Glucose metabolic disorders and diabetic retinopathy is linked to an increased risk of cataracts. The anatomical components of the eye work together to focus a picture on the retina. The cornea, one of the eye's two major focusing structures, receives light. The pupil is the eye's next focusing component, and it is positioned directly after the crystalline lens, which is the eye's second focusing component. The cornea and lens focus light rays onto the retina, which initiates image processing and transmission to the occipital area of the brain. The lens of the eye becomes clouded, limiting light from reaching the retina. Blurred vision, glare, and reduced contrast sensitivity are all symptoms of cataracts. Studies have demonstrated that diabetic lenses have aberrant levels of electrolytes, glutathione, nucleotides, and carbohydrates. Cataracts are more common in those with type 1 and type 2 diabetes. Diabetes-related alterations in lens metabolism and cataract development are linked to hyperglycemia. According to a study of glucose metabolism pathways, several hyperglycemia-initiated activities are linked to cataract formation. Metabolic alterations in galactosemia-related cataracts are identical, indicating a similar biochemical origin. Aldose reductase (NADP+ 1-oxidoreductase, EC 22.214.171.124) is a sugar alcohol synthase enzyme that transforms glucose or galactose into sugar alcohols (polyols). Increased intracellular polar alcohol levels promote lens fiber extension, vacuole formation, and opacification, while Aldose reductase inhibition prevents sugar cataract development. This article is a review on different studies and reports that encompasses diabetic retinopathy and cataracts.