Abstract

Mechanistic investigations in both animal models and human subjects have consistently elucidated a causal relationship between obesity, diabetes, and Alzheimer's disease (AD). Alzheimer's disease is the predominant etiology of dementia, marked by progressive cerebral degeneration characterized by the formation of intracellular neurofibrillary tangles and extracellular amyloid beta (Aβ) plaques. Adipose tissue secretes bioactive signaling molecules known as adipokines. Interactions between adipose tissue and the central nervous system serve as the foundational mechanism contributing to the elevated susceptibility of individuals with obesity to the onset of neurologic disorders, including cognitive and mood-related disturbances. Omentin is a recently discovered adipokine that has gained attention for study because of its pleiotropic effects on several disorders. The specific receptor responsible for binding with Omentin remains unidentified thus far. This investigation elucidates the variability in Omentin levels observed in multiple pathological conditions. Therapeutic methods to raise omentin-1 levels may be helpful for the treatment or prevention of several illnesses. Increases in circulating omentin-1 levels can be achieved with weight loss, an olive oil-rich diet, aerobic exercise, atorvastatin therapy, and the use of diabetes medications. It is also possible to use circulating omentin-1 as a biomarker of obesity, diabetes, metabolic syndrome, atherosclerosis, ischemic heart disease, inflammatory disease, cancer, and neurological diseases via AMP-activated protein kinase/Akt/nuclear factor-κB/mitogen-activated protein kinase (ERK, JNK, and p38) signaling. This review provides insights into the potential use of omentin-1 as a biomarker for Obesity, Diabetes, and associated metabolic and neurological disorders.

Keywords: Omentin, adipokines, adipose tissue, obesity, diabetes, Alzheimer's disease.