RESUMO
Heart failure (HF) is a worldwide pandemic that affects at least 26 million people and is becoming more prevalent. Heart failure health expenditures are substantial and will considerably increase with population aging. Newer medications for treating type 2 diabetes include sodium-glucose cotransporter-2 inhibitors (SGLT2). Recent clinical studies and research have shown the efficacy of this class in treating heart failure by lowering the risk of cardiovascular events, hospitalization, and mortality. In addition, there is undeniable evidence that SGLT2 inhibitors have a beneficial effect on metabolic function, even though the mechanisms responsible for these drugs' practical consequences have not been completely elucidated. In this narrative review, we discuss the effects of SGLT2 inhibitors on the provision of cardiac energy by ketone bodies, pathological remodeling of the ventricle, arterial stiffness, and inflammation in patients with HF.
RESUMO
AIM OF THE STUDY: Parkinson's disease and schizophrenia are disease end points of dopaminergic deficit and hyperactivity, respectively, in the mid brain. Accordingly, current medications aim to restore normal dopamine levels, overshooting of which results in adverse effects of psychosis and extra-pyramidal symptoms, respectively. There are currently no available laboratory tests to guide treatment decisions or help predict adverse side effects of the drugs. The aim was to therefore explore the possibility of using apolipoprotein E as a biomarker to monitor pharmacological intervention in dopamine dictated states of Parkinson's disease and schizophrenia for optimum therapy. METHODS: Naïve and treated, Parkinson's disease and schizophrenic patients were recruited from neurology and psychiatry clinics. Serum of healthy volunteers was collected as controls. Serum concentrations of apolipoprotein E was estimated by enzyme-linked immunosorbent assay (ELISA). Pathway analysis was carried out to delineate the interactions of apolipoprotein E in Parkinson's disease and schizophrenia. RESULTS: Apolipoprotein E levels are higher in Parkinson's disease patients as compared with schizophrenic samples (P < .05). Also, post-treatment apolipoprotein E levels in both disease states were at par with levels seen in healthy controls. The interactions of apolipoprotein E validate the results and place the differential expression of the protein in Parkinson's disease and schizophrenia in the right perspective. CONCLUSION: Apolipoprotein E concentration across the dopaminergic spectrum suggests that it can be pursued not only as a potential biomarker in schizophrenia and Parkinson's disease, but can also be an effective tool for clinicians to determine efficacy of drug-based therapy.