Exam 3: Ch 19 Regulation of Metabolism Flashcards
Pancreatic Islets of Langerhans
- Contain 2 cell types involved in energy homeostasis:
- a cells
- b cells
a cells
- secrete glucagon
- when glucose levels are low,
- causes increased glucose by stimulating glycogenolysis in liver
b cells
- secrete insulin
- when glucose levels are high
- reduces blood glucose by promoting its uptake by tissues
Normal fasting glucose level
65–105 mg/dl
After a meal is absorbed, blood glucose levels
- rise to ~ 140 – 150 mg/dl
- This rise stimulates secretion of insulin and inhibits glucagon secretion
Insulin & glucagon normally prevent
levels from rising above 170mg/dl after meals or falling below 50mg/dl between meals
Insulin Overall effect is to promote
anabolism
anabolism
- Promotes storage of digestion products (not only glucose)
- Inhibits breakdown of fat & protein
- Inhibits secretion of glucagon
Insulin: Anabolism stimulates
insertion of GLUT4 transporters (transport by facilitated diffusion) in cell membrane of skeletal muscle, liver, & fat
Oral Glucose Tolerance Test
- Assesses ability of b cells to secrete insulin & insulin’s ability to lower blood glucose
- Responses to drinking a glucose solution are measured
Oral Glucose Tolerance Test
in non-diabetics
glucose levels return to normal within 2 hrs
Oral Glucose Tolerance Test
in diabetics
Diabetes mallitus causes blood glucose >200 mg/dl after 2 hrs
Glucagon
- Maintains blood glucose concentration above 50mg/dl
- Stimulates glycogenolysis in liver
- Stimulates gluconeogenesis, lipolysis, & ketogenesis
- Skeletal muscle, heart, liver, & kidneys use fatty acids for energy
Effects of ANS on Insulin & Glucagon
ANS innervates islets
Activation of parasympathetic NS
stimulates insulin secretion
Activation of sympathetic NS
NS stimulates glucagon & inhibits insulin
Effects of Intestinal Hormones
Insulin levels increase more rapidly after glucose ingestion than after intravenous glucose infusion
after intravenous glucose infusion
due to hormones secreted by intestine during meals
- “in anticipation” of glucose rise: all stimulate insulin secretion
- GIP; GLP-1; CCK
GIP
= gastric intestine peptide (secreted by duodenum),
GLP-1
= glucagon-like peptide (secreted by ileum),
CCK
= cholecystokinin
Diabetes mallitus
characterized by chronic high blood glucose levels (hyperglycemia)
hyperglycemia
the major cause of kidney failure and amputations, and is the 2nd leading cause of blindness
Type I (insulin dependent or IDDM)
- due to insufficient insulin secretion by beta cells
- 5 – 10% of total cases
- requires exogenous insulin
Type II (insulin independent or NIDDM)
- due to lack of efficiency of insulin at target cells
- 90 – 95% of total cases
Type 1diabetes (formerly “juvenile on set”)
= b cells of islets are destroyed by autoimmune attack, thus beta cells secrete little or no insulin
Glucose is unable to enter resting muscle or adipose cells
–> rate of fat synthesis lags behind rate of lipolysis –> fatty acids are converted to ketone bodies, leading to ketosis (↑ [ketone] in blood) producing ketoacidosis (↓ pH) –> glucose and ketones in urine (glucosuria or ketonuria) + ↑ H2O excretion because glucose and ketones act like osmotic diuretics (severe dehydration)
–> ↑ glucagon levels stimulate
glycogenolysis in liver, which ↑ [glucose] in blood also ↑ [ketone] in blood–>serious electrolyte imbalances–> coma or death
Type II diabetes
due to lack of efficiency of insulin at target cells)=
Type II diabetes slow to develop
heredity plays a role and occurs most often in overweight people
Type II diabetes involves
insulin resistance; usually accompanied by normal-to-high insulin levels
Type II diabetes treatable by
- exercise & diet
- b/c being over weight causes insulin resistance, thus ↑ caloric expenditure and shrinking fat cells ↑ insulin responsiveness
- Is not usually accompanied by ketoacidosis