Glucose Metab and Digestive Endocrinology Flashcards
(40 cards)
What is the difference between the endocrine and exocrine functions of the pancreas?
- Exocrine: secreting outwardly via a duct. (i.e- pancreatic duct)
- Endocrine: secreting inwardly; applied to organs and structures who’s function is to secrete hormones into the blood or lymph that has a specific effect on another organ or part.
What are the cells of the pancreas?
What % of pancreas is endorcrine?
-acinar cells secrete enzymes into the pancreatic duct.
- Islets of Langerhan cells secrete hormones into the blood vessels.
- made up of alpha (glucagon), beta(insulin), gamma(secrete pancreatic peptide) and delta cells(somatostatin)
- beta, alpha, delta = layers of islet of langerhan cells, innermost to outermost.
- 2% of pancreatic mass.
Glucagon:
- secreted by what cells?
- function
- what happens when there is low glucose in the blood?
- alpha cells
function: produce an increase in blood glucose by creating glucose from glycogen via gluconeogensis.
Low glucose:
-Glucagon is released into portal circulation stimulated by low blood glucose or during strenuous exercise to prevent low BS. Glucagon initiates glycogenolysis (break down of glycogen in the liver to glucose). Glucagon also increases transport of AA into the liver and stimulates their conversion into glucose(gluconeogenesis).
What are some factors that stimulate glucagon secretion? Inhibit?
Stimulate:
- Hypoglycemia
- AA (arginine & alanine)
- GI Hormones (CCK & Gastrin)
- Fasting
- Exercise
- Neural influences (vagal activity-ACH, sympathetic activity; beta adrenergic-E and NE)
Inhibit:
- Glucose
- Somatostatin
- Insulin
- GI Hormones (Secretin, Glucagon Like Peptide-1)
- Free Fatty Acids
- Ketoacids
- Neural influences (alpha adrenergic)
What is DPP? What is it used for?
What is Incretin? What is it used for?
Dipeptidyl Peptidase; essential for glucose production
Incretin is a hormone, inhibits glucagon and stimulates insulin release.
What is occurring metabolically during anabolism and catabolism in regards to:
- Hormones insulin and glucagon
- Fuel source
- Metabolic Process
Anabolism:
- Hormones: Insulin increases and glucagon decreases.
- Fuel Source: diet
- Metabolic Process: Glycogen synthesis (insulin is pushing glucose into liver and producing glycogen). Triglyceride synthesis and Protein synthesis.
Catabolism:
- Hormones: decreased insulin and increased glucagon
- Fuel source: storage deposits
- metabolic process: Glycogenolysis, lipolysis, proteolysis, ketogenesis
Metabolic Effects of Epinepherine
During periods of stress E is released from adrenal medulla causing glycogenolysis in the liver, thus causing large quantities of glucose to be released into the blood. It also inhibits insulin release from the beta cells and thereby decreases the movement of glucose into the muscle cells, while at the same time increasing the breakdown of muscle glycogen stores. Glucose released from muscle glycogen cannot be released into the blood, the mobilization of these stores for muscle use conserves blood glucose for use by other tissues such as brain and nervous system.
E also has effects on adipose tissue, increasing the mobilization of fatty acids for use as an energy source.
pg 1307 porth.
How does blood glucose affect growth hormone?
- growth hormone is inhibited by insulin and increased levels of blood glucose. When insulin and glucose decrease GH increases.
- Chronic hypersection of GH (acromegaly) can lead to glucose intolerance and the development of DM.
Insulin
-function
Function:
- lowers blood glucose by:
- -promoting uptake of glucose by target cells
- -promotes glucose storage as glycogen
- -prevents fat and glycogen breakdown
- -inhibits gluconeogensis and increases protein synthesis.
- -increases triglyceride synthesis
- -promotes fat storage by increasing transport of glucose into fat cells.
Insulin synthesis
main steps of insulin synthesis and secretion is by the Beta cells in the islets of langerhands.
Preproinsulin is converted to proinsulin in the rough ER. It is released into cytoplasm and is then taken up into small vesicles. The gogli apparatus secretes granules that enable the conversion of proinsulin to insulin. Insulin is stored here until they are released into the capillary system(portal venous circulation).
What is the major regulator of insulin? How does this work?
- glucose is the regulator of insulin.
- Beta cell has GLUT 2 receptor allowing glucose to enter beta cell. This results in depolarization and excretion of insulin from beta cell.
Factors Affecting Insulin Secretion
- stimulation
- inhibition
Stimulation:
- Glucose
- AA (arginine, lysine, alanine, leucine)
- Free FA
- Keto Acids
- Glucagon
Inhibition:
- Somatostatin
- fasting
- exercise
- Leptin
Insulin Effect on Carbs
-carbs from a meal release glucose and stimulate secretion of insulin leading to uptake and storage of glucose in all tissues.
In muscle if not used glycogen is stored.
In liver stored as glycogen, once liver stores max amount of glycogen, insulin promotes conversion of glucose to FA.
Insulin effects on skeletal muscle and adipose tissue?
-insulin binds to receptor on skeletal muscle or adipose cell causing intracellular signal and insertion of GLUT-4 receptor into cell membrane leading to transport of glucose into cell. Resulting in increased glycogen via glycolysis, increased protein synthesis and triglycerides
1307 porth
Insulin Effects on the Liver
–insulin binds to receptor on liver causing intracellular signal and insertion of GLUT-2 receptor into cell membrane leading to transport of glucose into cell. Resulting in increased glycogen via glycolysis, increased protein synthesis and triglycerides
Effects of Insulin on Fat Metabolism
First Insulin increases the uptake of glucose by most of the body tissues, thereby decreasing utilization of fat.
Once liver glycogen is maxed, additional glucose forms fatty acids. These FA form triglycerides that are released into the blood stream and transported via VLDLV to adipose tissue where it must be cleaved by lipoprotein lipase into FA’s so it can be absorbed into the adipose tissues.
What blood sugar levels correspond with:
- normal
- decreased cognition
- coma
- convulsions
- permanent brain damage
Normal- 100-70 Sx- 55-50 cognition- 45-50 Coma- 30-35 Convulsions- 20-25 Permanent brain damage- 10-15
Action of Somatostatin
- inhibits secretion of growth hormone and thyro-tropin from pituitary.
- *inhibits insulin and glucagon
- *inhibits exocrine pancreas
What is the functional unit of the exocrine pancreas?
WHat cells make up this unit?
Compromises how much of
the pancreas?
- acinus and its draining ductule make up the functional unit.
- acinar cells(digestive enzymes) and centroacinar cells( fluid and electrolyte secretion) make the functional unit.
- 80-90% of pancreatic mass.
Describe the activation of the digestive enzymes in the pancreas.
- all enzymes are inactive in the pancreas, if they were activated while still in the pancreas they would dissolve/eat the pancreas.
- Trypsinogen is activated by glycoprotein peptidase creating trypsin. Typsin then activates all of the other inactive proenzymes.
Describe secretion of pancreatic enzymes into the gut.
-Ductule cells of the pancrease are stimulated by secretin released when acidic chyme enters the small intestine, they release large volumes of water and bicarb* to make the contents of the small intestine more alkaline. This allows the pancreatic enzymes to work better, these enzymes flow through the pancreatic duct, which joins with the hepatic hepatic duct and empties into the duodenum through teh ampulla of vater surrounded by the sphincter of Oddi.
WHat hormones regulate pancreatic secretion?
- Ach: from vagal nerve–gastric and cephalic phase
- Secretin: stimulates release of water and bicarb (alkaline pH)–intestinal phase
- Cholecystokinin: duodenal and upper jejunal cells; secreted when food enters leading to increased release of enzymes
- Trypsin inhibitor: in acini prevents activation of trypsinogen(which activates other enzymes enzymes) and prevents enzymes from beign activated and digesting pancreas.
Explain the pathophysiology of pancreatitis?
pancreas may become damaged or duct blocked, the secretions back up and overwhelm typsin inhibitor and pancreatic secretions become ACTIVATED and “digest” the pancreas causing acute pancreatitis!
signs and sx of hypoglycemia
what are the two types of hypoglycemia?
Sympathoadrenal: -sweating -palpitations -tremor -nervousness -irritability -paresthesias -hunger -n/v -tachycardia** (usually first sx) Neuroglycopenic: -HA -Blurred vision -confusion -seizures -coma -fatigue -diff speaking -loss of memory -LOC
- Fasting hypoglycemia (sx of neuroglycopenia d/t decreased glucose supply to the central and peripheral nervous system)
- Postprandial hypoglycemia (d/t adrenergic response w/ abrupt decrease in glucose levels leading to increased Epinephrine release.
