Search Results (417)

Background: Obesity is a growing global health concern and a modifiable risk factor for multiple pancreatic diseases, including acute pancreatitis (AP), chronic pancreatitis (CP), and pancreatic cancer (PC). While these conditions have distinct clinical courses, obesity contributes to their pathogenesis through shared mechanisms, such as visceral adiposity, systemic inflammation, insulin resistance, and ectopic pancreatic fat deposition. Methods: This narrative review synthesizes current evidence from clinical, epidemiological, and mechanistic studies exploring the relationship between obesity and pancreatic diseases. We also critically evaluate the effects of weight loss interventions—including lifestyle modifications, pharmacologic therapies, endoscopic approaches, and bariatric surgery—on the risk and progression of disease. Results: Obesity increases the risk and severity of AP via mechanisms such as gallstone formation, hypertriglyceridemia, and lipotoxicity. In CP, obesity-related intrapancreatic fat and metabolic dysfunction may influence disease progression, although some data suggest a paradoxical protective effect. In PC, obesity accelerates tumorigenesis through chronic inflammation, adipokine imbalance, and activation of oncogenic signaling pathways. Weight loss interventions, particularly bariatric surgery and incretin-based therapies (e.g., GLP-1 receptor agonists and dual agonists such as tirzepatide), show promising effects in reducing disease burden and improving metabolic and inflammatory profiles relevant to pancreatic pathology. Conclusions: Obesity plays a multifaceted role in the pathophysiology of pancreatic diseases. Therapeutic strategies targeting weight loss may alter disease trajectories, improve outcomes, and reduce cancer risk. Further research is needed to define optimal intervention strategies and to identify and validate biomarkers for personalized risk assessment and prevention. Full article

Background/Objectives: Although eating disorders (EDs) affect a large portion of the population and have a significant impact on health and productivity, they are understudied in the workplace. We assessed the frequency of EDs and studied the relationship between EDs and occupational and individual factors. Methods: All workers undergoing health surveillance were invited to fill in the Eating Disorder Examination Questionnaire, short form (EDE-QS) and, before their routine medical examination that included metabolic tests, measure their level of health literacy, stress, quality of sleep, anxiety, depression, and happiness. Out of a total of 2085 workers, 1912 (91.7%) participated. Results: Suspected EDs affected 4.9% (CI95% 3.9; 5.9) of workers, with no notable difference in gender (5.3% CI95% 4.1; 6.7 in female workers vs. 4.2%, CI95% 2.9; 5.9 in male). Cases were significantly associated with trauma and emotional factors (anxiety, depression, unhappiness), but also with work-related stress and poor sleep quality, and negatively associated with health literacy. Using a hierarchical logistic regression model, suspected cases of EDs were significantly predicted in Model II by life trauma (OR 2.21 CI95% 1.40; 3.48, p < 0.001) and health literacy (OR 0.94 CI95% 0.90; 0.98, p < 0.001), in Model III also by work-related stress (OR 2.57 CI95% 1.68; 3.94, p < 0.001), and in Model IV by depression (OR 1.19 CI95% 1.02; 1.38, p < 0.05) and happiness (OR 0.88 CI95% 0.78; 0.99, p < 0.05). An association was also found between EDs and overweight, obesity, increased abdominal circumference, hypercholesterolemia, hypertriglyceridemia, hyperglycemia, arterial hypertension, atherogenic index of plasma, and metabolic syndrome. Conclusions: The workplace is an ideal setting for the prevention of EDs and their consequences. Occupational health intervention should promote health literacy, improve sleep quality, and reduce work-related stress. Full article

Atherosclerotic cardiovascular disease (ASCVD) remains the leading global cause of morbidity and mortality, even in the era of aggressive low-density lipoprotein cholesterol (LDL-C) lowering. This persistent residual risk has prompted a reevaluation of atherogenic lipid markers, with non-high-density lipoprotein cholesterol (non-HDL-C) and apolipoprotein B (Apo B) emerging as superior indicators of the total atherogenic particle burden. Unlike LDL-C, non-HDL-C includes cholesterol from all atherogenic lipoproteins, while Apo B reflects the total number of atherogenic particles regardless of cholesterol content. Their clinical relevance is underscored in populations with diabetes, obesity, and hypertriglyceridemia, where LDL-C may not adequately reflect cardiovascular risk. This review explores the biological, clinical, and genetic foundations of non-HDL-C and Apo B as critical tools for risk stratification and therapeutic targeting. It highlights discordance analysis, inflammatory mechanisms in atherogenesis, the influence of metabolic syndromes, and their utility in specific populations, including those with chronic kidney disease and children with familial hypercholesterolemia. Additionally, the role of lipoprotein (a), glycation in diabetes, and hypertriglyceridemia are examined as contributors to residual risk. Clinical trials and genetic studies support Apo B and non-HDL-C as more robust predictors of cardiovascular events than LDL-C. Current guidelines increasingly endorse these markers as secondary or even preferred targets in complex lipid disorders. The incorporation of Apo B and non-HDL-C into routine clinical practice, especially for patients with residual risk, represents a paradigm shift toward personalized cardiovascular prevention. The review concludes with recommendations for guideline integration, emerging therapies, and future directions in biomarker-driven cardiovascular risk management. Full article

Background/Objectives: Extracellular volume (ECV) expansion reflects myocardial fibrosis and may play a role in subjects with severe aortic stenosis (AS) receiving transcatheter aortic valve implantation (TAVI). This study aimed to assess the relationship between cardiovascular risk factors (CVRF), AS severity and left ventricular myocardial ECV measured by cardiac computed tomography (CCT). Methods: 61 patients qualified for TAVI underwent pre-procedural CCT. CVRFs were recorded, including advanced age, male gender, obesity, hypertension, hypercholesterolemia, hypertriglyceridemia, type 2 diabetes, and smoking. The CCT protocol included non-contrast (for aortic valve calcium score, AVCS), angiographic (for vascular access planning), and delayed phases (for left atrial appendage thrombus assessment). ECV was calculated from attenuation values of the interventricular septum and left ventricular cavity assessed in native and delayed phases. Patients were stratified based on the presence/absence of individual CVRFs, median AVCS, and aortic valve area (AVA). Results: Mean ECV was higher in patients with hypertension (28.01% vs. 26.93%, p = 0.03), smokers (28.71% vs. 26.52%, p = 0.01), AVCS ≥ 2975 (28.08% vs. 26.95%, p = 0.02), and AVA < 0.95 cm² (28.63% vs. 26.53%, p = 0.01). Positive correlations were found between ECV and the number of CVRFs (r = 0.49, p = 0.01), BMI (r = 0.30, p = 0.01), systolic BP (r = 0.31, p = 0.02), and AVCS (r = 0.36, p = 0.01); AVA correlated negatively (r = −0.59, p = 0.01). Regression showed that hypertension, smoking, and smaller AVA were independent predictors of higher ECV. Conclusions: Among TAVI candidates, hypertension, smoking, and more advanced AS are independently associated with increased myocardial ECV on CCT. These findings may reflect subclinical myocardial remodeling and support the added diagnostic value of ECV in pre-TAVI assessment. Full article

Atopic dermatitis (AD) is a chronic, complex, and immunologically mediated skin disease. Its exact cause remains complex, multifaceted and yet to be discovered but is likely related to a combination of immunological, genetic and environmental factors. A medical literature search of PubMed (1992–present), Google Schoolar and Embase was performed using appropriate terms without date limitations in accordance with the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines. Nevertheless, chronic inflammation is believed to be a major player in the development of AD and a causative element in the development of metabolic syndrome (MetS). Metabolic syndrome is a cluster of common metabolic abnormalities including hypertension, insulin resistance, abdominal obesity, reduced high-density lipoprotein (HDL)–cholesterol levels and elevated triglyceride levels. High waist circumference is positively correlated with the risk of atopic dermatitis, but there is no significant correlation between adult-onset atopic dermatitis and hypertension. Some evidence suggests an association between AD and hypertension but only in patients with severe AD. On the other hand, the relationship between AD and hyperglycemia or AD and cholesterol levels seems inconclusive. The aim of this review is to present current knowledge on the association between atopic dermatitis and metabolic syndrome, including each of the components of metabolic syndrome. Full article

Background/Objectives: Fatty liver disease (FLD) is currently the most common liver disorder, affecting 25–30% of the global population. Its occurrence is strongly associated with overweight, obesity, and type 2 diabetes. In 2020, the disease definition was revised from NAFLD (non-alcoholic fatty liver disease) to MAFLD (metabolic-associated fatty liver disease), emphasizing its link to metabolic dysfunction and marking a major shift in clinical evaluation and risk stratification. We assessed the association between MAFLD and cardiovascular risk factors in a geriatric population by comparing patients with and without fatty liver disease and evaluating the influence of selected metabolic and echocardiographic parameters on MAFLD prevalence. Methods: This retrospective study was conducted using data from patients treated at the Department of Geriatrics, the University Clinical Hospital, in Wrocław. The study included 237 patients diagnosed with fatty liver disease and 148 controls without liver pathology. The groups were compared in terms of comorbidities, laboratory abnormalities, body mass index (BMI), and left ventricular hypertrophy. Statistical analysis was performed to assess the association between the severity of selected variables and the risk of MAFLD. Results: Patients with MAFLD had significantly higher body weight and BMI compared to controls. Diabetes mellitus and hypertriglyceridemia were more frequent in the MAFLD group, whereas HDL and vitamin D3 levels were lower. Echocardiographic indicators of left ventricular hypertrophy [IVSd, LVPWd, (IVSd + LVPWd)/2] were significantly elevated in MAFLD patients. Conclusions: This study confirms a strong association between MAFLD and cardiovascular risk factors in elderly patients. The inclusion of a control group allowed for more precise evaluation, supporting the role of MAFLD as an independent cardiometabolic risk indicator in geriatric care. Full article

The discovery of new drugs offers valuable alternatives, particularly for treating diseases that are resistant to existing therapies or involving complex, multi-organ conditions such as metabolic syndrome. Although treatment algorithms are generally well established and primarily based on synthetic pharmaceuticals, they are increasingly being supplemented by biological and biosimilar agents. This trend is particularly evident in the development and advancement of anti-diabetic and hypolipemic therapies. This review explores advances in the treatment of hypercholesterolemia and hypertriglyceridemia, elevated lipoprotein(a) [Lp(a)], diabetes, and obesity associated with metabolic syndrome. It focuses mainly on biopharmaceuticals such as proteins and nucleotide-based drugs (antisense oligonucleotides, small interfering RNA), but also on dipeptidyl peptidase-4 (DPP-4) inhibitors classified as incretin drugs along with glucagon-like peptide-1 (GLP-1) analogues. Due to the substantial role of SGLT-2 (sodium/glucose cotransporter 2) inhibitors in novel diabetes therapies, especially for managing cardiovascular risk, this group of compounds was also included in this review. Many clinical data in the field of effectiveness of biopharmaceuticals in metabolic disorders are provided. Therefore, in this review, we mainly include a brief history of drug development and approval, first synthesis and structure modifications, which relevantly influence pharmacokinetics, and safety. We provide only brief comparison of biological drugs with metformin and sulphonylureas derivatives. Databases such as PubMed, Scopus, and Google Scholar are searched for the period between 2000 and 2024. Full article

1-Acylglycerol-3-phosphate O-acyltransferase (1-AGPAT) is an enzyme family composed of 11 isoforms. Notably, 1-AGPAT 2, the most studied isoform since its discovery, is a critical enzyme in the triglyceride synthesis pathway, converting lysophosphatidic acid to phosphatidic acid. In addition, AGPAT2 gene expression is shown to be essential for adipocyte development and maturation. Defects in AGPAT2 are responsible for significant pathophysiological alterations related to adipose tissue (AT). Pathogenic variants in this gene are the molecular etiology of Congenital Generalized Lipodystrophy type 1 (CGL1), in which fatty tissue is absent from birth. Metabolically, these individuals have several metabolic complications, including hypoleptinemia, hypoadiponectinemia, hyperglycemia, and hypertriglyceridemia. Furthermore, numerous AGPAT2 pathogenic variants that enormously affect the amino acid sequence, the tertiary structure of 1-AGPAT 2, and their transmembrane and functional domains were found in CGL1 patients. However, studies investigating the genotype–phenotype relationship in this disease are scarce. Here, we used bioinformatics tools to verify the effect of the main pathogenic variants reported in the AGPAT2 gene: c.366-588del, c.589-2A>G, c.646A>T, c.570C>A, c.369-372delGCTC, c.202C>T, c.514G>A, and c.144C>A in the 1-AGPAT 2 membrane topology. We also correlated the phenotype of CGL1 subjects harboring these variants to understand the genotype–phenotype relationship. We provided an integrative view of clinical, genetic, and metabolic features from CGL1 individuals, helping to understand the role of 1-AGPAT 2 in the pathogenesis of this rare disease. Data reviewed here highlight the importance of new molecular studies to improve our knowledge concerning clinical and genetic heterogeneity in CGL1. Full article

Background and Objectives: Metabolic syndrome (MetS) is characterized by a cluster of metabolic abnormalities, including abdominal obesity, hyperglycemia, insulin resistance, dyslipidemia, and hypertension. Growing evidence suggests that these components may contribute to the development of gastrointestinal (GI) malignancies. This review aims to explore the association between MetS and GI cancers, including esophageal, gastric, pancreatic, and colorectal cancers. Materials and Methods: A narrative literature review was conducted using PubMed, incorporating 22 sources published between 1991 and 2024. Search terms included “gastrointestinal malignant tumors”, “metabolic syndrome”, “diabetes mellitus”, and “obesity”. Priority was given to large-scale studies from Europe, America, and Asia. Case reports, commentaries, and conference abstracts were excluded. Results: By analyzing the available literature data, this study determined that hyperinsulinemia (IGF-1 pathway), hyperglycemia, and obesity (>102 cm in men and >88 cm in women) are highly associated with the development of esophageal cancer (primarily with Barret’s long and short segment as precancerosis), gastric cancer (through reactive oxygen species), and both pancreatic (1.5–2.4 higher risk) and colorectal cancer (30% higher risk). Patients with a high BMI (>40 kg/m²) show a 20%- or 1.18-times greater risk of developing colorectal cancer and a 1.72-times higher risk of developing pancreatic cancer. There is not enough evidence on the specific influence of hypertriglyceridemia, low HDL cholesterol, and high blood pressure on the development of gastrointestinal malignancy. However, those three conditions have shown a low to moderate association (from 6% to 12%) with the development of colorectal cancer. Conclusions: Metabolic syndrome (MetS) is increasingly being recognized as a significant risk factor for the development and progression of gastrointestinal cancers. Key components such as obesity, hyperglycemia, insulin resistance, and type 2 diabetes mellitus appear to contribute to carcinogenesis through mechanisms involving chronic inflammation, oxidative stress, and immune dysregulation. Further research is needed to clarify the biological pathways linking MetS to gastrointestinal malignancies and to inform effective prevention strategies. Full article

Background and Objectives: Hemophagocytic lymphohistiocytosis (HLH) is a rare hyperinflammatory condition characterized by excessive activation of cytotoxic lymphocytes and macrophages, resulting in a cytokine storm, multiorgan damage, and high mortality. HLH is classified into primary (genetic) and secondary (acquired) forms, with diagnosis often challenging due to nonspecific symptoms. Macrophage activation syndrome (MAS) refers to the secondary HLH triggered by rheumatic diseases. In this study, we retrospectively analyzed the clinical and laboratory features of patients with secondary HLH to enhance understanding of this life-threatening condition and summarize emerging management strategies. Materials and Methods: This single-center retrospective study analyzed medical records of patients hospitalized with HLH at the University Hospital in Kraków, Poland, from 2013 to 2024, based on HLH-2009 criteria and HScore > 169 points. Diagnostic criteria included clinical, laboratory, and histological findings, e.g., hemophagocytosis in bone marrow, circulating cytopenia, and elevated ferritin levels. Results: A total of 21 patients met the criteria for HLH diagnosis, with a median age of 35 (range: 19–67) years, including 12 women (57.1%). The median HScore among the patients was 244 (range: 208–304) points. Fever was the most common presenting symptom, occurring in all cases. High ferritin, hypertriglyceridemia, and hypofibrinogenemia in peripheral blood were also prevalent. Bone marrow hemophagocytosis was confirmed in 66.7% of cases (n = 12/18 of available data). Regarding immunosuppressive therapy, glucocorticosteroids were the most frequently used (used in all cases). Four (19.0%) patients died during HLH (cases triggered by lymphoma [twice], Epstein–Barr virus infection, unknown reason). Compared to survivors, these patients had lower counts of white blood cells, neutrophils, and lymphocytes at diagnosis (p < 0.05 for all). Conclusions: Secondary HLH is a severe syndrome requiring rapid diagnosis and timely intervention to improve patient outcomes. Lower white blood cell, neutrophil, and lymphocyte counts present worse prognostic factors. Full article

Background/Objectives: Supplementation with nicotinamide mononucleotide (NMN), a key nicotinamide adenine dinucleotide (NAD⁺) intermediate, exerts anti-aging, anti-obesity, and anti-diabetic effects in animal experiments. However, previous studies have evaluated NMN supplementation using oral administration in drinking water or by intraperitoneal administration. No studies have reported whether NMN exerts beneficial effects when incorporated into the diet. The diet is a multicomponent mixture of many nutrients that may interact with each other, thus weakening the effects of NMN. In the present study, we evaluated whether dietary NMN intake protects obese diabetic db/db mice from obesity-related metabolic disorders, such as dyslipidemia, hepatic steatosis, hyperglycemia, and hyperinsulinemia. Methods: Five-week-old male db/db mice were randomly assigned to two groups and fed for four weeks either a control diet containing 7% corn oil and 0.1% cholesterol (CON group, n = 6) or a diet supplemented with 0.5% NMN (NMN group, n = 5). Results: After 4 weeks of feeding, dietary NMN intake alleviated obesity, hypertriglyceridemia, and hepatic triglyceride accumulation in db/db mice. Respiratory gas analysis indicated that dietary NMN intake significantly enhanced energy expenditure by suppressing carbohydrate oxidation and increasing fat oxidation after 3 weeks of feeding. Additionally, the suppression of the increase in plasma triglyceride (TG) levels by dietary NMN intake was attributable to a reduction in hepatic TG levels through the suppression of fatty acid synthesis and the enhancement of fatty acid β-oxidation in the liver. Furthermore, the improvement in hepatic fatty acid metabolism induced by dietary NMN intake was partially responsible for the significant increase in plasma adiponectin and soluble T-cadherin levels. Conclusions: This is the first report to show that dietary NMN intake but not oral administration in drinking water or intraperitoneal administration alleviates body fat mass and hypertriglyceridemia by enhancing energy expenditure, with preferential promotion of fat oxidation, the enhancement of hepatic lipolysis, and the suppression of hepatic lipogenesis in db/db mice. Full article

Introduction/Objectives: Although monounsaturated fatty acids (MUFAs) are known as a healthy nutrient, their impact on the risk of metabolic syndrome (MetS) in the Asian population is not fully understood. This study aimed to determine the association between dietary MUFA intake and the prevalence of MetS among Korean adults. Materials and Methods: The 7th Korea National Health and Examination Survey (2016–2018) was analyzed. MetS was defined based on the guideline of the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) criteria, and MUFA intake was calculated using a single 24 h dietary recall. Data from 3932 younger adults (19–39 years), 6943 middle-aged adults (40–64 years), and 3942 older adults (≥65 years) were included and multivariable logistic regression models were applied to estimate odds ratios (OR) and 95% confidence intervals (CI). Results: Approximately 25.8% of Korean adults showed signs of MetS, and the average MUFA intake was 13.70 g/day. Middle-aged adults with a higher MUFA intake had a lower risk of MetS (OR 0.52, 95% CI 0.35–0.78 for men; OR 0.66, 95% CI 0.43–0.99 for women) compared to those with a lower MUFA intake after the adjustment of possible confounding variables, including age, body mass index, total energy intake, household income, alcohol consumption, smoking, aerobic exercise, and energy intake from carbohydrates. No significant associations were observed in younger and older adults. Conclusions: These results suggest that higher dietary MUFA consumption is associated with a lower risk of MetS in middle-aged Korean adults. These findings suggest that including MUFA-rich foods in the diet could be a practical strategy to reduce the burden of MetS in clinical and public heath settings. Full article

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease (NAFLD), is rapidly becoming the most prevalent form of chronic liver disease in both pediatric and adult populations. It encompasses a wide spectrum of liver abnormalities, ranging from simple fat accumulation to severe conditions such as inflammation, fibrosis, cirrhosis, and liver cancer. Major risk factors for MASLD include obesity, insulin resistance, type 2 diabetes, and hypertriglyceridemia. Methods: This narrative review employed a comprehensive search of recent literature to identify the latest studies on the relationship between MAFLD and obesity, the health consequences and the latest treatment options to prevent long-term damage to the liver and other organs. Additionally, the article presents perspectives on diagnostic biomarkers. Results: Childhood obesity is linked to a multitude of comorbid conditions and remains a primary risk factor for adult obesity. This abnormal fat accumulation is known to have long-term detrimental effects into adulthood. Scientific evidence unequivocally demonstrates the role of obesity-related conditions, such as insulin resistance, dyslipidemia, and hyperglycemia, in the development and progression of MASLD. Oxidative stress, stemming from mitochondrial dysfunction, is a leading factor in MASLD. This review discusses the interconnections between oxidative stress, obesity, dyslipidemia, and MASLD. Conclusions: Atherogenic dyslipidemia, oxidative stress, inflammation, insulin resistance, endothelial dysfunction, and cytokines collectively contribute to the development of MASLD. Potential treatment targets for MASLD are focused on prevention and the use of drugs to address obesity and elevated blood lipid levels. Full article

Acute pancreatitis is a common gastrointestinal condition, primarily caused by gallstones and alcohol abuse, with other causes including hypertriglyceridemia, trauma, infections, etc. While most cases are mild and self-limiting, up to 20% of patients develop severe pancreatitis with pancreatic necrosis, increasing the risk of multi-organ failure and mortality. Conservative management involves fluid resuscitation, nutritional support, and antibiotics for infected peripancreatic fluid collections (PFCs). When PFCs are infected or symptoms persist, invasive interventions such as endoscopic ultrasound (EUS)-guided drainage or percutaneous drainage are recommended. Dual modalities (endoscopic and percutaneous drainage) offer better outcomes with fewer complications. Direct endoscopic necrosectomy is considered for patients who do not improve with drainage. A multidisciplinary team, including endoscopists, interventional radiologists, surgeons, and specialists, is essential for optimal management of severe necrotizing pancreatitis. Full article

Background/Objectives: Propofol is a preferred agent for ICU sedation. Hypertriglyceridemia occurs in up to 45% of patients on propofol and has been linked with adverse effects. Data extrapolated from acute pancreatitis suggests intravenous (IV) insulin infusions may be effective in reducing serum triglyceride (TG) values in patients with propofol-induced elevated TG. The objective is to describe and compare serum TG levels in critically ill patients receiving concomitant insulin infusions and propofol versus propofol alone. Methods: This is a retrospective cohort study of mechanically ventilated adult patients admitted to a medical intensive care unit who received a propofol infusion alone or propofol and IV insulin infusions and who had a minimum of two serum TG levels while on propofol infusion. The primary outcome was median change in the serum TG concentration in patients receiving concomitant propofol and IV insulin infusions, as compared to those receiving propofol alone. Results: A total of 263 patients were screened and 32 met inclusion criteria (16 in each group). The median change between first and last obtained TG level was 0.35 (−0.31–1.33) vs. −0.07 (−1.08–+0.42) mmol/L (p = 0.051) in the propofol vs. propofol and IV insulin groups, respectively. Each day on propofol was associated with an estimated 0.21 mmol/L (95% confidence interval (CI) 0.0.004 to 0.41, p = 0.046) increase in TG, and each additional day of IV insulin was associated with a 0.14 mmol/L (95% CI −0.63 to 0.35, p = 0.571) decrease in TG. Conclusions: Each additional day of propofol was associated with an increase in serum TG levels. IV insulin infusions did not lead to a significant difference in triglyceride values. Full article