With a dramatic increase in the number of obese and overweight people, there is a great need for new anti-obesity therapies. With the discovery of the functionality of brown adipose tissue in adults and the observation of beige fat cells among white fat cells, scientists are looking for substances and methods to increase the activity of these cells. We aimed to describe how scientists have concluded that brown adipose tissue is also present and active in adults, to describe where in the human body these deposits of brown adipose tissue are, to summarize the origin of both brown fat cells and beige fat cells, and, last but not least, to list some of the substances and methods classified as BAT promotion agents with their benefits and side effects. We summarized these findings based on the original literature and reviews in the field, emphasizing the discovery, function, and origins of brown adipose tissue, BAT promotion agents, and batokines. Only studies written in English and with a satisfying rating were identified from electronic searches of PubMed.

Obesity poses a significant and escalating challenge in contemporary society, increasing the risk of developing various metabolic disorders such as dyslipidemia, cardiovascular diseases, non-alcoholic fatty liver disease (NAFLD), type 2 diabetes, and certain types of cancer. The current array of therapeutic interventions for obesity remains insufficient, prompting a pressing demand for novel and more effective treatments. In response, scientific attention has turned to the fibroblast growth factor 21 (FGF21) due to its remarkable and diverse impacts on lipid, carbohydrate, and energy metabolism. This comprehensive review aims to delve into the multifaceted aspects of FGF21, encompassing its discovery, synthesis, functional roles, and potential as a biomarker and therapeutic agent, with a specific focus on its implications for NAFLD.

Background and Objectives: This is a retrospective study conducted at the Clinical County Hospital of Craiova, Romania, providing valuable insights into hemorrhagic transformation (HT) in thrombolyzed patients with acute ischemic stroke (AIS). Hemorrhagic complications remain a significant concern after intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA). This study aims to analyze clinical and biological factors associated with HT following thrombolysis. Materials and Methods: A retrospective analysis was conducted on 356 patients who received rt-PA at the Clinical County Hospital of Craiova between January 2020 and December 2024. Patients were divided into three groups based on CT findings at 24 h post-thrombolysis: no HT, minimal HT, and massive HT. Baseline characteristics were analyzed, including demographics, medical history, NIHSS scores, imaging findings, and laboratory parameters. Statistical analysis was performed using ANOVA and chi-square tests, with a significance threshold of p < 0.05. Results: HT occurred in 12.08% of patients (minimal HT: 8.15%, massive HT: 3.93%). Mortality was significantly higher in the massive HT group (71.43%) compared to minimal HT (41.38%) and non-HT (13.42%) (p < 0.001). Lower platelet count (p = 0.003), elevated blood glucose (p = 0.004), prolonged QT interval (p = 0.004), and reduced fibrinogen levels (p = 0.005) were significantly associated with HT. Other risk factors included atrial fibrillation (p = 0.001), hypertension (p = 0.005), delayed door-to-needle time (p < 0.001), diabetes mellitus (p = 0.007), dense ACM sign on CT (p = 0.003), older age (p < 0.001), obesity (p = 0.001), early neurological deterioration at 2 h/24 h (p < 0.001), elevated GOT (p < 0.001), elevated GPT (p = 0.002), lower LDL cholesterol (p < 0.001), lower total cholesterol (p = 0.001), and lower triglycerides (p < 0.001). Conclusions: Patients with HT had worse clinical outcomes, with massive HT associated with the highest mortality. Risk factors include age, nutritional status, hyperglycemia, and low platelet and fibrinogen levels, among others.

Non-alcoholic fatty liver disease (NAFLD) is increasingly recognized as a systemic condition with neuropsychiatric comorbidities, including depression. Growing evidence for the neuroprotective, antidepressant, and anxiolytic potential of Portulaca oleracea (PO) extract, provides a compelling rationale for investigating its effects in the interaction between dietary models of NAFLD and vulnerability to stress-related disorders. Fifty-four 14- to 18-week-old male and female C57BL/6N mice were distributed in two equal groups and fed either a methionine- and choline-deficient diet (MCD) or a methionine- and choline-controlled diet (MC). Subsequently, half of each group was subjected to chronic unpredictable mild stress (CUMS) and PO treatment. MCD caused significant weight loss, whereas MC promoted weight gain. Behaviorally, MCD induced anhedonia- and anxiety-like behaviors, worsened by CUMS. MC diet reduced CUMS-induced anhedonia, though anxiety-like behavior emerged only under stress. Recognition memory was impaired in stressed MCD-fed mice, while MC-fed mice showed enhanced novel object preference. At the cellular level, MCD suppressed hippocampal microglia and caused cortical astrocyte dysfunction, whereas the MC diet promoted cortical neurogenesis potentiated through PO, abolished by chronic stress. These findings underscore the impact of dietary composition on PO’s systemic effects under chronic stress and support a mechanistic link between NAFLD-related dysfunction and depression-like phenotypes.

Fibroblast growth factor 21 (FGF21) is a hormone involved in regulating the metabolism, energy balance, and glucose homeostasis, with new studies demonstrating its beneficial effects on the heart. This study investigated the relationship between FGF21 levels and clinical, biochemical, and echocardiographic parameters in patients with acute coronary syndromes (ACSs). This study included 80 patients diagnosed with ACS between May and July 2023, categorized into four groups based on body mass index (BMI): Group 1 (BMI 18.5–24.9 kg/m²), Group 2 (BMI 25–29.9 kg/m²), Group 3 (BMI 30–34.9 kg/m²), and Group 4 (BMI ≥ 35 kg/m²). Serum FGF21 levels were measured by ELISA (Abclonal Catalog NO.: RK00084). Serum FGF21 levels were quantifiable in 55 samples (mean ± SD: 342.42 ± 430.17 pg/mL). Group-specific mean FGF21 levels were 238.98 pg/mL ± SD in Group 1 (n = 14), 296.78 pg/mL ± SD in Group 2 (n = 13), 373.77 pg/mL ± SD in Group 3 (n = 12), and 449.94 pg/mL ± SD in Group 4 (n = 16), with no statistically significant differences between groups (p = 0.47). Based on ACS diagnoses, mean FGF21 levels were 245.72 pg/mL for STEMI (n = 21), 257.89 pg/mL for NSTEMI (n = 9), and 456.28 pg/mL for unstable angina (n = 25), with no significant differences observed between these diagnostic categories. Significant correlations were identified between FGF21 levels and BMI, diastolic blood pressure, and serum chloride. Regression analyses revealed correlations with uric acid, chloride, and creatinine kinase MB. This study highlights the complex interplay between FGF21, BMI, and acute coronary syndromes. While no significant differences were found in FGF21 levels between the different BMI and ACS diagnostic groups, correlations with clinical and biochemical parameters suggest a multifaceted role of FGF21 in cardiovascular health. Further research with a larger sample size is warranted to elucidate these relationships.

Background: Little is known about the physiopathological factors or mechanisms that underlie tumor invasion of the serosa and lead to perforation in the peritoneal cavity. The aim of the work was to analyze the pathological and immunohistochemical factors of tumor neoangiogenesis which could influence tumor perforation in colorectal cancer. Results and discussions: 451 cases of complicated colorectal carcinomas were statistically analyzed, of which 19 cases were perforated sigmoid tumors. The immunohistochemical detection of mutant p53 proteins was the first molecular parameter examined in the context of the search for markers predicting the natural evolution mode in colorectal carcinomas. Conclusions: Both loss of p53 and overexpression of bcl-2 proteins confer immortalization on cancer cells by inhibiting the processes leading to apoptosis. The paper proposes a review of the specialized literature, but also the presentation of a clinical case.