied populations. [ABSTRACT FROM AUTHOR]

Background: Diabetes and older age are associated with an increased risk of malnutrition and mortality. Recently, the Global Leadership Initiative on Malnutrition (GLIM) provided a 2‐step approach for the malnutrition diagnosis. In this study, we aimed to determine whether GLIM nutrition status at admission was associated with long‐term survival in elderly patients with type 2 diabetes mellitus (T2DM). Additionally, we aimed to identify which GLIM criteria were more able to become prognostic indicators of early or late death. Methods: Our study included a convenience sample of 159 patients with T2DM older than 65 years and admitted to the internal medicine wards of different Spanish hospitals: the VIDA‐survival cohort. Nutrition status was retrospectively assessed with the new GLIM criteria. The main outcome was long‐term mortality in the cohort during an 8‐year follow‐up. Bivariate tables summarized the variables of interest. Kaplan‐Meier survival curves and adjusted Cox regressions were also performed. Results: According to the GLIM criteria, we observed that the 35.8% and 16.3% of the VIDA‐survival cohort were categorized as having moderate and severe malnutrition, respectively. Severe malnutrition was associated with increased mortality (hazard ratio [HR] = 2.09; 95% CI, 1.29–3.38), compared with nonmalnourished participants. Moderate malnutrition had a neutral effect on all‐cause mortality (HR = 1.30; 95% CI, 0.88–1.92). Low plasma albumin levels, a surrogate marker of inflammation, were strongly associated with early mortality. Conclusion: Our study provides evidence that severe malnutrition according to GLIM criteria is associated with increased long‐term all‐cause mortality among elderly individuals with T2DM. [ABSTRACT FROM AUTHOR]