Arch Dermatol Res. 2015 Aug;307(6):539-44.

Association between leptin gene expression in subcutaneous adipose tissue and circulating leptin levels in obese patients with psoriasis.

Mitsuyama S, Abe F, Kimura M, Yoshida M, Higuchi T.

Department of Dermatology, Sakura Medical Center, School of Medicine, Toho University, 564-1 Shimoshizu, Sakura, Chiba, 285-0841, Japan.

 

Abstract

Numerous reports have shown that psoriasis is associated with obesity and leptin. However, few reports are available on the association between serum leptin levels and leptin gene expression in SAT of psoriasis patients. To clarify this point, we examined serum leptin levels and expression levels of leptin messenger RNA (mRNA) in subcutaneous adipose tissue (SAT) of psoriasis patients. 17 psoriasis vulgaris patients and 6 non-obese control patients who underwent skin surgery were enrolled in this study. We measured serum leptin levels. SAT samples in psoriasis patients were taken from beneath the lesional psoriatic skin at the time of skin biopsy. Leptin mRNA expression in SAT was measured using quantitative real-time reverse transcription polymerase chain reaction (real-time RT-PCR) amplification. Leptin mRNA expression showed a positive correlation with serum leptin levels and BMI. We classified psoriasis patients into two groups according to BMI: the group of non-obese psoriasis patients (BMI < 25, n = 7), and the group of obese psoriasis patients (BMI ≥ 25, n = 10). PASI score, serum leptin levels and Leptin mRNA expression in SAT were significantly higher in the obese psoriasis patients than in the non-obese psoriasis patients. Leptin mRNA expression in SAT was correlated with circulating levels of leptin, the severity of psoriasis, and obesity in psoriasis patients. Serum leptin levels and leptin mRNA expression levels in SAT of non-obese psoriasis patients were not significantly different from those of non-obese controls. The altered secretion of leptin by SAT may be related to the severity of psoriasis.

PMID: 26054710

 

Supplementary

Psoriasis is a chronic inflammatory skin disease with joint manifestations and associated with several comorbidities, such as obesity, diabetes mellitus, dyslipidemia, hypertension, cardiovascular diseases, and metabolic syndrome. Obesity has long been considered a risk factor for the development of psoriasis. A number of studies demonstrated a strong association between obesity and psoriasis. Weight loss intervention induced by low calorie diet, physical exercise and gastric bypass surgery for losing weight is associated with reduction in the severity of psoriasis in obese patients (1, 2). However, the molecular links between psoriasis and obesity have not been fully elucidated. It is becoming apparent that adipose tissue is not only a reservoir for energy but also an active endocrine organ. Adipose tissue secrets a number of bioactive peptides and proteins, called adipokines. Leptin is one of adipokines derived from adipocyte (3). Several studies have reported that psoriasis is associated with leptin. However, the endocrine function of subcutaneous adipose tissue has not been fully elucidated. In the original article, we focused on the altered gene expression of leptin in obese patients with psoriasis. We demonstrated that the altered secretion of leptin by subcutaneous adipose tissue was related to the worsening of psoriasis severity in obese patients with psoriasis. We conclude that subcutaneous adipose tissue now emerges as a very important tissue affecting psoriasis severity.

 

TH fig1

Fig 1. Leptin linking obesity to worsening of psoriasis severity. (SAT, subcutaneous adipose tissue)

 

References

  1. Upala S, Sanguankeo A (2015) Effect of lifestyle weight loss intervention on disease severity in patients with psoriasis: a systematic review and meta-analysis. Int J Obes 39: 1197-202.
  2. Debbaneh M, Millsop JW, Bhatia BK, Koo J, Liao W (2014) Diet and psoriasis, part I: Impact of weight loss interventions. J Am Acad Dermatol 71: 133-40.
  3. Maury E, Bichard SM, (2010) Adipokine dysregulation, adipose tissue inflammation and metabolic syndrome. Mol Cell Endocrinol 314: 1-16.

 

Contact:

Tetsuya Higuchi, M.D., Ph.D. Department of Dermatology, Toho University Sakura Medical Center 564-1 Shimoshizu, Sakura, Chiba, Japan, 285-8741

higuchit@sakura.med.toho-u.ac.jp

http://www.kokusai.toho-u.ac.jp/english/mc/sakura/dermatology/index.html

http://www.lab.toho-u.ac.jp/med/sakura/dermatology/index.html

 

 

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