A high-fructose diet is supposed to induce the so-called metabolic syndrome, associated with increased fat deposition in adipose tissue. Physical exercise may counteract the induction of the metabolic syndrome. The present study aims to investigate the effect of voluntary physical activity (VPA) on cGMP-mediated lipolysis in retroperitoneal adipose tissue in a metabolic syndrome model induced in rats by a high-fructose diet.

Male Sprague-Dawley rats in control and fructose (F) groups had free access to either plain drinking water or a solution of 20% D-fructose, combined with a standard diet for 8 wk. Rats in the fructose + activity (F + A) group performed voluntary physical activity with a running wheel. Blood pressure, serum glucose, lipids and natriuretic peptide levels were measured on the last day of the feeding period. In retroperitoneal adipose tissue, cGMP, hormone-sensitive lipase (HSL), perilipin-1, aquaglyceroporin levels, and adipocyte diameter were analyzed.

Systolic blood pressure, glucose, and triacylglycerol were higher in the F groups compared to the control. The C-type natriuretic peptide was higher in the F group compared to the control. The cGMP level in retroperitoneal adipose tissue was higher in the F + A group than F group. Higher HSL and perilipin-1 levels were observed in the F + A group compared to the F and control groups. Adipocyte diameter was lower in the F + A group compared to the F group.

Regular physical exercise triggers lipolytic effects in adipose tissue through cGMP, HSL, and perilipin-1-mediated pathway in fructose-induced metabolic syndrome model in rats, preventing the increase in adipocyte diameter.

Atherosclerosis (AS), a chronic inflammatory vascular disease with lipid metabolism abnormalities, is one of the major pathological bases of coronary heart disease. As people's lifestyles and diets change, the incidence of AS increases yearly. Physical activity and exercise training have recently been identified as effective strategies for lowering cardiovascular disease (CVD) risk. However, the best exercise mode to ameliorate the risk factors related to AS is not clear. The effect of exercise on AS is affected by the type of exercise, intensity, and duration. In particular, aerobic and anaerobic exercise are the two most widely discussed types of exercise. During exercise, the cardiovascular system undergoes physiological changes via various signaling pathways. The review aims to summarize signaling pathways related to AS in two different exercise types and provide new ideas for the prevention and treatment of AS in clinical practice.

Amino-terminal pro C type natriuretic peptide (NT proCNP) is the N terminal fragment of the CNP precursor. NT proCNP occurs in an equimolar concentration with CNP in human plasma and is considered to be a marker of the extent of CNP biosynthesis. A recent study has shown associations between plasma NT proCNP and blood pressure; it is also an independent predictor of death and cardiac readmission in people with unstable angina. Beyond that, recent studies have focused on the applicability of assessing NT proCNP peptide levels in the diagnosis of diseases with different etiologies but the same denominator, i.e., inflammation.

This study reviewed recent results on the usability of NT proCNP peptide levels in the diagnosis of diseases accompanied by statistical analysis of previously reported results.

The data obtained confirmed the applicability of the assessment of NT proCNP levels in biological fluids in diseases, such as Parkinson's disease, sepsis, meningitis, and asthenozoospermia.

The reported results demonstrated that NT-proCNP is helpful in a variety of diseases. Furthermore, changes in serum or CSF levels of NT-proCNP reflect only inflammatory states related to general inflammation. Local inflammation does not trigger an increase in NT proCNP level.

One of the major obstacles that prevents an effective therapeutic intervention against ischemic stroke is the lack of neuroprotective agents able to reduce neuronal damage; this results in frequent evolution towards a long-term disability with limited alternatives available to aid in recovery. Nevertheless, various treatment options have shown clinical efficacy. Neurotrophins such as brain-derived neurotrophic factor (BDNF), widely produced throughout the brain, but also in distant tissues such as the muscle, have demonstrated regenerative properties with the potential to restore damaged neural tissue. Neurotrophins play a significant role in both protection and recovery of function following neurological diseases such as ischemic stroke or traumatic brain injury. Unfortunately, the efficacy of exogenous administration of these neurotrophins is limited by rapid degradation with subsequent poor half-life and a lack of blood-brain-barrier permeability. Regular exercise seems to be a therapeutic approach able to induce the activation of several pathways related to the neurotrophins release. Exercise, furthermore, reduces the infarct volume in the ischemic brain and ameliorates motor function in animal models increasing astrocyte proliferation, inducing angiogenesis and reducing neuronal apoptosis and oxidative stress. One of the most critical issues is to identify the relationship between neurotrophins and myokines, newly discovered skeletal muscle-derived factors released during and after exercise able to exert several biological functions. Various myokines (e.g., Insulin-Like Growth Factor 1, Irisin) have recently shown their ability to protects against neuronal injury in cerebral ischemia models, suggesting that these substances may influence the degree of neuronal damage in part via inhibiting inflammatory signaling pathways. The aim of this narrative review is to examine the main experimental data available to date on the neuroprotective and anti-ischemic role of regular exercise, analyzing also the possible role played by neurotrophins and myokines.

Paracrine actions of CNP and rapid degradation at source severely limit study of CNP's many roles in vivo. However provided sensitive and validated assays are used, there is increasing evidence that low concentrations of bioactive CNP in plasma, and the readily detectable concentrations of the bio-inactive processed product of proCNP (aminoterminal proCNP), can be used to advance understanding of the hormone's role in pathophysiology. Provided renal function is normal, concordant changes in both CNP and NTproCNP reflect change in tissue production of proCNP whereas change in CNP alone results from altered rates of bioactive CNP degradation and are reflected in the ratio of NTproCNP to CNP. As already shown in juveniles, where plasma concentration of CNP products are higher and are associated with concurrent endochondral bone growth, measurements of plasma CNP products in mature adults have potential to clarify organ response to stress and injury. Excepting the role of CNP in fetal-maternal welfare, this review examines evidence linking plasma CNP products with function of a wide range of tissues in adults, including the impact of extraneous factors such as nutrients, hormone therapy and exercise.

Physical exercise is one of the most effective methods to help prevent cardiovascular (CV) disease and to promote CV health. Aerobic and anaerobic exercises are two types of exercise that differ based on the intensity, interval and types of muscle fibers incorporated. In this article, we aim to further elaborate on these two categories of physical exercise and to help decipher which provides the most effective means of promoting CV health.