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Endocrine > Endocrine Pancreas > Flashcards

Endocrine Pancreas Flashcards

1
Q

what Hs do endocrine cells of the pancreas secrete?

A

insulin, glucagon, somatostatin

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2
Q

major fcns of the endocrine pancreas

A

regulate glucose, fatty acid, and AA metabolism

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3
Q

endocrine cells arrangement and innervation

A
  • arranged in clusters which are islets of Langerhans

- innervated by adrenergic, cholinergic, and peptidergic neurons

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4
Q

beta cells

A
  • 60-65% of islet
  • secrete insulin and peptide C
  • tend to be located in central core
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5
Q

alpha cells

A
  1. ~20% of the islet
  2. secrete glucagon
  3. tend to be located near the periphery of the islet
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6
Q

delta cells

A
  1. ~5% of the islet
  2. secrete somatostatin
  3. interspersed b/w alpha and beta cells
  4. neuronal appearance, send dendrite like processes to beta cells
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7
Q

how do cells of islets of langerhans communicate?

A

i. gap junctions:

1. permit rapid cell to cell communication (alpha-alpha, alpha-beta, beta-beta)

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8
Q

blood supply to the islets of Langerhans

A
  1. islets receive around 10% of the total pancreatic blood flow
  2. venous blood from one cell type bathe the other cell types
  3. venous blood from the beta cells carries insulin to the alpha and delta cells
    a. blood flows first to capillaries in the center of the islet and picks up insulin
    b. then, blood flows to the periphery of the islets, where it acts on alpha cells to inhibit glucagon secretion
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9
Q

paracrine mechanisms of Hs in the endocrine pancreas

A

i. delta cells’ Hs act on alpha cells and beta cells
ii. alpha cells’ Hs act on beta cells
iii. beta cells’ Hs act on alpha cells

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10
Q

why is insulin secreted?

A
  1. secreted in response to carbohydrate and/or protein containing meal
    a. glucose, AAs, FFA act on the pancreatic islets/beta cells to release insulin to the target cells
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11
Q

synthesis and secretion of insulin

A

a. preproinsulinproinsulininsulin
i. preproinsulin—4 peptides: signal peptide, A abd B chains of insulin, and connecting C peptide
ii. proinsulin
1. no signal peptide
2. C peptide still attach to insulin, disulfide bridges form in the ER
3. packed in secretory vesicles in the golgi
4. during packaging, proteases cleaved proinsulin
iii. insulin and cleaved C peptide are packed together in secretory vesicles
1. secreted in equimolar quanities into the blood

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12
Q

what is C peptide used for

A
  1. C peptide is used to test beta cell function in type 1 diabetes mellitus patients receiving insulin injections
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13
Q

transport of glucose into the beta cell

A

beta cell membrane contains GLUT2 that moves glucose from the blood into the cell by facilitated diffusion (1)

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14
Q

metabolism of glucose inside the beta cell

A

i. Once inside the cell, glucose is phosphorylated to glucose 6 phosphate by glucokinase (2) and glucose 6 phosphate is subsequently oxidized (3)
1. ATP—one of the products of the oxidation step is a key factor that regulates insulin secretion, b/c when inc ATP, K channels close

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15
Q

ATP, K channels, and C VG cells

A

a. ATP closes ATP sensitive K channels
i. K channels in the beta cell membrane are regulated by changes in ATP levels
ii. When ATP levels inside the beta cell increase, the K channel close (4), which depolarizes the beta cell membrane (5)
b. Depolarization opens voltage sensitive Ca channels
i. Ca channels, also in the beta cell membrane, are regulated by changes in voltage
1. They are opened by depolarization and closed by hyperpolarization.
2. The depolarization caused by ATP opens these Ca channels (6)
3. Ca flows into the beta cell down its electrochemical gradient and the intracellular Ca conc increases (7)
c. Increased intracellular Ca causes insulin secretion
i. Increases in intracellular Ca concentration cause exocytosis of the insulin containing secretory granules (8).
ii. Insulin is secreted into pancreatic venous blood and then delivered to the systemic circulation
iii. C peptide is secreted in equimolar amounts with insulin and is excreted unchanged in the urine
iv. Therefore, the excretion rate of C peptide can be used to assess and monitor endogenous beta cell function

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16
Q

sulfonylurea drugs

A

i. promotes the closing of ATP dependent Kinc insulin secretion
1. Used in the treatment of type II diabetes mellituis

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17
Q

biphasic manner of insulin secretion

A

a. When glucose is released into the bloodstream, in the first 10-15 min, there is an immediate upstroke in the plasma insulin—phase 1
b. Insulin then decreases rapidly from 10-20 min
c. Insulin then slowly increases over the next 2 hours—phase 2

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18
Q

CCK

A

i. Bind to a R to activate Gq which facilitates the activation of PLC
ii. PLC goes on to release IP3 and DAG
1. DAG binds to PKC and activates the secretion of insulin
2. IP3 acts on the ER and Ca-calmodulin to inc Ca and stimulate insulin secretion

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19
Q

somatostatin

A

i. Binds to Gi and inhibits adenylyl cyclase

20
Q

glucagon

A

i. Binds to Gs and stimulates adenylyl cyclase

ii. Activates ATP to cAMP which activates PKA and causes the release of insulin

21
Q

insulin and insulin R

A

a. When occupied by insulin, insulin R phosphorylates itself and other proteins
i. Phosphorylation either activates or inhibits these proteins to produce the metabolic actions of insulin
b. Insulin R complex is internalized by its target cell
c. Insulin down regulates its own receptor

22
Q

insulin secretion and clearance

A

a. Insulin release from the pancreas oscillates with a period of 3-6 min changing from generating a blood insulin concentration more than 800 pmol/L to less than 100

23
Q

MOA of insulin

A

a. Action of insulin on target cells begins when the H binds to the R in the cell membrane which is a R composed of 2 alpha and 2 beta subunits
i. they have intrinsic tyrosine kinase activity
b. insulin acts on target cells by the following steps:
i. insulin binds to the alpha subunits of the R and induces conformational change in the R
1. the conformational change activates the tyrosine kinase activity of the Beta subunits which phosphorylate themselves in the presence of ATP
ii. activated tyrosine kinase phosphorylates other proteins or enzymes that are involved in the actions of insulin
1. phosphorylation either inhibits or stimulates these proteins to produce the actions of insulin
c. insulin R complex is internalized by its target cell in endocytosis
i. either degraded by intracellular proteases, stored, or recycled to be reused
ii. insulin downregulates its own receptor by dec the rate of synthesis and inc the rate of degradation of the R

24
Q

peripheral uptake of glucose

A

a. glucose is taken up by peripheral cells by facilitated diffusion
b. insulin facilitates the uptake in some tissues
i. insertion of glucose transporters in the membrane (GLUT4)
ii. adipose tissue, resting skeletal muscle, and liver requires insulin for effective glucose uptake

25
Q

action of insulin on muscle

A

a. inc glucose uptakeinc GLUT4 transporter
b. inc glycogen synthesisinc hexokinase (in liver and beta cells is glucokinase)
i. activates glycogen synthase
c. inc glycolysis and carbohydrate oxidation
i. causes increased hexokinase, phosphofructokinase, and pyruvate dehydrogenase
d. dec gluconeogenesis
e. inc protein synthesis and dec protein breakdown

26
Q

insulin effects on triglyceride and fatty acid metabolism in adipose tissue

A

a. overall effect of insulin on fat metabolism is to inhibit the mobilization and oxidation of fatty acids, and, simultaneously, to increase the storage of fatty acids
i. as a result, insulin decreases the circulating levels of fatty acids and ketoacids.
b. In adipose tissue, insulin stimulates fat deposition and inhibits lipolysis
c. Insulin also inhibits ketoacid formation in the liver b/c decreased fatty acid degradation means that less acetyl coenzyme A substrate will be available for the formation of ketoacids

27
Q

how does insulin affect amino acid concentration?

A
  1. Insulin decreases blood AA concentration
    a. Overall effect of insulin on protein metabolism is anabolic
    b. Insulin increases AA and protein uptake by tissuesdecreases blood levels of AAs
    c. Insulin stimulates AA uptake into target cells (muscle), increases protein synthesis, and inhibits protein degradation
28
Q

insulin actions in the liver

A

i. GLUT 2 transportersinc glucokinase
ii. Inc glycogen synthesis
iii. Dec glucose release (by dec gluconeogenesis)dec glucose 6 phosphatase
iv. Inc glycolysisinc acetyl CoA and inc FA synthesis
v. Inc triglyceride storage and export
vi. Inc protein synthesis and dec protein degradation

29
Q

insulin action in adipose tissue

A

i. Inc GLUT4 transporters
ii. Inc glycolysisinc alpha glycerol phosphate, inc acetyl CoA, inc FA synthesis
iii. Inc triglyceridesdec H sensitive lipase (HPL)—dec lipolysis, inc lipoprotein lipase (LPL)—inc uptake

30
Q

insulin action on muscle

A

i. Inc GLUT4 transporters
ii. Inc glycogen synthesis
iii. Inc glycolysis
iv. Inc protein synthesis, dec protein degradation
v. Inc triglycerides (FA’s from circulation)

31
Q

stimulatory factors affecting insulin secretion

A
  • inc glucose conc
  • inc AA conc
  • inc FA and ketoacid conc
  • glucagon
  • cortisol
  • glucose dependent insulinotropic peptide (GIP)
  • vagal stimualtion, ACh
  • K+
  • sulfonylurea drugs
  • obesity
32
Q

inhibitory factors on insulin secretion

A
  • dec blood glucose
  • fasting
  • exercise
  • somatostatin
  • alpha adrenergic agonists
  • diazoxide
33
Q

type 1 diabetes mellitus

A
  • inadequate insulin secretion
  • onset early in childhood
  • autoimmune disease due to destruction of beta cells
  • Symptoms do not become evident until 80% of the beta cells are destroyed
34
Q

symptoms of T1D

A
  1. Inc blood glucose
    a. Dec uptake of glucose
    b. Dec glucose utilization
    c. Inc gluconeogenesis
  2. Inc blood FA and ketoacid
    a. Dec FA synthesis
    b. Dec triglyceride synthesis
    c. Inc triglyceride breakdown
    d. Inc level of circulating free FA
    e. Inc conversion of FA to ketoacids and dec ketoacid utilization by tissues
    i. Results in diabetic ketoacidosis—metabolic acidosis
  3. Inc AA concentration
    a. Inc protein breakdown
    b. Dec protein synthesis
    c. Inc catabolism of AA
    i. Loss of lean body mass
    d. Inc ureagenesis
  4. Osmotic diuresis
    a. Inc blood glucose concentration results in inc filtered load of glucose, exceeding reabsorptive capacity of the PCT
    b. Water and electrolyte reabsorption is also prevented
    c. Polyuria: inc excretion of Na and K even though urine conc of electrolytes is low
    d. Thirst
  5. Hyperkalemia—shift of K out of cell
    a. Intracellular conc is low
    b. Lack of insulin effect on Na/K ATP pump
    c. Even though plasma levels may be above normal, total body K is usually below normal due to the polyuria and dehydration
35
Q

treatment of T1D

A

a. Insulin replacement—objective is to recreate normal physiology (basal and bolus insulin)
b. Drawbacks of insulin replacement therapy
i. Painful and time consuming
ii. Lab b/w glucose measurement and insulin dosing
iii. Delayed absorption of insulin following subcutaneous injection
iv. Poor blood glucose control—periods of hyperglycemia

36
Q

type 2 diabetes mellitus

A
  1. Vast majority of diabetics are type II
  2. Patients able to make insulin, but not enough to overcome insulin resistance
  3. Normal or elevated insulin concentration initially and relative insulin deficiency
  4. prevalence in middle aged or older
37
Q

obesity and T2D

A
  1. Often associated with obesity
    a. Reactive hyperinsulinemia followed by relative hypoinsulinemia
    b. 3 causes for obesity induced insulin resistance:
    i. dec GLUT4 uptake of glucose in response to insulin release
    ii. dec ability of insulin to repress hepatic glucose production
    iii. inability of insulin to repress H sensitive lipase (HSL) or increase lipoprotein lipase (LPL) in adipose tissue
38
Q

what causes insulin resistance?

A
  1. insulin resistance mechanisms not well understood
    a. might be due to post-receptor signaling, which ultimately results in dec of glucose transporter number
    i. dec plasma glucose; plasma insulin can inc receptor sensitivity toward normal
39
Q

why do non-obese patients develop T2D?

A
  1. in non-obese patients, T2D can occur due to dec in insulin release by the pancreas, varying degrees of insulin resistance can also occur
40
Q

signs of T2D

A
  1. inc hepatic glucose production
  2. hyperglucagonemia
  3. not as prone to ketoacidosis as type I
    a. presence of some insulin secretion appears to protect from the development of ketoacidosis
41
Q

treatment of T2D

A

a. caloric restriction and weight reduction
b. insulin secretagogues
i. sulfonylurea drugs
ii. incretin analog of GLP1 (exenatide)—injection needed
c. slow absorption of carbs
i. alpha glucosidase inhibitors—acarbose, miglitol
ii. amylin analogs—pramlintide
d. insulin sensitizers
i. biguanide drugs—metformin—upregulates insulin Rs on target tissues

42
Q

plasma glucose concentration reflects the balance b/w the hypoglycemic action of insulin and the hyperglycemic action of the anti-insulin Hs

A

a. insulin inhibits the the synthesis and secretion of glucagon
b. other inhibitory factors:
i. somatostatin
ii. inc FA and ketoacid concentration

43
Q

glucagon

A
  1. single straight chain polypeptide
  2. member of a family of peptide that includes the GI Hs secretin and GIP
  3. synthesized as preproglucagon
  4. stored in dense granules until alpha cells are stimulated
44
Q

stimulatory factors of glucagon

A
  1. the major stimulatory factor of glucagon secretion is decrease blood glucose concentration
    a. inc AA (arginine and alanine) also stimulate glucagon secretion
    b. other stimulatory factors:
    i. fasting
    ii. CCK
    iii. Beta adrenergic agonists
    iv. ACh
45
Q

major actions of glucagon

A
  • work on the liver
    a. Glucagon increases blood glucose concentration
    i. Inc glucogenolysis and inhibits glycogen formation from glucose
    ii. Inc gluconeogenesis by dec the production of fructose 2,6 phosphate which dec phosphofructokinase activity
    iii. Substrates are directed towards glucose formation
    b. Increase blood fatty acid and ketoacid concentration
    i. Glucagon increases lipolysis and inhibits FA synthesis which shunts substrates toward gluconeogenesis
    ii. Ketoacids are produced from FAs
46
Q

diabetes mellitus type II

A

a. insulin resistance
i. In insulin resistance, the ability of insulin to suppress lipolysis in adipose tissue and glucagon secretion by alpha cells in the islet results in increase of gluconeogenesis

47
Q

incretin Hs

A
  1. Intestine derived Hs
    a. GLP1, GIP
    b. Short T1/2
    c. Secreted in response to GI glucose and fat
  2. Simulate insulin secretion—glucose dependent
  3. Inhibit glucagon secretion
  4. Slow gastric emptying

Endocrine (15 decks)

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