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Endo/Repro I Exam 1 > Lecture 7: Endocrine Pancreas > Flashcards

Lecture 7: Endocrine Pancreas Flashcards

1
Q

What cells are found in the Islets of Langerhans; where are they located and what do they secrete?

A

β cells: secrete insulin and C-peptide; located in central core

α cells: secrete glucagon; located near the periphery

D cells: secrete somatostatin, interspersed between α and β cells

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2
Q

How do the cells of the islets of Langerhans communicate w/ eachother?

A

Gap junctions:

  • Rapid cell-to-cell communication
  • β-β; α-α; and α-β
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3
Q

What is the blood supply like to the Islets of Langerhans; how does this relate to the paracrine mechanism of the hormones within the endocrine pancreas?

A
  • Receive 10% of the total pancreatic blood flow
  • Venous blood from one cells type bathes the other cells types
  • Venous blood from the β carries insulin to the α and D cells
  • Blood flows first to center (for insulin), then:
  • Flows through periphery acting on α-cells inhibiting glucagon release.
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4
Q

What is the main stimulatory factor for insulin secretion?

A

Glucose

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5
Q

What are the components of preproinsulin vs. proinsulin vs. insulin?

A

Preproinsulin: signal peptide, A and B chains and C peptide

Proinsulin: no signal peptide, C peptide still attached

Insulin: is packaged w/ C peptide, but only consists of the A and B chains whilst inside secretory vesicles

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6
Q

Why is C peptide significant?

A
  • Is released in equimolar amounts into the blood w/ insulin and excreted unchanged in urine
  • Can be used as a long-term marker of endogenous insulin secretion, specifically endogenous B cell function
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7
Q

What are Sulfonylurea drugs (i.e., tolbutamide, glyburide) and what are they used for?

A

Promote the closing of the ATP-dependent K+ (inward-rectifier K+ channel); increasing insulin secretion; used in the treatment of Type II DM

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8
Q

Describe the 6 steps upon glucose binding pancreatic B-cell to insulin release

A

1) Glucose enters cell via GLUT-2
2) Phosphorylated by Glucokinase
3) G-6-P is oxidized promoting ATP generation
4) ATP closes the ‘inward-rectifying’ K+ channel; membrane depolarization
5) Activation of voltage-gated Ca2+ channels; Ca2+ enters cell
6) Vesicles of insulin mobilized to plasma membran and exocytosis

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9
Q

What is the proportionality of insulin secretion in relation to blood glucose?

A

Insulin secretion is basically proportional to plasma glucose changes

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10
Q

What does biphasic secretion of insulin refer to; which phase is lost first in diabetic patients?

A

First phase: rapid and transient release

Second phase: delayed/longer chronic phase of release

*First phase is the first thing to dissapear in diabetic individuals*

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11
Q

What are the other modulators of insulin secretion?

A
  • GI peptides, glucagon, somatostatin, and ACh
  • Different intracellular pathways
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12
Q

How is GLUT-4 translocated to the plasma membrane; what else stimulates this process and why is this significant?

A
  • Activation of AMP-kinase (AMPK) upon insulin binding its receptor
  • Muscle contractions stimulate this process, highlighting the importance of exercise in the management of insulin resistance and/or diabetes
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13
Q

How is glucose taken up by peripheal cells?

A

Facilitated diffusion

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14
Q

Insulin is important for glucose uptake into what tissues?

A

Adipose tissue, resting skeletal muscle, and liver

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15
Q

What are the major effects of insulin on skeleal muscle?

A
  • Increased glucose uptake and GLUT 4 transporter
  • Activates glycogen synthase = increased glycogen synthesis
  • Increased glycolysis and CHO oxidation (hexokinase, PFK, PDH)
  • Increased protein synthesis and decreased breakdown
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16
Q

What are the major effects of insulin on the liver?

A
  • Promotes glycogen synthesis (glucokinase and glycogen synthase)
  • Increased glycolysis and CHO oxidation
  • Decreases gluconeogenesis
  • Increases hexose monophosphate shunt
  • Increase pyruvate oxidation
  • Increase lipid storage and decrease lipid oxidation
  • Increase protein synthesis and decrease breakdown
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17
Q

What are insulins actions on Adipose Tissue?

A
  • Increases glucose uptake (GLUT 4 trasnlocation)
  • Increases glycolysis (increased production of α-glycerol phosphate for esterification and lipogenesis)
  • Decreased lipolysis (inhibits HSL)
  • Promotes uptake of FA’s (LPL activity/synthesis), favoring the formation of TAG’s
18
Q

What is the effect of insulin on the blood levels of K+, glucose, FA’s, ketoacids, and AA’s?

A

Decreases them all!

19
Q

What is one of the common treatments for hyperkalemia?

A

The administration of some insulin w/ small amount of glucose.

20
Q

What are some of the stimulatory factors for the secretion of insulin?

A
  • Increased [Glucose]
  • Increased [AA]
  • Increased [FA] and [Ketoacid]
  • Glucagon
  • GIP (glucose-dependent insulinotropic peptide)
  • Vagal stimulation; ACh
  • K+
  • Sulfonylurea rugs
  • Obesity
21
Q

What are some of the inhibitory factors for the secretion of insulin?

A
  • Decreased blood glucose
  • Fasting
  • Exercise
  • Somatostatin
  • α-adrenergic agonists
  • Diazoxide (K+ channel activator)
22
Q

How is the signal for insulin shut down?

A

Lysosomes will internalize the receptor from the plasma membrane, shutting down the signal

23
Q

What is Type I DM; symptoms seen when and what metabolic problems occur?

A
  • Inadequate insulin secretion
  • Destruction of β cell, often the result of autoimmune disease
  • Symptoms do not become evident until > 80% of β cells are destroyed
  • Increased blood glucose, fatty acids, ketoacids, amino acids, increased conversion of fatty acids to ketoacids
  • Results in diabetic ketoacidosis (DKA): metabolic acidosis
24
Q

How does hyperkalemia develop in Type I DM patients; what are the total body K+ levels like?

A
  • Shift of K+ out of the cell
  • Intracellular concentration is low
  • Lack of insulin effect on Na+/K+ ATPase
  • Even though plasma levels may be able normal, total body K+ is usually below normal due to the polyuria and dehydration
25
Q

How does Osmotic diuresis result from Type I DM?

A
  • Increased blood [glucose] results in increased filtered load of glucose, exceeding reabsorptive capacity of the proximal tubule
  • Water and electrolyte reabsorption is also prevented
  • Polyuria: increases excretion of Na+ and K+ even though urine concentration of electrolytes is low
  • Thirst (polydipsia)
26
Q

What is the goal w/ insulin replacement treatment for Type I DM?

A

To recreat normal physiology (basal and bolus insulin)

27
Q

What is Type 2 DM

A
  • Insulin resistance
  • Progressive exhaustion of β-cells due to enviornmental factors, including a sedentary lifestyle, malnutrition, or obestiy
  • Patients ARE able to make insulin, but NOT enough to overcome insulin resistance
28
Q

What is the progression of insulin resistance seen in Type II DM?

A

Reactive hyperinsulinemia (at first) followed by relative hypoinsulinemia as β-cells begin to fail

29
Q

What are 3 causes of obestity-induced insulin resistance?

A
  • Decreased GLUT-4 uptake of glucose in response to insulin
  • Decreased ability of insulin to repress hepatic glucose production
  • Inability of insulin to repress adipose tissue FA uptake (via LPL) and lipolysis (via HSL)
30
Q

What are some more of the pathophysiologies seen w/ Type II DM; is ketoacidosis an issue?

A
  • Post-receptor signaling, which ultimately results in decrease of glucose transportr number
  • Increased hepatic glucose production
  • Hyperglucagonemia
  • NOT as prone to ketoacidosis as type I, but may still occur
  • In non-obese pt’s, Type II DM can occur due to decreases in insulin release by the pancreas; varying degrees of insulin resistance can also occur
31
Q

What are some of the contributing factors to activation of stress kinases and disruption of insulin signaling?

A
  • Fatty acyl carnitines
  • Ceramides
  • DAGs

*Intermediates produced by mitochondrial overload that activate pathways which inhibit insulin signaling

32
Q

What are some of the TX for Type II DM?

A
  • Caloric restriction, exercise, weight reduction
  • Insulin secretagogues
  • Slow absorption of CHO’s
  • Insulin sensitizers (i.e., Metformin)
  • Bariatric surgery good option for BMI >40/obese pre-diabetic
33
Q

What is the incretin effect?

A
  • You get a much more robust insulin response when intaking glucose orally vs. an IV injection of glucose
  • Due to the potent incretin hormones GLP-1 and GIP
34
Q

What are the incretin hormones; secreted when; half-life; and function?

A
  • Intestine derived hormones: GLP-1 and GIP
  • Short half-life
  • Secreted in response to GI glucose and fat
  • Stimulate insulin secretion (glucose dependent)
  • Inhibit glucagon secretion
  • Slow gastric emptying
35
Q

What type of receptor do the incretin hormones act on and what are the downstream signaling molecules?

A

GPCR; Gs pathway —> increased adenylyl cyclase —> increased cAMP—–> Increased PKA —-> insulin secretion

36
Q

What happens to the incretin effect in Type II DM?

A
  • Reduced Incretin effect
37
Q

What are some of the associated conditions commonly seen w/ Type I DM?

A
  • Autoimmune thyroid disease
  • Celiac Disease
  • Addison’s disease
38
Q

Glucagon is a member of a family of peptide that includes what other hormones?

A

Secretin and GIP

39
Q

What is the major stimulatory factor of glucagon secretion and what are some other sitmulatory factors?

A

Major = decreased blood [glucose]

Other:

  • Increased AA’s (arginine and alanine)
  • Fasting
  • CCK
  • β-adrenergic agonists
  • ACh
40
Q

What inhibits glucagon?

A
  • Insulin inhibits the synthesis and secretin of glucagon
  • Somatostatin
  • Increased [FA] and [Ketoacid]
41
Q

What are the major actions of glucagon on the liver?

A
  • Increases blood [glucose]
  • Increased glycogenolysis and inhibits glycogen formation
  • Increased gluconeogenesis by decreasing the production of fructose-2,6-bisphosphate
  • Substrates are directed toward glucose formation
42
Q

What are the effects of glucagon on adipose tissue?

A
  • Increases lipolysis and inhibits FA synthesis, which shunts substrates towards gluconeogenesis
  • Ketoacids are produced from FA’s, but not to the extent of a diabetic

Endo/Repro I Exam 1 (12 decks)

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