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GIGU - Week 2 > 16- Endocrine Pancreas > Flashcards

16- Endocrine Pancreas Flashcards

1
Q

Endocrine cells of the pancreas secrete what hormones?

A

Insulin
Glucagon
Somatostatin

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2
Q

Endocrine cells of the pancreas have a large role in regulating lipid, CHO, and AA metabolism. These cells are arranged in clusters called…

A

Islets of Langerhans

***Innervated by adrenergic, cholinergic, and peptidergic neurons

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3
Q

These cells make up 60-65% of islets and are centrally located. They secrete insulin and C peptide.

A

Beta Cells

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4
Q

These cells make up 20% of islets and are peripherally located. They secrete glucagon.

A

Alpha Cells

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5
Q

These cells make up 5$ of islets and are interspersed between alpha and beta cells. They secrete somatostatin. Have a neuronal appearance and send ‘dendrite-like’ processes to beta cells.

A

Delta Cells

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6
Q

These cells secrete pancreatic polypeptide, which acts like a satiety signal (neuropeptide Y, peptide YY family).

A

F Cells

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7
Q

Cells of islets of Langerhans communicate with each other. Ion concentrations can change signals. _______ ______ provide rapid cell-to-cell communication between a-a, B-B, and a-B cells.

A

Gap Junctions

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8
Q

Islets receive 10% of the pancreatic blood flow, and venous blood from one cell type will bathe other cell types. Describe this path of blood flow.

A

Venous blood from Beta cells carries insulin to Alpha and Delta Cells. Blood flow is first to the center (for insulin) and flows through the periphery (on Alpha cells to inhibit glucagon release).

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9
Q

This is secreted in response to CHO and/or protein ingestion. Glucose is the major stimulatory factor of this.

A

Insulin

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10
Q

Insulin is a peptide hormone that consists of 2 chains linked by…

A

Disulfide Bridges

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11
Q

List the steps in insulin production.

A

Preproinsulin — Proinsulin — Insulin and C Peptide

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12
Q

This is a signal peptide with A and B chains with connecting peptide (C peptide). There are no disulfide bonds.

A

Preproinsulin

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13
Q

This is not a signal peptide. C peptide is still attached in Insulin and packaged into secretory granules. Proteases cleave it into Insulin and C peptide.

A

Proinsulin

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14
Q

_______ and cleaved ________ are packaged together in secretory vesicles. They are secreted in equimolar quantities into the blood.

A

Insulin

C Peptide

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15
Q

This can be used as a tool to measure function Beta cells and endogenous insulin secretion. It is typically secreted in urine.

A

C Peptide

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16
Q

Put the following steps of insulin release in order:

A. Ca2+ enters the cell

B. Glucose is phosphorylated by glucokinase

C. ATP closes the ‘inward-rectifying’ K+ channel

D. Activation of voltage-gated Ca2+ channels

E. Glucose enters cell via GLUT2

F. G6P is oxidized promoting ATP generation

G. Plasma membrane is depolarized

H. Ca2+ initiates mobilization of insulin (and C peptide) containing vesicles to plasma membrane and exocytosis

A

1) E.
2) B.
3) F.
4) C.
5) G.
6) D.
7) A.
8) H.

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17
Q

For insulin release, rises in ATP closes the ______ channels.

A

K+ (ATP-dependent K+ channels)

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18
Q

________ _________ are associated with ATP-dependent K+ channels. They detect the ATP and cause the closure of the channel, allowing membrane depolarization to occur more easily and more Ca2+ entry to occur. Used for treatment of T2DM.

A

Sulfonylurea Receptor

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19
Q

Insulin release is biphasic. The (FIRST/SECOND) phase is lost first in diabetic individuals.

A

First

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20
Q

Once insulin binds to its receptor, the insulin receptor will ___________ itself and _________ other proteins. The Insulin-receptor complex is then internalized by the target cell.

A

Autophosphorylate

Phosphorylate

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21
Q

Downregulation of the Insulin receptor occurs by ________ itself.

A

Insulin

22
Q

Insulin binds to receptor and results in phosphorylation of ________ and other proteins. These proteins activate/inactivate downstream pathways including ________ and ________ which mediate metabolic and mitogenic responses.

A

IRS (Insulin Receptor Substrate)
PI3K/AKT/mTOR
MAP kinases

23
Q

Downstream pathways also cause translocation of vesicles containing _________ to the membrane so glucose can enter the cell via facilitated diffusion.

A

GLUT4

24
Q

Activation of _______ results in GLUT4 translocation to the plasma membrane. Muscle contractions stimulate this process. This is why blood sugar drops during exercise.

A

AMPK (AMP-kinase)

25
Q

ACh, CCK, and GLP-1 (INHIBIT/ACTIVATE) insulin release, while Somatostatin and Glucagon (INHIBIT/ACTIVATE) insulin release.

A

Activate

Inhibit

26
Q

This is a single straight-chain polypeptide with 29 AAs. It’s a member of the same peptide family as secretin and GIP, and it stored in dense granules of Alpha cells.

A

Glucagon

27
Q

Glucagon is initially synthesized as…

A

Preproglucagon

28
Q

Glucagon is stimulated by…

A

Decreased blood sugar

29
Q

T/F. Blood glucose reflects balance between hypoglycemic actions of insulin and hyperglycemic actions of anti-insulin hormones.

A

True

30
Q

Insulin inhibits _________ production and secretion. Other inhibitor factors include Somatostatin, FAs, and ketoacids.

A

Glucagon

31
Q

Glucagon increases blood glucose, so substrates are directed toward glucose formation. What are some of its actions on the liver?

A

Increases Gluconeogenesis
Increased Glycogenolysis
Inhibits Glycogenesis

***Remember, Insulin decreases blood glucose so its effects would be opposite of these!

32
Q

Glucagon stimulate ________ in both adipose tissue and skeletal muscle. Ketoacids are produced from the FAs.

A

Lipolysis

33
Q

What are the “3 P’s” of diabetes?

A

Polyuria
Polydipsia
Polyphagia

34
Q

Look at slide 28, be able to describe what’s going on!

A

Review 5 minutes

35
Q

This type of diabetes mellitus, formerly known as juvenile onset diabetes, is due to inadequate insulin secretion.

A

Type 1 DM

36
Q

T1DM occurs from the destruction of _______ _______. Symptoms do not become evident until > 80% of these are destroyed.

A

Beta Cells

37
Q

T1DM results in increased blood glucose, ketoacids, amino acids, and increased conversion of FAs to ketoacids. Decreased utilization of these ketoacids results in ________ ________.

A

Diabetic Ketoacidosis (DKA)

38
Q

T1DM causes __________, which is a shift of K+ out of cells, resulting in a low intracellular concentration. This is due to a lack of insulin effect on Na+/K+ ATPase.

A

Hyperkalemia

39
Q

In T1DM, plasma K+ levels may be normal, but total K+ is usually low due to…

A

Polyuria and dehydration

40
Q

In T1DM, increased blood glucose increases filtered load of glucose, which exceeds the reabsorptive capacity of the proximal tubule. Water and electrolyte reabsorption is also blunted. This causes polyuria, which increases excretion of ______ and ______ even though urine concentration of electrolytes is low. Also results in thirst (polydipsia) due to volume loss.

A

Na+

K+

41
Q

Treatment for T1DM is _________ replacement, but it has its drawbacks (see slide 32).

A

Insulin

42
Q

A big advance in T1DM treatment is transplantation. _______ ________ ________ cells showed glucose-induced insulin release performance comparable to that of Beta cell lines and human islets. Worked in T1D mice.

A

Beta-cell Mimetic Designer Cells (HEK-ß)

43
Q

This type of diabetes develops due to insulin resistance. It is the progressive exhaustion of active Beta-cells due to environmental factors (amongst others). Includes sedentary lifestyle, malnutrition, or obesity. Patients produce insulin, but often need to produce more and more.

A

Type 2 DM (T2DM)

***95% of diabetes cases!

44
Q

T2DM results in reactive hyperinsulinemia. Obesity-induced insulin resistance causes decreased ________ uptake of glucose in response to insulin (classical skeletal muscle impairment).

A

GLUT4

45
Q

T2DM also has decreased ability of insulin to repress hepatic ________ production (may be earliest response), as well as the inability of insulin to repress adipose tissue uptake (via LPL) and ________ (via HSL).

A

Glucose
Lipolysis

***Glucose is high in the blood because insulin isn’t working for it to uptake. Also, because insulin isn’t working then glucagon acts to increase glucose even more.

46
Q

In non-obese patients, T2DM can occur due to decreased insulin release by the _________ independent of peripheral insulin resistance. However, both can and often do occur.

A

Pancreas

47
Q

These are intestine derived hormones, like GLP-1 and GIP. They have a short half-life and are secreted in response to GI glucose and fat.

A

Incretins

48
Q

Incretin hormones (GLP-1, GIP) stimulate ________ secretion (glucose dependent) and inhibit ________ secretion. They also aid in slow gastric emptying.

A

Insulin

Glucagon

49
Q

T2DM patients have a (NORMAL/REDUCED) incretin hormone effect.

A

Reduced

50
Q

What are some treatments for T2DM?

A
    • Caloric restriction, weight reduction, exercise
    • Insulin secretagogues
    • Slow absorption of CHO
    • Insulin sensitizers
    • Bariatric surgery
51
Q

What are common conditions associated with T1DM?

A

Autoimmune Thyroid Disease
Celiac Disease
Addison’s Disease

52
Q

What are common conditions associated with T2DM?

A

Obesity
Lipid Abnormalities
PCOS
NAFLD

GIGU - Week 2 (10 decks)

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