Insulin resistance (IR) has become a common health issue in medical practice. There are no detailed data on IR prevalence, but it is an increasing problem due to its close association with obesity. However, IR is not considered as a separate nosological entity and the diagnostic criteria are not well defined, which leads to overdiagnosis of IR and an inappropriate approach. This review aims to summarize the available literature on IR pathophysiology, its relationship with obesity, as well as diagnostic methods, clinical presentation and treatment. Excessive energy intake results in cell overload that triggers mechanisms to protect cells from further energy accumulation by reducing insulin sensitivity. Additionally, hypertrophied adipocytes and macrophage infiltration causes local inflammation that may result in general inflammation that induces IR. The clinical picture varies from skin lesions (e.g., acanthosis nigricans) to metabolic disorders such as diabetes mellitus or metabolic-associated fatty liver disease. There are numerous IR laboratory markers with varying sensitivities and specificities. Nutrition changes and regular physical activity are crucial for IR management because a reduction in adipose tissue may reverse the inflammatory state and consequently reduce the severity of insulin resistance. In cases of obesity, anti-obesity medications can be used.

Regenerative medicine combines elements of tissue engineering and molecular biology aiming to support the regeneration and repair processes of damaged tissues, cells and organs. The most commonly used preparation in regenerative medicine is platelet rich plasma (PRP) containing numerous growth factors present in platelet granularities. This therapy is increasingly used in various fields of medicine. This article is a review of literature on the use of PRP in gynecology and obstetrics. There is no doubt that the released growth factors and proteins have a beneficial effect on wound healing and regeneration processes. So far, its widest application is in reproductive medicine, especially in cases of thin endometrium, Asherman’s syndrome, or premature ovarian failure (POF) but also in wound healing and lower urinary tract symptoms (LUTS), such as urinary incontinence or recurrent genitourinary fistula auxiliary treatment. Further research is, however, needed to confirm the effectiveness and the possibility of its application in many other disorders.

Organism survival depends on oxygen delivery and utilization to maintain the balance of energy and toxic oxidants production. This regulation is crucial to the brain, especially after acute injuries. Secondary insults after brain damage may include impaired cerebral metabolism, ischemia, intracranial hypertension and oxygen concentration disturbances such as hypoxia or hyperoxia. Recent data highlight the important role of clinical protocols in improving oxygen delivery and resulting in lower mortality in brain-injured patients. Clinical protocols guide the rules for oxygen supplementation based on physiological processes such as elevation of oxygen supply (by mean arterial pressure (MAP) and intracranial pressure (ICP) modulation, cerebral vasoreactivity, oxygen capacity) and reduction of oxygen demand (by pharmacological sedation and coma or hypothermia). The aim of this review is to discuss oxygen metabolism in the brain under different conditions.

Transporters of the solute carrier 6 (SLC6) family translocate their cognate substrate together with Na⁺ and Cl⁻. Detailed kinetic models exist for the transporters of GABA (GAT1/SLC6A1) and the monoamines dopamine (DAT/SLC6A3) and serotonin (SERT/SLC6A4). Here, we posited that the transport cycle of individual SLC6 transporters reflects the physiological requirements they operate under. We tested this hypothesis by analyzing the transport cycle of glycine transporter 1 (GlyT1/SLC6A9) and glycine transporter 2 (GlyT2/SLC6A5). GlyT2 is the only SLC6 family member known to translocate glycine, Na⁺, and Cl⁻ in a 1:3:1 stoichiometry. We analyzed partial reactions in real time by electrophysiological recordings. Contrary to monoamine transporters, both GlyTs were found to have a high transport capacity driven by rapid return of the empty transporter after release of Cl⁻ on the intracellular side. Rapid cycling of both GlyTs was further supported by highly cooperative binding of cosubstrate ions and substrate such that their forward transport mode was maintained even under conditions of elevated intracellular Na⁺ or Cl⁻. The most important differences in the transport cycle of GlyT1 and GlyT2 arose from the kinetics of charge movement and the resulting voltage-dependent rate-limiting reactions: the kinetics of GlyT1 were governed by transition of the substrate-bound transporter from outward- to inward-facing conformations, whereas the kinetics of GlyT2 were governed by Na⁺ binding (or a related conformational change). Kinetic modeling showed that the kinetics of GlyT1 are ideally suited for supplying the extracellular glycine levels required for NMDA receptor activation.

Obesity continues to be a significant global health concern, giving rise to various complications. This review article explores the current standards and emerging innovations in diagnosing and treating obesity, including recent disease name change, staging system or therapeutic goals. This narrative review has been based on recent scientific articles from PubMed database, limiting the scope of topics to current standards and upcoming developments and breakthroughs in the diagnosis and treatment of obesity. The educational and informative nature of the review has been maintained in order to make the information presented accessible to both researchers and clinical practitioners. The recognition of diverse obesity phenotypes has prompted a paradigm shift towards a complex and patient-centered approach to diagnosis and therapy. Pharmacotherapy for obesity is evolving rapidly, with ongoing research focusing on novel molecular targets and metabolic pathways. Promising developments include dual or triple incretin analogs, oral incretin drugs, neurotransmitter-based therapies, muscle mass-increasing treatments, and therapies targeting visceral adipose tissue browning. Despite current evidence-based international standards, the field of obesity diagnosis and treatment continues to expand, with new diagnostic tools and pharmacotherapies potentially replacing current practices. Therapeutic management should be tailored to individual patients, considering obesity phenotype, health status, lifestyle, and preferences. Looking ahead, the future holds promising opportunities for obesity management, but further research is required to assess the efficacy and safety of emerging therapies. A multifactorial and personalized approach will be pivotal in addressing the diverse challenges posed by obesity.

The health of post-menopausal women has become of paramount concern due to the aging of the world’s population. Concurrently, the prevalence of obesity among postmenopausal women is expected to increase, presenting a significant public health challenge. Although weight gain during menopause is a well-observed phenomenon, its underlying causes and mechanisms remain incompletely understood. This manuscript reviews the literature to explore potential hormonal factors and pathomechanisms contributing to obesity during perimenopause, aiming to identify pathogenic factors that can guide treatment selection. Menopause-induced hormonal changes, including hypoestrogenaemia, hypergonadotropinaemia, relative hyperandrogenaemia, growth hormone deficiency, leptin resistance, and chronic stress affecting the hypothalamic-pituitary-adrenal axis, have been implicated in the onset of obesity in perimenopausal women. These hormonal fluctuations, alongside lowered daily energy expenditure, lead to metabolic alterations that elevate the risk of developing metabolic disorders and cardiovascular diseases. Weight gain in perimenopausal women is associated with higher total and abdominal adipose tissue and lower lean body mass. Addressing this issue requires individualized behavioural management, supported by effective pharmacological therapy, and, when warranted, complemented by bariatric surgery. Modern obesity treatment therapies have demonstrated safety and efficacy in clinical trials, offering the potential to reduce excess body fat, improve metabolic profiles, lower cardiovascular risk, and enhance the quality and longevity of women’s lives. In addition to standard obesity therapies, the article examines different treatment strategies based on obesity’s pathogenic factors, which may offer promising options for treating obesity with or without complications in perimenopausal women. One such potential approach is menopausal hormone therapy (MHT), which hypothetically targets visceral obesity by reducing visceral adipose tissue accumulation, preserving metabolically active lean body mass, and improving lipid profiles. However, despite these reported benefits, gynaecological and endocrinological societies currently do not recommend the use of MHT for obesity prevention or treatment, necessitating further research for validation. Emerging evidence suggests that visceral obesity could result from hypoestrogenaemia during perimenopause, potentially justifying the use of MHT as a causal treatment. This highlights the importance of advancing research efforts to unravel the intricate hormonal and metabolic changes that occur during perimenopause and their role in obesity development. The health of post-menopausal women has become of paramount concern due to the aging of the world’s population. Concurrently, the prevalence of obesity among postmenopausal women is expected to increase, presenting a significant public health challenge. Although weight gain during menopause is a well-observed phenomenon, its underlying causes and mechanisms remain incompletely understood. This manuscript reviews the literature to explore potential hormonal factors and pathomechanisms contributing to obesity during perimenopause, aiming to identify pathogenic factors that can guide treatment selection. Menopause-induced hormonal changes, including hypoestrogenaemia, hypergonadotropinaemia, relative hyperandrogenaemia, growth hormone deficiency, leptin resistance, and chronic stress affecting the hypothalamic-pituitary-adrenal axis, have been implicated in the onset of obesity in perimenopausal women. These hormonal fluctuations, alongside lowered daily energy expenditure, lead to metabolic alterations that elevate the risk of developing metabolic disorders and cardiovascular diseases. Weight gain in perimenopausal women is associated with higher total and abdominal adipose tissue and lower lean body mass. Addressing this issue requires individualized behavioural management, supported by effective pharmacological therapy, and, when warranted, complemented by bariatric surgery. Modern obesity treatment therapies have demonstrated safety and efficacy in clinical trials, offering the potential to reduce excess body fat, improve metabolic profiles, lower cardiovascular risk, and enhance the quality and longevity of women’s lives. In addition to standard obesity therapies, the article examines different treatment strategies based on obesity’s pathogenic factors, which may offer promising options for treating obesity with or without complications in perimenopausal women. One such potential approach is menopausal hormone therapy (MHT), which hypothetically targets visceral obesity by reducing visceral adipose tissue accumulation, preserving metabolically active lean body mass, and improving lipid profiles. However, despite these reported benefits, gynaecological and endocrinological societies currently do not recommend the use of MHT for obesity prevention or treatment, necessitating further research for validation. Emerging evidence suggests that visceral obesity could result from hypoestrogenaemia during perimenopause, potentially justifying the use of MHT as a causal treatment. This highlights the importance of advancing research efforts to unravel the intricate hormonal and metabolic changes that occur during perimenopause and their role in obesity development.