The aryl hydrocarbon receptor (AhR) is a receptor found in the cytoplasm as a part of a protein complex. It becomes active by ligand binding and translocates into the nucleus. There it forms a hetero-dimer with the aryl hydrocarbon nuclear translocator (Arnt)1. This hetero-dimer then binds to a specific DNA sequence2 in order to induce the transcription of a variety of genes called the AhR gene battery3.
It was found that AhR is implicated in apoptosis, cell proliferation and development4. Researchers have also implicated this receptor in the development of hepatocytes and adipocytes5. Although AhR has many known exogenous ligands, its specific endogenous ligand is still unknown.
Diets that are high in carbohydrates encourage fatty-acid synthesis and results in obesity6. Numerous studies have specified that central obesity; visceral fat is a prime cause of metabolic syndromes i.e. insulin resistance, inflammatory diseases, type 2 diabetes and obesity-related pathologies6, 7. In obese individuals, macrophages penetrate in the adipose tissue and discharge cytokines that lead to low-grade inflammation. Distinctively, tumor necrosis factor alpha results in insulin resistance in adipocytes8.
In recent studies it has been find that is implicated in obesity and related metabolic pathologies. Therefore scientists conducted a study in order to evaluate the AhR expression in the prostates of lean and obese rats, an area which had not been previously explored. This will provide an idea of AhR distribution in the prostate and will shed a light on AhR’s therapeutic potential as a novel drug target for managing obesity’s complications9.
Researcher studied the animal model; obesity and metabolic syndrome were induced in them. Rats were divided into 2 groups. Both groups received standard rat food and drinking water but the obese group also received a continued supply of fructose. Morpho-metric, biochemical, histological and immune-histochemical methods were used.
It was found that AhR was expressed in both the lean and obese rats but it showed higher regulation in the obese group, which had diffused cytoplasmic and nuclear staining in the prostatic epithelium, in lean rats, the expression was only nuclear. This higher expression pattern led to the obese rats having a shorter prostatic epithelium than the lean rats had. AhR was also expressed in the mast cells of both groups.
It was established that higher regulation of AhR in the prostatic epithelium during the induction of metabolic syndrome points to AhR’s direct involvement in prostate pathology. It thus may be possible to use AhR as a therapeutic target to control metabolic syndrome-induced prostate problems.
Written by: Rabeeia
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17 November, 2019