ABSTRACT
Obesity and cognitive decline including dementia and Alzheimer's Disease (AD) affect millions worldwide. Several studies have shown that obese individuals suffer from cognitive decline. Here, we suggest that adiponectin and leptin, protein hormones secreted by white adipose tissue explain the relationship between obesity and cognitive decline. We systematically searched PubMed and World Health Organization (WHO) websites with the keywords obesity and dementia and compiled literature that explains how adiponectin and leptin impact obesity and cognitive decline. Full-text, free-access articles on PubMed published after 2009 have been included. Whereas articles published before 2009, books, and reports were excluded. We concentrated on mechanisms via which adiponectin and leptin affect energy expenditure, fatty acid catabolism, satiety, hunger, Body Mass Index (BMI), neurogenesis, and brain structures that lead to the development of cognitive dysfunction. Moreover, we hypothesized that adiponectin and leptin hormones explain how obesity and dementia are connected. After compiling the research studies, we summarized that adiponectin and leptin negatively correlate to BMI. Adiponectin arbitrates energy expenditure and fatty acid catabolism to prevent obesity. In the presence of adiponectin, hippocampal cells proliferate, whereas neurogenesis is reduced in its absence. However, leptin prevents obesity by promoting satiety, reducing hunger, and increasing insulin sensitivity. It also has neuroprotective effects thus reducing the risk of developing cognitive decline. So, physical exercise, diet alteration, weight reduction, adiponectin, and leptin supplementation should be carried out to protect against obesity-induced cognitive decline. Therefore, further research studies should be done in this area.
ABSTRACT
Diabetes mellitus (DM) and hepatic steatosis are two of the most common metabolic syndromes that affect the health of people globally. Empagliflozin (EMPA) is a promising drug of choice for the diabetic population. Recent studies have shown its beneficial effects not only on diabetic patients but also on patients suffering from cardiac, hepatic, neurological, or pancreatic anomalies. In this paper, we systematically searched electronic databases to compile literature that focuses on EMPA's effect on the prediabetic population, diabetic population, and hepatic lipid metabolism. We focus on the mechanism of EMPA, specifically by which it increases insulin sensitivity and fat browning and reduces fat accumulation. Overall, we hypothesized that by its effect on weight loss and reducing inflammatory markers and insulin resistance (IR), EMPA decreases the rate of prediabetes to diabetes conversion. We concluded that by improving hepatic and serum triglyceride, decreasing visceral fat, and its positive impact on hepatic steatosis, the drug improves hepatic lipid metabolism. Further research should be done on this matter.
