With the recent urbanization and globalization, the adult obesity rate has been increasing, which was paralleled with a dramatic surge in the incidence and prevalence of nonalcoholic fatty liver disease (NAFLD). NAFLD poses a growing threat to human health as it represents the most common cause of chronic liver disease in developed countries. It encompasses a wide spectrum of conditions starting from a build-up of fat in hepatocytes (steatosis), to developing inflammation (steatohepatitis), and reaching up to cirrhosis. It is also associated with higher rates of cardiovascular mortalities. Therefore, proper timely treatment is essential and weight loss remains the cornerstone in the treatment of obesity-related liver diseases. When diet, exercise, and lifestyle changes are not successful, the current recommendation for weight loss includes antiobesity medications and bariatric endoscopic and surgical interventions. These interventions have shown to result in significant weight loss and improve liver steatosis and fibrosis. In the current literature review, we highlight the expected outcomes and side effects of the currently existing options to have a weight-centric NAFLD approach.

Radiation therapy (RT) has dramatically improved cancer survival, leading to several inevitable complications. Unintentional irradiation of the heart can lead to radiation-induced heart disease (RIHD), including cardiomyopathy, pericarditis, coronary artery disease, valvular heart disease, and conduction system abnormalities. Furthermore, the development of RIHD is aggravated with the addition of chemotherapy. The screening, diagnosis, and follow-up for RIHD in patients who have undergone RT are described by the consensus guidelines from the European Association of Cardiovascular Imaging (EACVI) and the American Society of Echocardiography (ASE). There is compelling evidence that chest RT can increase the risk of heart disease. Although the prevalence and severity of RIHD are likely to be reduced with modern RT techniques, the incidence of RIHD is expected to rise in cancer survivors who have been treated with old RT regimens. However, there remains a gap between guidelines and clinical practice. Currently, therapeutic modalities followed in the treatment of RIHD are similar to the non-irradiated population. Preventive measures mainly reduce the radiation dose and radiation volume of the heart. There is no concrete evidence to endorse the preventive role of statins, angiotensin-converting enzyme inhibitors, and antioxidants. This review summarizes the current evidence of RIHD subtypes and risk factors and suggests screening regimens, diagnosis, treatment, and preventive approaches.

It well known that long-lasting hyperglycaemia disrupts neuronal function and leads to neuropathy and other neurodegenerative diseases. The α-ketoglutarate analogue (DMOG) and the caspase-inhibitor “Ac-LETD-CHO are potential neuroprotective molecules. Whether their protections may also extend glucotoxicity-induced neuropathy is not known. Herein, we evaluated the possible cell-protective effects of DMOG and Ac-LETD-CHO against hyperglycaemia-induced reactive oxygen species and apoptosis in ND7/23 neuronal cells. The impact of glucotoxicity on the expression of HIF-1α and a panel of micro-RNAs of significance in hyperglycaemia and apoptosis was also investigated.ND7/23 cells cultured under hyperglycaemic conditions showed decreased cell viability and elevated levels of ROS production in a dose- and time-dependent manner. However, presence DMOG (500 µM) and/or Ac-LETD-CHO (50 µM) counteracted this effect and increase cell viability concomitant with reduction in ROS production, DNA damage and apoptosis. AcLETD-CHO suppressed hyperglycaemia-induced caspase 3 activation in ND7/23 cells. Both DMOG and Ac-LETD-CHO increased HIF-1α expression paralleled with the suppression of miR-126–5p, miR-128–3p and miR-181 expression and upregulation of miR-26b, 106a-5p, 106b-5p, 135a-5p, 135b-5p, 138–5p, 199a-5p, 200a-3p and 200c-3p expression.We demonstrate a mechanistic link for the DMOG and Ac-LETD-CHO protection against hyperglycaemia-induced neuronal dysfunction, DNA damage and apoptosis and thereby propose that pharmacological agents mimicking these effects may represent a promising novel therapy for the hyperglycaemia-induced neuropathy.

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