Abstract
11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which converts inactive cortisone to active cortisol, has been reported to play an important role in metabolic diseases as well as chronic inflammatory diseases. The involvement of 11β-HSD1 in chronic periodontitis was investigated in the present study. The relationship between the levels of 11β-HSD1, chronic periodontitis, and body mass index (BMI) was analyzed. The expression of 11β-HSD1 mRNA was significantly higher in the chronic periodontitis group than in the control group. Since the expression of 11β-HSD2, which converts active cortisol to inactive cortisone, was slightly lower in the chronic periodontitis group than in the controls, the ratio of 11β-HSD1 versus 11β-HSD2 was significantly higher in the chronic periodontitis group than in the controls. A correlation was not observed between BMI and the level of 11β-HSD1 or between BMI and the ratio of 11β-HSD1 versus 11β-HSD2. These results suggested that an increase in the ratio of 11β-HSD1 versus 11β-HSD2 was associated with chronic periodontitis irrespective of obesity.
Highlights
Cortisol, a major glucocorticoid hormone in humans, is known to have various effects on the metabolism of carbohydrates, fat, and proteins as well as immune responses: briefly, it promotes the conversion of proteins and lipids into glucose, and limits and resolves the inflammatory process (Rhen and Cidlowski 2005; Gross and Cidlowski 2008)
We further investigated the expression of 11β-HSD1 as well as 11β-HSD2, and analyzed the relationships between the expression of 11β-HSD1/2, chronic periodontitis, and obesity
The expression levels of RANKL, RANK, and OPG mRNA were examined, since these molecules are involved in osteoclast differentiation and it was reported that the expression of RANKL was higher and that of OPG was lower in the periodontitis group than healthy control (Vernal et al 2006; Bostanci et al 2007; Wara-aswapati et al 2007)
Summary
A major glucocorticoid hormone in humans, is known to have various effects on the metabolism of carbohydrates, fat, and proteins as well as immune responses: briefly, it promotes the conversion of proteins and lipids into glucose, and limits and resolves the inflammatory process (Rhen and Cidlowski 2005; Gross and Cidlowski 2008). Transgenic mice selectively overexpressing 11βHSD1 in adipose tissue showed phenotypes similar to metabolic diseases including visceral fat obesity, insulin resistance, dyslipidemia, and hypertension (Masuzaki et al 2001, 2003). Inhibitors of 11β-HSD1 have been shown to ameliorate metabolic diseases and prevent atherosclerosis in mice (Hermanowski-Vosatka et al 2005; Nuotio-Antar et al 2007). These findings suggest that 11β-HSD1 plays a crucial role in metabolic diseases, to which inhibitors of 11β-HSD1 may be applied as novel therapeutics. Several highly potent and selective 11β-HSD1 inhibitors have been developed for the treatment of metabolic diseases including type 2 diabetes mellitus (Rosenstock et al 2010; Feig et al 2011; Anil et al 2014; Okazaki et al 2014; Hamilton et al 2015)
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