ArticleEndocrinology and metabolism (Seoul, Korea)2022
Stimulation of Alpha-1-Adrenergic Receptor Ameliorates Obesity-Induced Cataracts by Activating Glycolysis and Inhibiting Cataract-Inducing Factors.
Article in Endocrinology and metabolism (Seoul, Korea), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Causal effect of obesity on cataract and mediating roles of metabolites: a Mendelian randomization study.International journal of ophthalmology · 2026Article
- Global regional and national burden of cataract attributable to high body mass index from 1990 to 2019.BMJ open · 2025Article
- αInternational journal of molecular sciences · 2023Review
- A new use for old drugs: identifying compounds with an anti-obesity effect using a high through-put semi-automatedHeliyon · 2022Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundObesity, 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.
methodsTo 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.
resultsMidodrine 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.
conclusionThe 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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