Today, both type 1 and type 2 diabetes mellitus affect 33.3 million people in the United States and nearly 500 million adults worldwide, and there is concern that this number may increase steadily in the future. Previous studies have linked the development of type 2 diabetes to multiple lifestyle factors, including physical activity level and diet, and biological characteristics, such as body composition, age, and race; however, current research suggests that gender may also have an impact on one’s risk of developing type 2 diabetes. Variations in type 2 diabetes diagnosis, prevalence, and progression have been found between males and females.

The protein hormone adiponectin regulates glucose and fatty acid metabolism by binding to two PAQR-family receptors (AdipoR1 and AdipoR2). Both receptors feature a C-terminal segment which is released by proteolysis to form a freely circulating C-terminal fragment (CTF) found in the plasma of normal individuals but not in some undefined diabetes patients.

Diabetes is a metabolic disease that compromises the integrity of multiple organs and systems including the nervous system. Not only does neurodegeneration occur in peripheral nerves of diabetic subjects but also in brain structures. Particularly, diabetes impairs olfactory functions which suggests the alteration of regions of the central nervous system related with olfaction, however, few studies have shed light on the mechanisms that cause these alterations.

Currently, there are no effective treatment methods for Alzheimer's disease (AD), Parkinson's disease (PD), and olfactory dysfunction (OD). Given common pathophysiological features of neurodegenerative diseases such as AD and type 2 diabetes mellitus (T2DM), antidiabetic drugs such as exenatide and liraglutide, which act as incretin mimetics, are tested as a potential treatment option. 

Ischemic stroke is the main cause of disability worldwide affecting around 6 million deaths per year. A cascade of events following the ischemic insult induce energy failure, excitotoxicity and release of inflammatory mediators that provoke cell death and brain injury. In this process, astrocytes undergo a change on gene expression that leads to reactive astrocytes.