Glucose Control and Diabetes (week 4) Flashcards
mellitus
honey
insipidus
invisible; nothing to it
where are islets of langerhans found
pancreas
fxn of islets of langerhans
regulate metabolism of fat, carbohydrate, and protein by release of hormones
what kind of organ is the pancreas
exocrine and endocrine
islets of langerhans innervated by
autonomics
islets of langerhans composed of
alpha cells
beta cells
delta cells
F cells
islets of langerhans alpha cells location
located at periphery of islets
islets of langerhans alpha cells secrete
glucagon
catecholamines and corticosteroids (increase/decrease) glucagon output
increase
what does glucagon do
promotes release of glucose
secretion of glucagon controlled by
blood glucose levels
insulin levels
autonomic input
sypathetic tone (increses/decreases) glucagon output
increases
parasympathetic tone (increases/decreases) glucagon output
decreases
if blood glucose drops, what is stimulated
glucagon output increases
hyperglycemic agent
will cause elevation in blood glucose
what does insulin do to glucagon output
suppresses it
normal range of blood glucose
80-120 mg/dL
hypoglycemic agent
decreases blood glucose
islets of langerhans beta cells location
middle of islets
islets of langerhans beta cells secrete
insulin
insulin release controlled by
blood glucose
glucagon
GI hormones
autonomics
what does insulin promote
storage of glucose
what forms can glucose be stored as
glycogen
amino acid
fat
islets of langerhans delta cells location
periphery of islets
islets of langerhans delta cells release
gastrin
somatostatin
(both are GI hormones)
islets of langerhans delta cells play a role in release of
glucagon
insulin
& balance between these 2 chemicals
only certainties of islets of langerhans F cells
release pancreatic polypeptide
found in pancreatic islet
what stimulates release of insulin
elevation of blood glucose
elevation of blood amino acids
GI hormones
parasympathetic stimulation to beta cells
what inhibits release of insulin
decreasing blood glucose
increasing levels of blood insulin
parasympathetic stimulation to alpha cells
increased glucagon output
general effects of insulin
facilitates uptake of glucose into cells
promotes synthesis of proteins, carboydrates, lipids, nucleic acids
insulin action at liver produces
increases glucose uptake
promotes synthesis of glycogen and fatty acids
decreases gluconeogenesis
decreases glycogenolysis
decreases ketogenesis (by inhibiting breaking down of fat)
insulin action at muscle produces
facilitation of production of carbohydrates
insulin action at adipose tissue produces
facilitation of production of lipid
gluconeogenesis
making new glucose
ketogenesis
making ketone bodies by breaking down of fat
insulin effects on muscle
promotes uptake of glucose and amino acids
increases glycogen synthesis
increases protein synthesis
decreases proteolysis
what do glucocorticoids do to muscle
decrease utilzation of glucose by muscle
decrease numbers of insulin receptors on muscle
insulin’s effects on adipose tissue
promotes glucose uptake
stimulates fatty acid synthesis
decreases lipolysis (causes decrease in ketone bodies)
glucose intolerance
inability to control blood glucose within range of normal during various perturbations (80-120 mg/dL)
diagnostic criteria for diabetes
- more than 1 fasting plasma glucose level greater than 126 mg/dL
- oral glucose tolerance test plasma glucose level greater than 200 mg/dL in a 2 hr sample
- glucose level of 200 mg/dL at anytime of day combined with polydipsia, polyphagia, and polyuria
polydipsia
excessive thirst
polyphagia
excessive appetite
polyuria
excessive urine output
impaired glucose tolerance (pre-diabetic)
- higher than normal blood glucose levels but lower than those considered to indicate DM
- increased risk of type II diabetes and cardiovascular disease
is it possible to recover from impaired glucose tolerance
yes, with lifestyle changes (diet and exercise), a person can be put back into normal range
Type I Diabetes Mellitus
absolute insulin deficiency
due to genetic/environmental interaction
peaks at age 12
insulin dependent
what happens to beta cells in Type I DM
beta cells get destroyed and therefore do not produce insulin
subtypes of Type I DM
immune
nonimmune
immune subtype of Type I DM
cell mediated destruction of beta cells
nonimmune subtype of Type I DM
presence of genetic defect in beta cells (unusual)
what happens to you in type I DM
hyperglycemia
unexplained weight loss
ketoacidosis
hyperglycemia leads to
osmotic diuresis
polyuria
thirst
explanation for unexplained weight loss in type I DM
protein and fat are broken down for fuel due to unavailability of glucose
ketoacidosis results from
excessive fat breakdown
