Because non-genomic pathways include any mechanism that is not a genomic effect, there are various non-genomic pathways. However, all of these pathways are mediated by some type of steroid hormone receptor found at the plasma membrane.  Ion channels, transporters, G-protein coupled receptors (GPCR), and membrane fluidity have all been shown to be affected by steroid hormones.  Of these, GPCR linked proteins are the most more information on these proteins and pathways, visit the steroid hormone receptor page.
Diabetes results from inadequate levels of insulin. Type I diabetes is characterized by inadequate levels of insulin secretion, often due to a genetic cause. Type II usually develops in adults from both genetic and environmental causes. Loss of response of targets to insulin rather than lack of insulin causes this type of diabetes. Diabetes causes impairment in the functioning of the eyes, circulatory system, nervous system, and failure of the kidneys. Diabetes is the second leading cause of blindness in the US. Treatments involve daily injections of insulin, monitoring of blood glucose levels and a controlled diet.
Terminal prostaglandin synthases have been identified that are responsible for the formation of other prostaglandins. For example, hematopoietic and lipocalin prostaglandin D synthases (hPGDS and lPGDS) are responsible for the formation of PGD 2 from PGH 2 . Similarly, prostacyclin (PGI 2 ) synthase (PGIS) converts PGH 2 into PGI 2 . A thromboxane synthase ( TxAS ) has also been identified. Prostaglandin-F synthase (PGFS) catalyzes the formation of 9α,11β-PGF 2α,β from PGD 2 and PGF 2α from PGH 2 in the presence of NADPH. This enzyme has recently been crystallized in complex with PGD 2  and bimatoprost  (a synthetic analogue of PGF 2α ).