Therapeutic Diets Exam #3

Group of diseases characterized by high blood glucose concentrations resulting from defects in insulin secretion, insulin action, or both.

A hormone produced by beta cells of the pancreas that is necessary for the use or storage of body fuels; essential to type 1; may be needed to store glycemia in type 2; onset, peak, duration; inhaled types; insulin pump

Elevated blood glucose levels; develops on when greater than 90% of the secretory capacity of the beta cells mass has been destroyed; first exhibited as elevation of postprandial bg

140-190 mg/dl; 2 hours postchallenge glucose; plasma glucose elevated after 75 g glucose load, typically 8-24 hrs before

Stage of impaired glucose homeostasis that includes IFG and GT. People with pre-diabetes have IFG, IGT, or both.

Fasting plasma glucose 100-125 mg/dl; fasting plasma glucose above normal level

People affected often lean, excessive thirst, frequent urination, significant weight loss. Pancreatic beta cell destruction, usually leading to absolute insulin deficiency and resulting in hyperglycemia, polyuria, polydipsia, weight loss, dehydration, electrolyte distrubance, and ketoacidosis. Two types: immune mediated and idiopathic

Forms of the disease that have no known etiology; falls most with blacks or asian origin; cause of the beta cell function loss unknown
beta cells destroyed by autoimmune process

• result of combo of HLA-DQ coded genes for disease susceptibility offset by genes that are related to disease resistance

Islet cell ab's; insulin auto-ab; antibodies against islet tryronsine phosphatase (IA2); autoantibodies to glutamic acid decarboxylase (GAD) (protein on surface of beta cells)

Glutamic acid decarboxylase; a protein on the surface of beta cells. Appear to provoke an attack by the T cells, which may be what destroys the beta cells in diabetes

Period after initial diagnosis of type 1 diabetes when there may be some recovery be beta cell function and a temporary decrease in exogenous insulin requirement. During, exogenous insulin requirement decrease dramatically for up to 1 year

Results from: combo of insulin resistance and beta cell failure; inadequate insulin levels to overcome insulin resistance causing hyperglycemia. Formerly NIDDM

Decreased tissue sensitivity or responsiveness to insulin; first demonstrated in target tissue (muscle, liver, adipose cells); in fat cels, leads to lipolysis and an elevation in circulating free fatty acids

After a meal bg; bg levels 1-2 hours after eating