This transport protein is stored in vesicles of insulin-target cells, especially muscle cells and adipocytes.

T1DM is mediated by this type of hypersensitivity reaction, resulting in the destruction of pancreatic beta cells.

This phenomenon describes the failure of target tissues to normally respond to insulin.

In DKA, epinephrine release blocks the secretion of insulin, while stimulating the secretion of this hormone.

The forms of insulin consisting of this molecular unit diffuse readily into the blood and have a fast onset of action.

The production of insulin in the pancreas is inhibited by this hormone during the fight or flight response.

The genetic susceptibility of T1DM is associated with these 2 HLA haplotypes.

This pattern of obesity results in adipocytes that carry out more lipolysis than adipocytes of subcutaneous fat, resulting in increased free fatty acids.

The accumulation of this substance causes the osmotic damage that mediates cataracts and diabetic neuropathy.

This type of insulin is administered IV to treat DKA and HHS.

Though glucagon typically acts as a counter-regulatory hormone, both insulin and glucagon increase cellular uptake of these molecules.

This environmental factor is hypothesized to have epidemiological association with the development of T1DM due to phenomena such as the "bystander effect" or "molecular mimicry".

This skin finding of hyperpigmented plaques in the folds of the neck and axillae is commonly associated with insulin resistance.

Advanced glycosylation end products (AGEs) cause the cross-linking of this protein, leading to hyaline arteriolosclerosis.

In addition to glargine, this type of insulin also controls basal levels of glucose and is known as "peakless".

Insulin stimulates fatty acid uptake in peripheral tisues by stimulating capillary lipoprotein lipase synthesis; it also decreases the plasma fatty acid level by inhibiting this hepatic enzyme.

The fundamental immune abnormality in T1DM is the result of defective negative selection that takes place in this organ.

This complication of T2DM manifests as mental status changes in elderly patients who can't mainain adequate fluid intake.

This finding on fundoscopic exam represents optic nerve infarction due to retinal ischemia.

This class of drugs cannot be used in T1DM because they bind to the beta cells of the pancreas to stimulate insulin release and thus require functional islets.

The intrinsic tyrosine kinase activity of the insulin receptor activates this downstream sequence via IRS proteins, leading to the metabolic effects of insulin on glucose transport.

This beta-cell enzyme important for neurotransmitter synthesis is a proposed target of auto-antibody attack in T1DM.

This peptide packaged and secreted in beta cells with insulin can form fibrils that stain Congo Red.

In DKA, beta oxidation of fatty acids results in the excess production of this intermediate at a rate faster than it can enter the TCA cycle, resulting in the formation of ketones.

This class of drugs known for causing side effects mimicking lactose intolerance is the only diabetes drug that inhibits glucose absorption in the small intestine.