Thus, when fatty acids are being broken down for energy, all of the remaining glucose is made available for use by the brain.After two or three days of fasting, the liver begins to synthesize ketone bodies from precursors obtained from fatty acid breakdown. The brain uses these ketone bodies as fuel, thus cutting its requirement for glucose. After fasting for three days, the brain gets 30% of its energy from ketone bodies. After four days, this may increase to 70% or more. Thus, the production of ketone bodies cuts the brains glucose requirement from 80 g per day to 30 g per day, about 35% of normal, with 65% derived from ketone bodies. But of the brains remaining 30 g requirement, 20 g per day can be produced by the liver from glycerol (itself a product of fat breakdown). This still leaves a deficit of about 10 g of glucose per day that must be supplied from another source; this other source will be the bodys own proteins. After exhaustion of fat stores, the cells in the body begin to break down protein. This releases alanine and lactate produced from pyruvate, which can be converted into glucose by the liver. Since much of human muscle mass is protein, this phenomenon is responsible for the wasting away of muscle mass seen in starvation. However, the body is able to choose which cells will break down protein and which will not.
Ophthalmoparesis  refers to weakness (-paresis) or paralysis (-plegia) of one or more extraocular muscles which are responsible for eye movements. It is a physical finding in certain neurologic, ophthalmologic, and endocrine disease. Internal ophthalmoplegia means involvement limited to the pupillary sphincter and ciliary muscle. External ophthalmoplegia refers to involvement of only the extraocular muscles. Complete ophthalmoplegia indicates involvement of both. Causes
Ophthalmoparesis can result from disorders of various parts of the eye and nervous system:

Infection around the eye. Ophthalmoplegia is an important finding in orbital cellulitis. The orbit of the eye, including mechanical restrictions of eye movement, as in Graves disease. The muscle, as in progressive external ophthalmoplegia or Kearns–Sayre syndrome. The neuromuscular junction, as in myasthenia gravis. The relevant cranial nerves (specifically the oculomotor, trochlear, and abducens), as in cavernous sinus syndrome or raised intracranial pressure. The brainstem nuclei of these nerves, as in certain patterns of brainstem stroke such as Fovilles syndrome. White matter tracts connecting these nuclei, as in internuclear ophthalmoplegia, an occasional finding in multiple sclerosis. Dorsal midbrain structures, as in Parinauds syndrome. Certain parts of the cerebral cortex (including the frontal eye fields), as in stroke. Toxic envenomation by mambas, taipans, and kraits.Thiamine deficiency can cause ophthalmoparesis in susceptible persons; this is part of the syndrome called Wernicke encephalopathy. The causal pathway by which this occurs is unknown. Intoxication with certain substances, such as phenytoin, can also cause ophthalmoparesis.