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.

Hypoxic-ischemic encephalopathy (HIE) continues to be an important cause of long-term neurologic disability among newborn infants. The estimated incidence ranges from 2-3/1000 live births in developed countries, to as high as 10-20/1000 in developing countries [1]. Affected infants who survive are at a 25% risk for cerebral palsy, epilepsy, and cognitive deficits and may require lifelong medical care.

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.

Angiopoietin-like 4 (ANGPTL4) is a multifaceted secreted protein discovered by three different institutions in 2000 simultaneously [1]. It is expressed in adipose tissues, liver, muscle, heart, kidney, skin, and other tissues. The nutritional, metabolic, and inflammatory status of the organism regulate the expression of ANGPTL4 [2-4].

Metabolic dysfunction-associated steatotic liver disease (MASLD) is comprised of a spectrum of conditions, which is a progressive form of liver disease ranging from simple steatosis to steatohepatitis. The liver regulates fat metabolic homeostasis through de novo lipogenesis, fatty acid uptake and oxidation, low-density lipoprotein secretion in hepatocytes.