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New causal relationship between psoriasis and non-alcoholic steatohepatitis

NAFLD is a multisystem disease affecting various extrahepatic organs and increases the risk of cardiovascular disease.

The term obese describes a person who's very overweight, with a lot of body fat. Obesity is believed to account for 80-85 percent of the risk of developing type 2 diabetes. — © Digital Journal
The term obese describes a person who's very overweight, with a lot of body fat. Obesity is believed to account for 80-85 percent of the risk of developing type 2 diabetes. — © Digital Journal

Non-alcoholic fatty liver disease (NAFLD) is the term for a range of conditions caused by a build-up of fat in the liver. This disease is usually seen in people who are overweight or obese.

A new study reveals that co-occurring non-alcoholic steatohepatitis (NASH) exacerbates psoriasis in STAM mice. This comes from a study conducted by Kawasaki Medical School (JPN) and SMC Laboratories, a non-clinical contrast research organisation specializing in inflammation, fibrosis, and cancer. NAFLD is a multisystem disease affecting various extrahepatic organs and increases the risk of cardiovascular disease, type 2 diabetes, and chronic kidney disease. Psoriasis, a skin disease, is also recognized as a complication of NAFLD, and its prevalence and severity are known to increase in NAFLD patients. Conversely, psoriasis patients have a higher incidence of NAFLD. Based on this, a bidirectional relationship between psoriasis and NAFLD has been suggested by researchers.

Non-alcoholic steatohepatitis (NASH) is a more serious form of NAFLD, where the liver has become inflamed.

For the study, NASH was induced in mice by streptozotocin injection at two days of age and by high-fat diet feeding (the STAM model). Psoriasis, a chronic inflammatory skin disease, was induced by topical application of imiquimod (IMQ) on the ear.

The severities of liver damage and psoriatic skin changes were then assessed using histological analysis. In addition, gene expression in the skin tissues was evaluated using quantitative PCR analysis. The researchers also determined the serum cytokine levels by using an enzyme-linked immunosorbent assay.

To examine the innate immune responses of normal human epidermal keratinocytes (NHEKs), the cells were treated with interleukin (IL)-17A, tumour necrosis factor (TNF)-α, and AdipoRon, acting as an adiponectin receptor agonist.

The experimental results showed there were no differences in the degree of liver tissue damage (fat deposition, inflammation, and fibrosis) between NASH mice with and those without psoriasis.

Whereas, the co-occurrence of NASH significantly augmented psoriatic skin changes, represented by epidermal hyperplasia, in psoriatic mice.

What appears to be happening within the body is increased inflammatory cytokine levels and decreased adiponectin levels. These are likely promote innate immune responses in the epidermal keratinocytes within psoriatic skin lesions.

The study has been published in Frontiers in Immunology. The research is titled “Co-occurrence of non-alcoholic steatohepatitis exacerbates psoriasis associated with decreased adiponectin expression in a murine model.”

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Dr. Tim Sandle is Digital Journal's Editor-at-Large for science news. Tim specializes in science, technology, environmental, business, and health journalism. He is additionally a practising microbiologist; and an author. He is also interested in history, politics and current affairs.

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