Aging is characterized by gradual deterioration of organ or tissue function and its ability to maintain homeostasis of the different physiological processes. This leads to the development of structural and functional alterations accompanied by an increased risk for diverse pathologies. Cellular senescence is a controlled biological process that could contribute to the development of many age-related diseases and related metabolic dysfunctions. Two major chronic diseases associated with premature accumulation of senescent cells that impose an enormous burden on global health systems are obesity and type 2 diabetes mellitus with its related complications. The purpose of this review is to highlight the links between aging, obesity, and type 2 diabetes mellitus, focusing on the role of cellular senescence in disease development and progression. Additionally, this review will discuss the potential of targeting cellular senescence as a promising therapeutic strategy for managing these interrelated diseases, therefore offering a novel approach to prevention and treatment.

• Keywords
• cellular senescence, metabolic complications, obesity, senolytics, type 2 diabetes mellitus,
• Publication type
• Journal Article MeSH
• Review MeSH

Chlorinated paraffins (CPs) are environmental pollutants extensively used in industries. While the use of short-chain chlorinated paraffins (SCCPs) has been restricted since 2017, the use of medium-chain chlorinated paraffins (MCCPs) has risen as their replacement. Due to lipophilic character, it can be expected that CPs enter the cells; however, the in vitro accumulation potential of CPs remains poorly understood. In this study, we aimed to explore the ability of SCCPs and MCCPs to accumulate in fat cells. We utilized an in vitro model of mouse 3T3-L1 preadipocytes and adipocytes. Using gas chromatography coupled with high-resolution mass spectrometry operated in negative chemical ionization mode, we determined the intracellular amounts of CPs. These compounds accumulated at rates of 8.5 ± 0.1 µg/gcells/h for SCCPs and 7.8 ± 0.3 µg/gcells/h for MCCPs when an initial concentration of 120 ng/ml was present in the medium. This rate increased approximately tenfold when the concentration of CPs was raised to 1200 ng/ml. CPs content in adipocytes steadily increased over 5 days, whereas preadipocytes accumulated 15-20 times less CPs. This highlights the importance of cellular lipid content, which was about 12 times higher in adipocytes. Furthermore, we found that the level of chlorine content in the CPs molecules significantly influenced their accumulation. Our results demonstrate that MCCPs exhibit a similar accumulation potential to SCCPs, with lipid content playing a crucial role. As with SCCPs, restrictions on the use of MCCPs in industry should be considered to mitigate their environmental and health impacts.

• Keywords
• 3T3-L1 cells, Adipocytes, Chlorinated paraffins, Persistent organic pollutants,
• MeSH
• 3T3-L1 Cells MeSH
• Hydrocarbons, Chlorinated * metabolism   toxicity   MeSH
• Halogenation MeSH
• Environmental Pollutants * metabolism   toxicity   MeSH
• Lipids analysis   MeSH
• Lipid Metabolism * drug effects   MeSH
• Mice MeSH
• Paraffin * metabolism   toxicity   chemistry   MeSH
• Gas Chromatography-Mass Spectrometry MeSH
• Adipocytes * metabolism   drug effects   MeSH
• Animals MeSH
• Check Tag
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Hydrocarbons, Chlorinated * MeSH
• Environmental Pollutants * MeSH
• Lipids MeSH
• Paraffin * MeSH

Sodium glucose transporter type 2 (SGLT2) molecules are found in proximal tubules of the kidney, and perhaps in the brain or intestine, but rarely in any other tissue. However, their inhibitors, intended to improve diabetes compensation, have many more beneficial effects. They improve kidney and cardiovascular outcomes and decrease mortality. These benefits are not limited to diabetics but were also found in non-diabetic individuals. The pathophysiological pathways underlying the treatment success have been investigated in both clinical and experimental studies. There have been numerous excellent reviews, but these were mostly restricted to limited aspects of the knowledge. The aim of this review is to summarize the known experimental and clinical evidence of SGLT2 inhibitors' effects on individual organs (kidney, heart, liver, etc.), as well as the systemic changes that lead to an improvement in clinical outcomes.

• Keywords
• SGLT2, SGLT2 inhibitors, chronic kidney disease, diabetes, heart failure,
• MeSH
• Diabetes Mellitus, Type 2 * drug therapy   metabolism   MeSH
• Sodium-Glucose Transporter 2 Inhibitors * pharmacology   therapeutic use   MeSH
• Glucose therapeutic use   MeSH
• Cardiovascular System * metabolism   MeSH
• Humans MeSH
• Sodium metabolism   MeSH
• Sodium-Glucose Transporter 2 metabolism   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Review MeSH
• Names of Substances
• Sodium-Glucose Transporter 2 Inhibitors * MeSH
• Glucose MeSH
• Sodium MeSH
• Sodium-Glucose Transporter 2 MeSH