NSG 322 - Exam 2 Study Guide.
LECTURE 6 – ENDOCRINE SYSTEM
Glucose Regulation Key Players
● Insulin
○ When blood sugar is high
○ Produced by Beta Cells in pancreas (islets of Langerhans)
○ Function:
■ Move glucose into the cells/metabolism
■ Stimulates storage of glucose in liver/muscle
■ Stimulates storage of dietary fat in adipose tissue
■ Signals liver to stop releasing glucose
■ Inhibits breakdown of glycogen *(PREVENTS glycogenolysis)
■ *Signals to inhibit lipolysis = breakdown of fat
● Glucagon
○ When blood sugar is low
○ Produced by the Alpha Cells in pancreas (Islets of Langerhans) go to liver
○ Function:
■ Stimulates liver cells to convert glycogen into glucose = (STIMULATES glycogenolysis)
■ Stimulates production of glucose from non-carb substances =
(STIMULATES gluconeogenesis)
● Glycogen = stored form of glucose
● Incretins
○ Peptides produced in the GI tract
○ Functions:
■ Stimulate insulin release
■ Decrease glucagon release
■ Stimulate satiety center
,NSG 322 - Exam 2 Study Guide.
■ Slow GI emptying
○ Example: Glucagon-like polypeptide 1 (GLP-1)
,NSG 322 - Exam 2 Study Guide.
● Dipeptidyl peptidase 4 (DDP-4)
○ Enzyme that metabolizes GLP-1
● Adiponectin (hormones produced by fat cells) plays role in metabolism
○ Increase insulin sensitivity
○ Decrease glucose released from liver
○ Protect blood vessels from inflammatory changes
Biphasic Insulin Release
● Post Prandial Insulin Production
○ “After meals” – when there’s sudden high levels of glucose
● Basal Insulin Production
○ “Maintain steady state”
○ During ‘fasting period’
○ What else occurs –
■ Glycogenolysis occurs
● By glucagon
■ Gluconeogenesis occurs
Types of Diabetes Mellitus
● Type 1 Diabetes
○ Pathophysiology:
■ Beta cells in the pancreas are destroyed by an autoimmune process
● Beta cells produce what? insulin
■ Often common +autoantibodies to pancreatic Beta cells
■ Cause of autoimmune destruction:
● Genetic susceptibility
● Environmental trigger agents
■ Little to no endogenous insulin
● Will require insulin therapy
● Ketosis can occur
■ Common acute complication:
● Hyperglycemic diabetic ketoacidosis
○ Without insulin…
■ Glucose can’t enter tissues
■ Accumulates in the blood = hyperglycemia
○ Hyperglycemia causes intracellular dehydration…..how? pulls water from body
○ Dehydration stimulates hypothalamus polydipsia develops
○ Amount of glucose filtered by kidneys exceeds its limits
■ Results in glucose ‘spilling’ into the urine
■ ….What will follow high glucose? water
■ Result in fluid loss (large volumes that are dilute) polyuria (going to the bathroom a
lot)
○ 3 Things get activated (body attempts to create more glucose b/c cells aren’t getting the
glucose needed)
■ Glycogenolysis via glucagon
, NSG 322 - Exam 2 Study Guide.
■ Gluconeogenesis
■ Ketosis (breakdown of fats & proteins ATP)
○ Result:
■ Polyphagia (hunger)
LECTURE 6 – ENDOCRINE SYSTEM
Glucose Regulation Key Players
● Insulin
○ When blood sugar is high
○ Produced by Beta Cells in pancreas (islets of Langerhans)
○ Function:
■ Move glucose into the cells/metabolism
■ Stimulates storage of glucose in liver/muscle
■ Stimulates storage of dietary fat in adipose tissue
■ Signals liver to stop releasing glucose
■ Inhibits breakdown of glycogen *(PREVENTS glycogenolysis)
■ *Signals to inhibit lipolysis = breakdown of fat
● Glucagon
○ When blood sugar is low
○ Produced by the Alpha Cells in pancreas (Islets of Langerhans) go to liver
○ Function:
■ Stimulates liver cells to convert glycogen into glucose = (STIMULATES glycogenolysis)
■ Stimulates production of glucose from non-carb substances =
(STIMULATES gluconeogenesis)
● Glycogen = stored form of glucose
● Incretins
○ Peptides produced in the GI tract
○ Functions:
■ Stimulate insulin release
■ Decrease glucagon release
■ Stimulate satiety center
,NSG 322 - Exam 2 Study Guide.
■ Slow GI emptying
○ Example: Glucagon-like polypeptide 1 (GLP-1)
,NSG 322 - Exam 2 Study Guide.
● Dipeptidyl peptidase 4 (DDP-4)
○ Enzyme that metabolizes GLP-1
● Adiponectin (hormones produced by fat cells) plays role in metabolism
○ Increase insulin sensitivity
○ Decrease glucose released from liver
○ Protect blood vessels from inflammatory changes
Biphasic Insulin Release
● Post Prandial Insulin Production
○ “After meals” – when there’s sudden high levels of glucose
● Basal Insulin Production
○ “Maintain steady state”
○ During ‘fasting period’
○ What else occurs –
■ Glycogenolysis occurs
● By glucagon
■ Gluconeogenesis occurs
Types of Diabetes Mellitus
● Type 1 Diabetes
○ Pathophysiology:
■ Beta cells in the pancreas are destroyed by an autoimmune process
● Beta cells produce what? insulin
■ Often common +autoantibodies to pancreatic Beta cells
■ Cause of autoimmune destruction:
● Genetic susceptibility
● Environmental trigger agents
■ Little to no endogenous insulin
● Will require insulin therapy
● Ketosis can occur
■ Common acute complication:
● Hyperglycemic diabetic ketoacidosis
○ Without insulin…
■ Glucose can’t enter tissues
■ Accumulates in the blood = hyperglycemia
○ Hyperglycemia causes intracellular dehydration…..how? pulls water from body
○ Dehydration stimulates hypothalamus polydipsia develops
○ Amount of glucose filtered by kidneys exceeds its limits
■ Results in glucose ‘spilling’ into the urine
■ ….What will follow high glucose? water
■ Result in fluid loss (large volumes that are dilute) polyuria (going to the bathroom a
lot)
○ 3 Things get activated (body attempts to create more glucose b/c cells aren’t getting the
glucose needed)
■ Glycogenolysis via glucagon
, NSG 322 - Exam 2 Study Guide.
■ Gluconeogenesis
■ Ketosis (breakdown of fats & proteins ATP)
○ Result:
■ Polyphagia (hunger)
