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Shusaku Tamaki, Takaaki Inaba, Motoko Kawashima, Akiko Ito, Tetsuya Kawakita, Kazuo Tsubota; Molecular Mechanism Of Lacrimal Gland Dysfunction In db/db Mice. Invest. Ophthalmol. Vis. Sci. 2012;53(14):625.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate molecular mechanism of lacrimal gland dysfunction and metabolic changes in db/db mice as a rodent model of type 2 diabetes.
Female db/db and non-diabetic db/m mice were used in all experiments. Tear secretion was measured every month using a phenol red-impregnated thread method. All mice were euthanized to extirpate the lacrimal glands. Serum samples were collected for biochemical analysis. To investigate energy metabolism-related genes, total RNA was extracted from the lacrimal glands and evaluated by real-time PCR. Pathological analyses were performed to analyze the lacrimal gland tissue sections using an optical microscope and electron microscope.
Body weight was significantly increased in the db/db mice as compared to the db/m mice. In the biochemical analysis using the serum samples, blood glucose level in the db/db mice was significantly higher than in the db/m mice. Three months after the start of the experiment, tear secretion decreased in the db/db mice as compared to the db/m mice. In the histological assessment, inflammatory cell infiltration into the lacrimal glands was increased in the db/db mice as compared to the db/m mice. Electron microscopic assessment also showed increased inflammatory cell infiltration in the db/db mice. Further, examination of gene expression levels revealed that the expression of energy metabolism genes such as PGC-1 alpha and NAMPT decreased in the lacrimal glands of the db/db mice as compared to the db/m mice.
Energy metabolism-related genes might be key molecules for tear secretion.
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