Normal Pancreas, Islets Of Langerhans, And Metabolism

Front 1

insulin sensitivity

Back 1

ability of the body to respond normally to insulin

Front 2

insulin resistance

Back 2

failure of the body to respond normally to insulin

Front 3

glucose sensitivity/tolerance

Back 3

ability of the body to metabolize glucose

Front 4

glucose insensitive/intolerant

Back 4

failure of the body to metabolize glucose

Front 5

glucose toxicity

Back 5

impaired beta cell function due to chronic high blood glucose levels

Front 6

hyperlipidemia

Back 6

elevated lipid concentrations in blood

Front 7

dyslipidemia

Back 7

alteration in ratio of FFAs, TAGs, and cholesterol in blood

Front 8

lipodystrophy

Back 8

lipid deposition in organs that don't normally store TAGs

Front 9

lipotoxicity

Back 9

theory that high levels of lipids cause insulin resistance in target tissues

Front 10

diabetes mellitus - what is it??

Back 10

a derangement of fuel metabolism: NOT a disease of elevated blood sugar, NOT a disease of the vascular system

Front 11

Type 1 diabetes mellitus

Back 11

insulin-dependent, juvenile-onset; autoimmune, unrestrained hepatic glucose output, minimal glucose uptake

Front 12

diagnosis of DM - clinical clues

Back 12

polydipsia, polyuria, polyphagia

Front 13

type 2 diabetes

Back 13

non-insulin dependent; insulin-resistant/adult onset; not autoimmune, relative failure of beta cells; some insulin is produced (prevent DKA and uncontrolled lipolysis)

Front 14

80% rule

Back 14

80% of type 2 diabetics are obese, but 80% of obese patients will not have diabetes

Front 15

short term complications of type 2

Back 15

hyperosmolar coma

Front 16

microvascular complications (long term)

Back 16

non-enzymatic glycosylation of proteins -> AGE production => retinopathy, nephropathy & peripheral neuropathy

Front 17

macrovascular complications (long term)

Back 17

CVD - HTN & altered lipid profiles; sorbitol production increases osmotic pressure -> cataracts

Front 18

Rx Type 1

Back 18

insulin required

Front 19

Rx type 2

Back 19

diet/exercise, acarbose, metformin, sulfonylureas, meglitinides, extenatide, glitizones

Front 20

blood glucose regulation

Back 20

beta cells -> insulin release -> inhibit FA release, glucose production + stimulate glucose uptake by liver, muscle & adipocytes

Front 21

fuel sources

Back 21

glucose (required by brain), fatty acids, protein (last resort)

Front 22

normal plasma glucose levels

Back 22

65-100 mg/dl

Front 23

hypoglycemia

Back 23

mild = <50 mg/dl; palpitations, sweating, anxiety, HTN, hunger

severe = <35; seizures, coma, brain death

Front 24

hyperglycemia

Back 24

mild = >180; exceeds renal threshold (glucosuria)

severe = >300; DKA or hyperosmolar coma

Front 25

insulin facts

Back 25

released in response to high glucose; liver = glycogenesis, glycolysis, FA synthesis; muscle = glucose uptake; inhibits HSL in adipose tissue, inhibits glucagon release from islets

Front 26

counterregulatory hormones

Back 26

glucagon, epinephrine, cortisol, growth hormone

Front 27

glucagon

Back 27

released when glucose is low; liver = glycogenolysis and gluconeogenesis, insulin release from islets

Front 28

epinephrine

Back 28

released during acute stress, low glucose states; liver = glycogenolysis; muscle = glycogenolysis to lactate; adipose = HSL; islets = inhibit insulin release

Front 29

cortisol

Back 29

released during chronic stress, low glucose; liver = gluconeogenesis, glycogenesis; muscle = protein catabolism, inhibit glucose uptake & utilization; adipose = lipolysis, inhibit glucose uptake

Front 30

growth hormone

Back 30

released in response to GHRH, low glucose, inhibited by somatostatin; liver = gluconeogenesis, glycogenesis, lipolysis + inhibit glucose uptake; muscle = uptake of AAs and protein synthesis, lipolysis; inhibit glucose uptake; adipose = lipolysis, inhibit glucose uptake

Front 31

insulin biphasic release

Back 31

initial spike = insulin secretory granules; sustained higher levels attributed to other beta cells (docking - like neurons!!)

Front 32

GLUT2

Back 32

sensor on liver & pancreatic beta cells; high Km = linear increase in uptake as glucose concentrations increase

Front 33

GLUT4 & insulin

Back 33

upon insulin binding, the number of receptors increases; expressed on skeletal muscle & adipose cells

Front 34

insulin release

Back 34

glucose enters cell -> ATP released -> K+ channel closes -> plasma membrane of beta cell is depolarized -> voltage gated Ca channels open -> intracellular incr. in ca -> release of insulin

Front 35

determine ratio of exogenous/endogenous insulin

Back 35

connecting peptide (c peptide) that is only present in endogenous insulins

Front 36

sulfonylureas

Back 36

inhibit potassium channel on beta cells from opening = increase membrane depolarization and insulin release

Front 37

GLP-1= glucagon like peptide

Back 37

produced after a large meal, increases the release of insulin by "priming" beta cells = incretin

Front 38

exenatide

Back 38

drug that acts like GLP-1

Front 39

adipose tissue

Back 39

endocrine organ; stores fatty acids to use as fuel in the future; carbohydrates are the source of triglyceride synthesis; cycle of FA and triglycerides w/in adipose tissue

Front 40

cortisol & adipose tissue

Back 40

decrease storage of fatty acids, increases levels in the blood

Front 41

lipotoxicity problem

Back 41

too much triglyceride = exceeds storage ability of adipose tissue = leaked free fatty acids

Front 42

glitazone drugs

Back 42

bind & stimulate expression of genes (PEPCK) that increase storage of fatty acids

Front 43

metformin

Back 43

increases AMPK levels = inhibit synthesis of fats, proteins & glycogen, increases uptake of glucose into muscle

Front 44

metabolic syndrome = insulin resistance syndrome

Back 44

abdominal obesity + insulin resistance + HTN + dyslipidemia; high risk for type 2 DM, CVD, essential HTN, polycystic ovary syndrome, cancer, sleep apnea, non-alcoholic fatty liver