Stimulation of Alpha-1-Adrenergic Receptor Ameliorates Obesity-Induced Cataracts by Activating Glycolysis and Inhibiting Cataract-Inducing Factors
Endocrinology and Metabolism
; : 221-232, 2022.
Article
em En
| WPRIM
| ID: wpr-924950
Biblioteca responsável:
WPRO
ABSTRACT
Background@#Obesity, the prevalence of which is increasing due to the lack of exercise and increased consumption of Westernized diets, induces various complications, including ophthalmic diseases. For example, obesity is involved in the onset of cataracts. @*Methods@#To clarify the effects and mechanisms of midodrine, an α1-adrenergic receptor agonist, in cataracts induced by obesity, we conducted various analytic experiments in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a rat model of obesity. @*Results@#Midodrine prevented cataract occurrence and improved lens clearance in OLETF rats. In the lenses of OLETF rats treated with midodrine, we observed lower levels of aldose reductase, tumor necrosis factor-α, and sorbitol, but higher levels of hexokinase, 5’-adenosine monophosphate-activated protein kinase-alpha, adenosine 5´-triphosphate, peroxisome proliferator-activated receptordelta, peroxisome proliferator-activated receptor gamma coactivator 1-alpha, superoxide dismutase, and catalase. @*Conclusion@#The ameliorating effects of midodrine on cataracts in the OLETF obesity rat model are exerted via the following three mechanisms direct inhibition of the biosynthesis of sorbitol, which causes cataracts; reduction of reactive oxygen species and inflammation; and (3) stimulation of normal aerobic glycolysis.
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Base de dados:
WPRIM
Tipo de estudo:
Prognostic_studies
Idioma:
En
Revista:
Endocrinology and Metabolism
Ano de publicação:
2022
Tipo de documento:
Article