Kisspeptins are the family of neuropeptide products of the KISS-1 gene that exert the biological action by binding with the G-protein coupled receptor 54 (GPR54), also known as the KISS-1 receptor. The kisspeptin level dramatically increases during pregnancy, and the placenta is supposed to be its primary source. The role of kisspeptin has already been widely studied in hypogonadotropic hypogonadism, fertility, puberty disorders, and insulin resistance-related conditions, including type 2 diabetes mellitus, polycystic ovary syndrome, and obesity. Gestational diabetes mellitus (GDM), preeclampsia (PE), preterm birth, fetal growth restriction (FGR), or spontaneous abortion affected 2 to 20% of pregnancies worldwide. Their occurrence is associated with numerous short and long-term consequences for mothers and newborns; hence, novel, non-invasive predictors of their development are intensively investigated. The study aims to present a comprehensive review emphasizing the role of kisspeptin in the most common pregnancy-related disorders and neonatal outcomes. The decreased level of kisspeptin is observed in women with GDM, FGR, and a high risk of spontaneous abortion. Nevertheless, there are still many inconsistencies in kisspeptin concentration in pregnancies with preterm birth or PE. Further research is needed to determine the usefulness of kisspeptin as an early marker of gestational and neonatal complications.

Gestational diabetes mellitus (GDM) is defined as a glucose tolerance disorder with onset or first recognition during pregnancy. GDM is associated with several adverse maternal and neonatal outcomes. Management to reduce the incidence of GDM could decrease the incidence of these complications. Modification of nutrition in the prevention of GDM is postulated. The vital issue in GDM prevention is the implementation of proper dietary patterns, appropriate physical activity, and a combination of diet and lifestyle modifications. However, intervention studies examining the effects of diet and lifestyle on GDM prevention are contradictory. The aim of this study was to review the scientific evidence on nutritional prevention strategies, including diet and supplementation of some substances such as probiotics, micro/macroelements, fiber, myoinositol, and vitamins that may be effective in reducing the risk of GDM. The presented article is a narrative review. This article indicates that certain nutritional factors may have some benefit in preventing GDM. However, further studies in a variety of populations and large groups of patients are needed. At present, no definitive conclusions can be drawn as to the best intervention in the prevention of GDM.

Graves’ orbitopathy (GO) is an autoimmune disease with a chronic inflammatory background. Smoking behavior is the main environmental factor responsible for the transition of this major extra thyroidal manifestation of Graves’ disease (GD) from the subclinical to the overt form. Complete blood count-derived parameters are suggested to be novel inflammatory indices. The aim of this retrospective study was to investigate the association between neutrophil-to-lymphocyte (NLR), monocyte-to-lymphocyte (MLR), and platelet-to-lymphocyte ratios (PLR) with selected clinical parameters and smoking status in 406 GD patients with (n = 168) and without GO (n = 238). The control group consisted of 100 healthy individuals. The activity of GO was graded according to Clinical Activity Score. Significantly higher white blood cells (WBC), neutrophil, and NLR (p < 0.05) values were observed in GD patients with GO compared with those without GO. PLR values were significantly higher in GO patients than in the controls. WBC (6.81 ± 1.56 vs. 5.70 ± 1.23) and neutrophils (3.89 ± 1.06 vs. 3.15 ± 0.95) count was higher in active GO patients than in those with inactive GO. Positive correlation (p < 0.05) between CAS score and WBC, neutrophil and monocyte count, and NLR was found. Smoking was associated with higher WBC (p = 0.040), neutrophil (p = 0.049), PLR (p = 0.032) values. Multivariate analysis revealed that WBC, NLR may be risk factors for GO development. WBC, neutrophil, NLR and PLR values seem to be useful tools in the assessment of inflammation in GD.

Acromegaly is a rare disease caused by overproduction of growth hormone (GH) by a pituitary adenoma, and consequently increased insulin-like growth factor 1 (IGF-1) concentration. The GH/IGF-1 axis and immune cells interactions are hypothesized to be involved in subclinical inflammation. This retrospective study aimed to investigate the differences in neutrophil-to-lymphocyte (NLR), platelet-to-lymphocyte (PLR) ratios, and systemic immune-inflammation index (SII) in GH-secreting adenomas compared with non-functioning pituitary adenomas (NFPAs) concerning clinical and radiological findings. After evaluation of 665 patients with pituitary tumors, 62 individuals with newly diagnosed acromegaly and 134 with NFPAs were enrolled in the analysis. The control group consisted of 120 healthy individuals. Fifty-eight patients with acromegaly were re-evaluated after medical or surgical therapies. NLR, PLR, SII values, and neutrophil count were significantly higher (p ≤ 0.001), whereas lymphocyte count was lower in acromegaly than in NFPAs (p = 0.001). No significant differences between NFPAs and controls were observed in analyzed ratios. Higher preoperative NLR, PLR, SII values were found in patients who failed to achieve a cure with surgery (p < 0.05). Although NLR, PLR, and SII values were significantly higher in acromegaly, these indices cannot be used to discriminate GH-secreting pituitary tumors from NFPAs. Treatment of acromegaly decreased the value of NLR and SII, but it requires further studies to consolidate the real clinical role of these inflammation-related ratios.

Introduction: Obesity is a chronic fatal disease with still growing incidence among children, adolescents, and adults worldwide. The subclinical inflammatory process together with hipoadiponectinemia may lead to the development of various comorbidities, including cardiovascular complications. That is why, the relationship between adipose tissue activity, obesity, insulin resistance, and endothelial function is in high interest and an object of extensively studies. Aim of the study: This article summarizes the current knowledge on the anti-atherogenic effects of adiponectin and its properties to improve endothelial function in obesity-related insulin resistance. Description of knowledge: Adiponectin, an adipose tissue-derived pleiotropic hormone with anti-inflammatory, anti-atherogenic, anti-diabetic, and insulin-sensitizing actions, is not only engaged in modulation of type 2 diabetes mellitus, hypertension or coronary artery disease, but the latest researches highlight its role in improving vascular wall integrity. It affects complex signaling pathways in endothelial cells and influence inflammatory responses in the subendothelial space. Pre-clinical and clinical studies suggest that agents leading to increase in adiponectin levels, simultaneously contribute to decrease insulin resistance, and improve endothelial dysfunction. Conclusions: Adiponectin may be a predictive factor of endothelial dysfunctionality and vascular remodeling development in the group of patients with overweight, obesity, and insulin resistance. Discovering pharmacological agents and non-pharmacological interventions that increase the level of circulating adiponectin will become novel and innovative therapeutic strategy to ameliorate obesity-related comorbidities. Therefore, further studies are required to determine the exact role of adiponectin in the pathogenesis of metabolic diseases.

Background. Maternal diabesity, defined as the coexistence of obesity and diabetes during pregnancy, is an increasingly prevalent metabolic condition associated with adverse maternal, placental, and fetal outcomes. Beyond hyperglycemia, it is characterized by chronic inflammation, insulin resistance, oxidative stress, endothelial dysfunction, which impair placental development and function. The fetoplacental unit represents a critical interface through which maternal metabolic disturbances shape fetal growth and long-term health. Aim. To integrate current evidence on placental diabesity, focusing on key mechanisms linking maternal metabolic dysfunction to placental maladaptation and its clinical implications for pregnancy and offspring outcomes. Material and methods. This research was based on a literature review of PubMed and Web of Science articles published between 2010-2025. Peer-reviewed experimental, clinical and translational studies, meta-analyses were included and synthesized narratively. Description of knowledge. The available evidence indicates that maternal diabesity induces early and persistent fetoplacental dysfunction, characterized by impaired endothelial insulin signaling, reduced nitric oxide bioavailability, enhanced oxidative and inflammatory stress, mitochondrial impairment, and activation of endoplasmic reticulum stress pathways. These interconnected alterations compromise placental blood flow, nutrient transport, and metabolic adaptability, thereby increasing fetal exposure to an adverse intrauterine environment and contributing to developmental programming of metabolic and cardiovascular disease. Conclusions. Fetoplacental dysfunction is a key mechanism linking maternal diabesity to impaired fetal development and long-term offspring health. Understanding placental maladaptation in diabesity is essential for developing preventive and therapeutic strategies beyond glycaemic control to reduce intergenerational metabolic risk.