Ametropic amblyopia is a medical condition in which the retina cannot focus on the image of a distant object, a condition often described as reduced visual acuity. This is due to large uncorrected refractive errors in the patients optic system of the eyes. Astigmatism is one of the most frequent causes of ametropic amblyopia. References
Further reading
Moseley, Merrick J., et al. "Effectiveness of occlusion therapy in ametropic amblyopia: a pilot study." British Journal of Ophthalmology 81.11 (1997): 956–961. Cavazos, H.;  et al. (1993). "Ametropic Amblyopia". Strabismus. Informa Plc. 1 (2): 63–67. doi:10.3109/09273979309087719. PMID 21314500. Abraham, S. V. "Bilateral ametropic amblyopia." J Pediatr Ophthalmol Strabismus 1 (1964): 57–61. Werner, D. B., and W. E. Scott. "Amblyopia case reports--bilateral hypermetropic ametropic amblyopia." Journal of pediatric ophthalmology and strabismus 22.5 (1984): 203–205. Moseley, Merrick J;  et al. (1997). "Effectiveness of occlusion therapy in ametropic amblyopia: a pilot study". British Journal of Ophthalmology. BMJ Publishing Group Ltd. 81 (11): 956–961. doi:10.1136/bjo.81.11.956. PMC 1722055. PMID 9505818.
Defects in nuclear-encoded mitochondrial genes are associated with hundreds of clinical disease phenotypes including anemia, dementia, hypertension, lymphoma, retinopathy, seizures, and neurodevelopmental disorders.A study by Yale University researchers (published in the February 12, 2004, issue of the New England Journal of Medicine) explored the role of mitochondria in insulin resistance among the offspring of patients with type 2 diabetes. Other studies have shown that the mechanism may involve the interruption of the mitochondrial signaling process in body cells (intramyocellular lipids). A study conducted at the Pennington Biomedical Research Center in Baton Rouge, Louisiana showed that this, in turn, partially disables the genes that produce mitochondria. Mechanisms
The effective overall energy unit for the available body energy is referred to as the daily glycogen generation capacity, and is used to compare the mitochondrial output of affected or chronically glycogen-depleted individuals to healthy individuals. This value is slow to change in a given individual, as it takes between 18 and 24 months to complete a full cycle.The glycogen generation capacity is entirely dependent on, and determined by, the operating levels of the mitochondria in all of the cells of the human body; however, the relation between the energy generated by the mitochondria and the glycogen capacity is very loose and is mediated by many biochemical pathways. The energy output of full healthy mitochondrial function can be predicted exactly by a complicated theoretical argument, but this argument is not straightforward, as most energy is consumed by the brain and is not easily measurable.