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BIOCHEMISTRY > EXAM3_L28_Insulin_Glucagon > Flashcards

EXAM3_L28_Insulin_Glucagon Flashcards

1
Q

What is diabetes fasting glucose levels?

A

> 126mg/dL

7mmol/L

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2
Q

1 hour postprandial Normal blood glucose

A

up to 145 mg/dL

8mmol/L

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3
Q

Normal Fasting blood glucose?

A

70-110mg/dL

3.9-6.1mmol/L

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4
Q

Symptomatic Hypoglycemia

A
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5
Q

What are the responsibilities of the Pancreas?

What 3 cell types of the pancreas?

A 
DIGESTION
GLUCOSE HOMEOSTASIS (insulin/glucagon)

Exocrine, Endocrine, ductal cell types

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6
Q

What 4 cell types in the islets of langerhans of the endocrine pancreas?

A
  1. Alpha- glucagon (15-20%)
  2. Beta- INSULIN (60-80%)
  3. Gamma- Somatostatin (5-10%)
  4. PP-cells - Pancreatic polypeptide (15-20%)
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7
Q

3 beta cell functions

A

synthesize, store, regulate INSULIN

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8
Q

Synthesis of Insulin
Describe the 6 steps of how its made
from transcription->prepro>pro>insulin + c pep

Where it happens and what is modified

A

1st. Beta cell gene for insulin is transcribed into mRNA in the nucleus
2. mRNA code for insulin is transported to RER in Cytosol
3. N-terminal signal penetrates RER and insulin is made/injected into the lumen of RER as pre-pro-insulin
4. Pre-pro-insulin is cleaved and now Pro-insulin
5. Pro-insulin is transported to the golgi where it is cleaved and forms Insulin and C-Peptide
6. Insulin and C peptide are secreted in secretory vessicles via exocytosis

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9
Q

What does PDI & Chaperone do? (Protein Disulfide Isomerase)

A

Helps correct folding of pro-insulin and forms the disulfide bonds in the RER

so that it can be transported to the Cis golgi for cleavage into insulin and Cpeptide

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10
Q

Where is 3 places glucagon made?

A

Alpha cells of the endocrine pancreas (outside perimeter)

AND

L-Cells of Intestines

(some in brain too)

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11
Q

What are incretins? Where are they synthesized?

A

GI hormones released in response to meal w/ carbs

Insulin-secretion-stimulating agents

made during the post-translational processing of
pro-glucagon

(when it is made by intestinal L-Cells)

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12
Q

What is GLP-1?

Where does it come from?

A

GLP1 is created during post-translational processing of the glucagon from LCELLS.

L-Cells secrete glucagon in the small intestines (colon-ilium)
undergo post-processing and incretins are made as a result.

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13
Q

What does GLP-1 do?

A

LOWERS BLOOD GLUCOSE LEVELS by:

Stimulating insulin and inhibiting Glucagon release

Increases the IG ratio

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14
Q

What is GLP-1 degraded by? how fast?

A

-GLP1 degraded by DPP-4 (dipeptidyl peptidase-4) within minutes

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15
Q

What is responsible for increasing the IG ratio after a carbohydrate rich meal?

A

INCRETIN GLP1 released by the L-cells of the small intestines (colon and ilium) minutes after eating a meal

prepares the pancreas for the nutrient load to enter the blood

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16
Q

What type of drugs are used to treat diabetes mellitus?

A

Incretin mimetic drugs:

EXENATIDE (Byetta)- GLP-1 mimetic, resists degradation by DPP-4 w/ long half life (12 hours).

Mimetic drugs resemble incretins- which are decreased in diabetes mellitus patients

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17
Q

What is Exenatide (Byetta)?

A

GLP-1 Incretin mimetic drug used to treat diabetes mellitus

-long half-life (12 hours) by resisting degradation by DPP-4

18
Q

What are secretagogues?

A

Insulin is stored in secretory granules and secretagogues initiate release of insulin upon being signaled

19
Q

What does Glucokinase do?

A

Converts Glucose to G6P inside the cell.

Once G6p, glucose is STUCK inside the cell

20
Q

Describe how beta cells Detect blood glucose

A

Increased [Glucose] > increased ATP/ADP ratio
ATP inhibits (atp sensitive K channel) > DEPOLARIZATION
depolarization> CamKinase2 > Exocytosis of INSULIN

21
Q

What is Sulfonylurea? What does it target?

Overall Function?

A

Sulfonylurea is a secretagogue of insulin release
Targets the atp-sensitive K+ channel

LOWERS BLOOD GLUCOSE LEVELS

(risk of hypoglycemia b/c they act independent of existing blood glucose levels)

22
Q

Type II diabetes (mellitus) can be treated with what drug that acts on atp-sensitive K+ Channels?

A

Sulfonylurea

blocks K+ channel causing a depolarization and release of insulin (independent of current blood glucose levels)

23
Q

What is the first pass effect?

A

Blood pancreas to portal vein into liver (50-60% IG) metabolized before hitting systemic circulation.

24
Q

how long is half life of IG?

Why?

A

3-5 minutes

50-60% metabolized in liver (first pass effect)
Kidney degrades 1/2 of systemic IG
Proteases destroy IG in systemic circulation

25
Q

If IG has such a short half-life, its unreliable to use as a determining factor of diabetes. What Should you measure to determine levels of Beta-cell activity?

A

C-Peptide (secreted 1:1 ratio w/ insulin)

  • not degraded by liver or other organs
  • HL ~30 min
26
Q

What REGULATES Insulin release?

looking for 1 major and 3 minor regulators

A

GLUCOSE! (almost entirely regulated by glucose)

  • Epinephrine (stress hormone)- Inhibits Insulin Release
  • incretins help release insulin (GLP1)
  • AA’s stimulate insulin in absence of glucose
27
Q

What is a counter-regulatory hormone?

What 4 are the counter-regulatory hormones ?

A

Hormones that oppose the action of insulin on glucose:

Glucagon, Epinephrine, Cortisol, growth hormone

28
Q

How does epinephrine affect Pancreatic Beta Cells?

A
  • promotes fuel mobilization during stress, exercise, and fasting)

Epinephrine (stress hormone) DECREASES/Inhibits INSULIN

29
Q

How does epinephrine affect Pancreatic Alpha Cells?

A

Alpha cells produce GLUCAGON (increase blood glucose)

Epinephrine (stress hormone) INCREASES Glucagon and blood glucose

30
Q

How do Dietary amino acids affect alpha and beta pancreatic cells?

A

CAN INCREASE BOTH insulin and glucagon secretion… ?

Why?

If there is no carbs in the diet, (PROTEIN ONLY DIET- ATKINs) - we use AA’s to make glucose

31
Q

Glucose uptake is insulin-dependent in many tissues of the body (brain, RBC, intestine, cornea, kidney, liver)

What tissues REQUIRE Insulin/Glucagon for glucose uptake?
What transporter expressed on these cells?

A

MUSCLE & ADIPOSE

Insulin-dependent GLUT-4 TRANSPORTER

32
Q

Muscle and Adipose are unique in that they require Glucose transporters to take up glucose.

Describe what signals initiate what transporters to get glucose into the cell.

A
  1. Insulin stimulates endosome to release GLUT4 transporter
  2. GLUT4 fuses with cell membrane of muscle/adipose and glucose is taken into the cell
  3. GLUT4 reabsorbed into endosome when insulin levels fall
33
Q

General Fed state (charging mode)

A

High IG
Fuel storage (make TAGs, glycogen, proteins)
Use Glucose as energy source
Glucose uptake (GLUT4)

34
Q

General Fasting State (battery mode)

A
  • Low IG
  • Battery Power (TAGs, Glycogen, Proteins)
  • Use FA’s and Ketone Bodies for energy (except RBC and Brain- Always use glucose)
  • Glucose synthesis in liver for export (for brain & RBC)
35
Q

Where does Lipolysis Take Place?

Where does Beta Oxidation take Place?

A

ADIPOSE TISSUE_ NOT THE LIVER!!!!

Beta oxidation takes place in the liver

36
Q

How much glucose does the brain require per day?

How much required for total body per day?

A

Brain requires 130grams glucose/ day
Total body requires 180grams glucose /day

72% of total required glucose is used by the BRAIN!!!

37
Q

If we eat atkins Protein only Diet

where does glucose come from?

A

Low IG ratio:
small insulin release prevents muscle protein degradation, but not the rest of fasting responses

Synthesize glucose from scratch but uses dietary AA’s

38
Q

LONG TERM FASTING

A

Muscles degrade to make glucose from scratch

39
Q

What type of cell does glp1 work on?

A

Beta cell - helps release insulin

40
Q

Which does what? Insulin/Glucagon phosphorylate/dephosphorylate target enzymes?

A

INSULIN- Dephosphorylates target enzymes

GLUCAGON- phosphorylates target enzymes

BIOCHEMISTRY (33 decks)

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