In this article, we aim to explore the rapidly developing role of artificial intelligence (AI) in cardiac metabolism research, highlighting its impact on biomarker discovery, precision medicine, and patient stratification. Cardiac metabolism, a key determinant of cardiovascular health, is often disrupted in cardiovascular diseases (CVDs) like heart failure and coronary artery disease. AI’s ability to process and analyze large-scale data offers new chances for understanding and addressing these metabolic dysfunctions. By integrating up-to-date technologies with molecular and clinical insights, AI enables the achievement of personalized treatments, more accurate diagnostics, and the discovery of potential novel therapeutic targets. The main challenges include ethical concerns around data privacy, algorithmic bias, and the need for representative datasets. Future directions focus on developing transparent, accountable, and collaborative AI models that integrate data and enable real-time monitoring, ensuring fairness and accessibility in healthcare. As AI continues to evolve, its role in advancing cardiovascular care is expected to grow, offering new trends in cardiovascular research.

In the present study by Dodig and colleagues, published in Metabolism and Target Organ Damage, the authors investigate the role of insulin in promoting type I collagen synthesis in hepatic stellate cells (HSCs) through α5β1 integrin signaling. Using L-SACC1 transgenic mice, which exhibit hyperinsulinemia and insulin resistance without fasting hyperglycemia, the researchers demonstrate that elevated insulin levels significantly increase type I collagen production in HSCs. This effect is mediated by α5β1 integrin signaling rather than the PI3 kinase pathway. These findings suggest that chronic hyperinsulinemia may preprogram HSCs for enhanced fibrogenesis following liver injury, contributing to advanced fibrosis associated with metabolic disorders such as metabolic dysfunction-associated steatosis liver disease (MASLD) and type 2 diabetes. It further suggests that chronic hyperinsulinemia increases the risk of significant fibrosis burden in chronic liver disease. In this commentary, the strengths and limitations of this study are discussed, along with the potential impact of these findings on current treatment strategies for insulin resistance, endogenous hyperinsulinemia, and exogenous hyperinsulinemia in the development of MASLD and disease progression to fibrosis, cirrhosis, and hepatocellular carcinoma.

An imbalance in the metabolism of glycolipids largely causes numerous metabolic diseases that negatively affect human health. Metrnl plays an important role in glycolipid metabolism and regulates glucose and lipid metabolism through multiple mechanisms. However, the expression level of Metrnl in diseases related to glycolipid metabolism remains controversial. Metrnl can increase the utilization of glucose by tissue cells in glucose metabolism and reduce the adverse effects of a high-glucose environment on the body; in lipid metabolism, it can affect the composition and level of blood lipids, reduce the accumulation of fat, and promote the browning of white fat. The clinical efficacy of exogenously administered recombinant Metrnl needs to be further investigated and verified. This review presents an overview of Metrnl, emphasizing its role in glycolipid metabolism and its association with related diseases. It offers a theoretical foundation for the clinical treatment of glycolipid metabolism-related conditions.

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are key agents in the treatment of type 2 diabetes mellitus (T2DM) and obesity. Small-molecule GLP-1RAs offer the advantage of oral administration while demonstrating efficacy comparable to that of peptide drugs. Despite synthetic challenges and solubility issues, compounds such as Pfizer’s PF-06882961 (Danuglipron), Eli Lilly’s LY3502970 (Orforglipron), and Hengrui Pharma’s HRS-7535 have shown potential to reduce glycosylated hemoglobin A1c (HbA1c) levels and body weight in Phase I-II trials, with mild to moderate gastrointestinal adverse effects, suggesting that they may be promising therapeutic options in the future.

Aim: To investigate the predictor of hypothalamic-pituitary-gonadal (HPG) axis recovery in male pituitary adenoma patients with trans-sphenoid extrapseudocapsular microsurgery.

Methods: From June 2019 to December 2021, we retrospectively analyzed the clinical data of gonadal hormone changes and resection degree before and after surgery in male patients with nonfunctioning pituitary adenoma (NFPA) who underwent microsurgical resection by pseudocapsule technique in the same treatment group at the Department of Neurosurgery, Tongji Hospital. We explored the predictors affecting postoperative testosterone recovery using logistics regression analysis.

Results: Among 291 male patients with pituitary adenomas, the mean age was 50 years. Preoperative testosterone was lower than normal in 127 patients (43.6%); total resection and subtotal were performed in 279 patients (95.9%) and 12 patients (4.1%), respectively. Postoperative follicle-stimulating hormone (FSH) was elevated in 224 (77.0%) patients, luteinizing hormone (LH) was elevated in 230 (79.0%) patients, and prolactin was significantly decreased in 259 (89.0%) patients. Seventy-one of 127 patients with low preoperative testosterone levels recovered to normal levels. Univariate and multivariate analysis suggested that tumor size, coagulative necrotic pituitary apoplexy (CNPA), and invasiveness were predictors of testosterone recovery in patients (P < 0.05).

Conclusion: For male NFPA, transsphenoidal extra-pseudocapsule microsurgery can effectively restore the function of the anterior pituitary gland and promote the recovery of testosterone. Tumor size, CNPA and invasiveness were predictors of testosterone recovery in postoperative patients.

Steatotic liver disease (SLD) is the most common cause of liver disease globally, with an ever-increasing burden. The two primary components of SLD are metabolic dysfunction-associated steatotic liver disease (MASLD) and Alcohol-Associated Liver Disease (ALD). Both entities have important knowledge gaps in differentiation, diagnosis, risk stratification, and prognosis. Given the enormous burden of both MASLD and ALD and their diverse presentation, they form an ideal ground for the application of artificial intelligence (AI) and machine learning (ML) techniques and algorithms. ML models can aid in disease prediction among large populations and estimate those at the highest risk of disease progression or mortality, while applications with AI technology can aid in better detection and monitored treatment approaches. The use of AI in digital pathology and digital therapeutics are attractive options in moving toward personalized medicine. This review briefly summarizes the knowledge gaps in SLD with emerging literature on the use of ML and AI technologies across domains of disease detection, diagnosis, and prognosis.

Wilson disease (WD) is a rare genetic disorder characterized by the excessive accumulation of copper in the body, leading to metabolic alterations and subsequent health complications due to mutations of the ATP7B gene. Despite advancements in medical science, diagnosing this condition remains challenging due to its variable presentation and overlap with other disorders. Traditional diagnostic methods are helpful in establishing WD, although in some cases, conflicting results may necessitate invasive procedures. The practicing physician may not always utilize the known diagnostic parameters or may not weigh their significance due to a lack of experience with the rare population of WD patients. In such cases, artificial intelligence (AI) can facilitate the diagnosis and management of WD, avoiding individual misinterpretation. By leveraging advanced algorithms and machine learning techniques, AI enhances diagnostic accuracy through predictive modeling and data analysis, while also facilitating personalized treatment plans tailored to individual patient profiles. Additionally, AI tools are reshaping disease monitoring through wearable technology and remote systems that provide real-time data integration with electronic health records. However, ethical considerations such as data privacy concerns and algorithmic bias must be addressed to ensure responsible implementation of AI in healthcare settings. The potential for broader applications across various genetic disorders further emphasizes the importance of continued research and interdisciplinary collaboration among tech developers, clinicians, and researchers. Ultimately, this paper highlights how AI can significantly improve patient outcomes and modulate copper metabolism in such a way that WD patients have a normal and worthwhile life expectancy.

The transition from non-alcoholic fatty liver disease (NAFLD) to metabolic dysfunction-associated steatotic liver disease (MASLD) represents a significant evolution in the nomenclature of steatotic liver disease. This updated terminology emphasizes metabolic dysfunction as a central criterion, offering greater precision and improved risk stratification. MASLD broadens the scope of liver disease classification by incorporating individuals with diverse metabolic profiles, including lean patients with hepatic steatosis, and aligns clinical practice with the multifactorial nature of this condition. The global adoption of MASLD creates opportunities for standardization in clinical and research settings, facilitating multicenter collaborations and enhancing the development of diagnostic tools and therapeutic strategies. However, the adoption of this new nomenclature poses challenges, including potential confusion during implementation, cultural and linguistic barriers, the integration of MetALD, and the need for educational initiatives targeting healthcare providers and patients. Further efforts are required to refine diagnostic criteria, address implementation challenges, and seamlessly incorporate MASLD into international coding systems. This review evaluates the key advantages and ongoing challenges associated with MASLD, providing a comprehensive analysis of its impact on clinical practice, research, and global health strategies.

Polycystic ovary syndrome (PCOS) is a complex disorder with a great heterogeneity of signs and symptoms. However, hyperandrogenism is considered a hallmark of PCOS, presented by most affected women. Women with PCOS are at high risk of developing type 2 diabetes mellitus (T2DM), which is associated with insulin resistance (IR) and hyperinsulinemia. In turn, hyperinsulinemia interferes with the androgen production by ovarian cells, and worsens the hyperandrogenism, initiating a feedback cycle. Women with PCOS are also at a greater risk of developing obesity. Indeed, a dysfunctional adipose tissue in obesity contributes to T2DM in PCOS by affecting insulin action and secretion through multiple mechanisms, such as lipotoxicity, inflammation, and adipokine signaling. Therefore, obesity-disrupted adipose tissue can be seen as an important target for T2DM development in women with PCOS. Because adipose tissue can be positively affected by non-pharmacological and easily accessible strategies such as physical exercise, this review provides a comprehensive summary of the benefits of physical exercise to improve adipose tissue health and decrease the risk of obesity and T2DM in women with PCOS.

Tissue spatial interaction in the liver, including the interplay among immune cells, blood vessels, sinusoidal endothelial cells, bile ducts, stellate cells, hepatic progenitor cells, and hepatocytes, is crucial not only for normal organogenesis but also for disease development. Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the most prevalent liver disease, with heterogeneous mechanisms involving cross-talk between hepatocytes and stromal cells under metabolic stress, inflammation, and fibrosis. Developing 3D coculture liver organoid platforms provides novel insights into the complex links of cell communication during disease progression. Thus, we recapitulate liver organoids as models for indicating reconstructed inter-tissue interactions of MASLD, highlighting the potential of transplanting liver organoids as a therapeutic application.

With the backset of the epidemic surge of type 2 diabetes (T2D), obesity, and metabolic dysfunction-associated steatotic liver disease (MASLD), the key role of jejunal mucosa in the development of metabolic disorders, beyond its normal function in nutrient absorption, has become increasingly appreciated. In humans, compared to non-diabetic controls, diabetic patients have jejunal mucosa hypertrophy, hyperplasia of enteroendocrine cells, and increased numbers of enteroendocrine cells and enterocytes. Moreover, functional changes have also been observed, including variations in glucose transporters, enteric nerves, and intestinal microbiota composition. Duodenal mucosa resurfacing (DMR) starts with the assumption that resurfacing the mucosal interface will reset and correct any abnormal signaling from the duodenal mucosa and will, therefore, result in improved pancreatic endocrine function and glucose tolerance owing to restored normal mucosal surface. The endoscopic technique of DMR involves the hydrothermal ablation of the more superficial duodenal mucosal layers. Data reviewed indicate that DMR is a safe and well-tolerated procedure, with favorable outcomes on glucose homeostasis among those with T2D, body weight among those with obesity, and liver tests among those with MASLD. Additional studies are therefore urgently needed to ascertain, among the various surgical, endoscopic and medical choices, the best precision medicine option to fit the individual patient with T2D, obesity, and MASLD.

Robotic metabolic and bariatric surgery (RMBS) has emerged as the most effective approach in the treatment of severe obesity in academic medical centers (AMCs) and community medical centers (CMCs) in the United States of America (USA). However, differences in their scientific productivity in their fields remain unexplored. This bibliometric analysis evaluates the differences in the scientific production related to RMBS in AMC vs. CMC in the USA from the point of view of bibliometric analysis. In the core collection of the Web of Science database, the research technique used in this bibliometric analysis includes specific keywords for “robotic” and “bariatric surgery”. Original articles released up until 2023 were included. A total of 89 articles were included in the study, with 73 originating from AMC and 16 from CMC. Compared with CMC, AMC had a higher average number of articles per year (3.48 vs. 1.1, P = 0.002) and a higher annual growth rate (13.23% vs. 7.6%). However, in terms of scientific impact, there was no difference in the average citations per article (22.73 ± 32.96 vs. 12.25 ± 9.59, P = 0.213) or the proportion of articles published in the highest quality scientific journals (54.8 vs. 56.3, P = 0.916). The scientific output of RMBS increased by 14.5% annually, showing a rising linear trend in AMC and an unclear trend in CMC. The University of Illinois was the most frequent AMC, while the Orlando Health network was the most common CMC. Both CMC and AMC play a pivotal role in the scientific production related to RMBS in the USA, with academic centers having a higher scientific production, but with similar scientific impact to the field at this time.

Fatty liver disease associated with metabolic dysfunction has emerged as a significant global health challenge. This condition often coexists with other liver diseases, such as alcohol-related liver disease and viral hepatitis, complicating both diagnosis and management. To address the limitations of the non-alcoholic fatty liver disease (NAFLD) classification, two alternative frameworks have been proposed: metabolic dysfunction-associated fatty liver disease (MAFLD) in 2020 and metabolic dysfunction-associated steatotic liver disease (MASLD) in 2023. A key difference between these definitions is how they consider fatty liver disease in relation to the coexistence of other liver conditions. MAFLD adopts a dual etiology concept, creating a unified classification system that aligns with contemporary clinical and epidemiological needs. In contrast, MASLD introduces a new term, MetALD (metabolic and alcohol-related/associated liver disease), to describe patients who have both metabolic dysfunction and excessive alcohol intake. This review critically examines the clinical, research, and epidemiological implications of the differing approaches of MAFLD and MASLD, offering insights into their potential to enhance the understanding and management of multi-etiology liver diseases.

Metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (ALD) are among the leading indications for liver transplantation (LT). The definition of metabolic dysfunction- and alcohol-associated liver disease (MetALD) identifies individuals with MASLD who consume moderate levels of alcohol, representing a severe phenotype within the steatotic liver disease (SLD) spectrum. Patients with MetALD face higher risks of post-LT complications, including metabolic syndrome, graft steatosis, and fibrosis. Despite the rising prevalence of MetALD due to increasing obesity and alcohol consumption, data on its recurrence or de novo development post-LT remain limited. The management of MetALD post-LT is particularly challenging due to the interplay of metabolic factors and potential alcohol relapse. Current evidence suggests that recurrent or de novo MetALD often progresses more rapidly to advanced fibrosis than in native livers, underscoring the importance of early detection and management. Integrated approaches addressing both metabolic syndrome and alcohol-related risks are essential for optimal management. Non-invasive diagnostic modalities, such as transient elastography and specific biomarkers like phosphatidylethanol (Peth), are promising in assessing graft health and alcohol relapse, respectively. Emerging therapies, including glucagon-like peptide-1 receptor agonists (GLP1-RAs) and fibroblast growth factor-21 (FGF21) analogs, offer potential dual-action benefits targeting metabolic dysfunction and alcohol consumption. These innovations, coupled with lifestyle interventions and tailored immunosuppressive regimens, may improve patient outcomes and reduce graft failure. This review highlights the need for multidisciplinary strategies and further research to optimize the management of MetALD post-LT, aiming to improve survival and quality of life in this high-risk population.

Alcohol-associated liver disease (ALD) is one of the most prevalent liver diseases and a leading indication for liver transplantation (LT). Alcohol use disorder (AUD), commonly present in patients with ALD, may also be associated with psychiatric comorbidities such as depression and anxiety. Early identification of ALD and timely treatment of AUD can help prevent the progression to advanced stages of ALD, including cirrhosis and alcoholic hepatitis. However, screening for alcohol use and managing AUD in ALD patients are often not performed due to various barriers at the patient, clinician, and administrative levels. This review highlights an integrated multidisciplinary care model, emphasizing the roles of hepatologists, psychiatrists, addiction counselors, and social workers in providing comprehensive management of both liver disease and AUD. It outlines laboratory assessments, pharmacological and behavioral therapies, and recommended follow-up evaluations by specialists. The goal of this article is to promote team-based comprehensive care for patients with ALD.