Open AccessThe hypomagnesic rat model: dermatitis‐prone hairless rats with mild magnesium depletion fed a diet low in lipids did not develop pruritic dermatitis
Author(s) -
Thomsen J. S.,
Nielsen P. L.,
Serup J.
Publication year - 2005
Publication title -
skin research and technology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.521
H-Index - 69
eISSN - 1600-0846
pISSN - 0909-752X
DOI - 10.1111/j.1600-0846.2005.00098.x
Subject(s) - hairless , transepidermal water loss , scratching , atopic dermatitis , endocrinology , medicine , magnesium , inflammation , chemistry , dermatology , biochemistry , pathology , physics , stratum corneum , organic chemistry , acoustics
Background/purpose: In the hypomagnesic dermatosis of rats, low‐dietary magnesium leads to lowered serum Mg 2+ , universal dermatitis and scratching. The model is postulated to work better if the diet also has a low content of lipids. Pruritus is seen in patients suffering from anorexia nervosa and resolves on weight restoration. Lipid depletion of the diet and/or lowered body weight may therefore be important in developing pruritus. The purpose of the present study was to investigate whether a diet low in lipids can induce pruritus in dermatitis prone rats because of mild magnesium depletion thereby focusing on the role of lipids in the hypomagnesic dermatosis rat model. Methods: Fourteen male hairless rats, 3 weeks of age, were fed a diet deficient in lipids and with a lower content of magnesium for a 4‐week period and compared with 11 controls fed a normal diet. The skin was inspected daily and transepidermal water loss (TEWL), serum Mg 2+ and scratching activity were measured. At the end, skin biopsies were taken from the flank and ears. Results: Serum Mg 2+ was significantly lowered in the diet group ( P <0.001) but the rats developed no dermatitis or increased TEWL compared with 11 rats in a control group. Biopsies were normal with no sign of inflammation. Rats in the diet group had inferior weight gain, were less active and spent more time asleep than control rats ( P <0.01). Furthermore, scratching activity monitored in the last week of the study as the number of scratch‐sequences per awake minute was reduced in the diet group ( P <0.001). Conclusion: The lipid‐deficient diet was not able to induce pruritic dermatitis despite the fact that the rats were dermatitis prone because of mild magnesium depletion. It is not confirmed that dietary lipid depletion plays any significant role in the hypomagnesic dermatitis rat model. The dermatitis and the model appear to be strictly dependent on efficient magnesium depletion manufactured with very low magnesium levels.