A new study from the Journal of Biomedical Science suggests that, contrary to the common “sugar hypothesis” of diabetic cataract development, cataract formation in patients with Type 2 diabetes may actually precede hyperglycemia.
First, what’s the sugar hypothesis?
The sugar hypothesis is the current widely-accepted hypothesis of diabetic cataract development. It posits that patients with diabetes experience a higher-than-normal concentration of glucose in the lens. This concentration leads to an accumulation of sorbitol molecules, which therefore leads to the known prevalence of cataracts in patients with Type 2 diabetes.
Tell me about the study.
According to the study authors from Brigham and Women’s Hospital in Boston, MA, the sugar hypothesis lacks supporting evidence from models that accurately mimic the pathophysiology of the human condition.
To develop a model that more closely maps to human Type 2 diabetes and cataract formation, the study used Nile grass rats, which develop Type 2 diabetes in captivity, and introduced diabetic cataracts. They then used an in-situ microscopy technique to track the immune cell migration to the lens. (via)
What did they find?
Researchers found microlesions in the lens that preceded hyperglycemia in 48% of the animals; additionally, they found immune cell migration to the lens from the ciliary bodies, and subsequent cataract progression.
So what does this mean?
As the predominating model for decades, the sugar hypothesis means that glucose has been seen as a primary culprit in diabetic cataract development.
This study suggests that diabetic cataract development is just one of the many complications of diabetes that can be sourced to normoglycemic phases, and all models based on the pathogenesis of the condition must proceed from there.
Ultimately, the study authors call for more research into the root of diabetic cataracts, as well as new investigations into diagnostics and treatment for this condition.