Even though type 2 diabetes mellitus (T2DM) represents a worldwide chronic health issue that affects about 462 million people, specific underlying determinants of insulin resistance (IR) and impaired insulin secretion are still unknown. There is growing evidence that chronic subclinical inflammation is a triggering factor in the origin of T2DM. Increased C-reactive protein (CRP) levels have been linked to excess body weight since adipocytes produce tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), which are pivotal factors for CRP stimulation. Furthermore, it is known that hepatocytes produce relatively low rates of CRP in physiological conditions compared to T2DM patients, in which elevated levels of inflammatory markers are reported, including CRP. CRP also participates in endothelial dysfunction, the production of vasodilators, and vascular remodeling, and increased CRP level is closely associated with vascular system pathology and metabolic syndrome. In addition, insulin-based therapies may alter CRP levels in T2DM. Therefore, determining and clarifying the underlying CRP mechanism of T2DM is imperative for novel preventive and diagnostic procedures. Overall, CRP is one of the possible targets for T2DM progression and understanding the connection between insulin and inflammation may be helpful in clinical treatment and prevention approaches.

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) play a fundamental role in regulating endothelial function and vascular tone in the physiological conditions of a vascular system. However, oxidative stress has detrimental effects on human health, and numerous studies confirmed that high ROS/RNS production contributes to the initiation and progression of cardiovascular diseases. The antioxidant defense has an essential role in the homeostatic functioning of the vascular endothelial system. Endogenous antioxidative defense includes various molecules and enzymes such as superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase. Together all these antioxidative enzymes are essential for defense against harmful ROS features. ROS are mainly generated from redox-active compounds involved in the mitochondrial respiratory chain. Thus, targeting antioxidative enzymes and mitochondria oxidative balance may be a promising approach for vascular diseases occurrence and treatment. This review summarized the most recent research on the regulation of antioxidative enzymes in vascular diseases.

Introduction: Insulin-like growth factor-1 (IGF-1) promotes survival and inhibits cardiac autophagy disruption.Methods: Male Wistar rats were treated with IGF-1 (50 µg/kg), and 24 h after injection hearts were excised. The level of interaction between Beclin-1 and the α1 subunit of sodium/potassium-adenosine triphosphates (Na+/K+-ATPase), and phosphorylated forms of IGF-1 receptor/insulin receptor (IGF-1R/IR), forkhead box protein O1 (FOXO1) and AMP-activated protein kinase (AMPK) were measured.Results: The results indicate that IGF-1 decreased Beclin-1’s association with Na+/K+-ATPase (p < 0.05), increased IGF-1R/IR and FOXO1 phosphorylation (p < 0.05), and decreased AMPK phosphorylation (p < 0.01) in rats’ hearts.Conclusions: The new IGF-1 therapy may control autosis and minimize cardiomyocyte mortality.

Due to present-day lifestyle habits, obesity is a disease of modern society. Obesity is characterized by excessive fat accumulation and lipid disturbance, which further leads to alterations in liver enzyme activity and redox signaling. We aimed to explore the effect of a high-fat (HF) diet on the concentrations of aspartate aminotransferase (AST), alkaline phosphatase (ALP), and alanine aminotransferase (ALT) in serum, and levels of nuclear factor erythroid 2-related factor 2 (NRF2) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) in rat liver. Our results showed a significant elevation of ALP concentration and no change in AST and ALT concentrations in serum. Additionally, protein levels of NRF2 and PGC1-α were reduced in liver of HF diet-fed rats compared to control rats. These findings indicate an increased inflammatory response and impaired antioxidant defense signaling in the liver of HF diet-fed rats, predisposing them to the development of insulin resistance.