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Biochem Quiz 4 Winter > Adipocytes Energy Balance 2 > Flashcards

Adipocytes Energy Balance 2 Flashcards

1
Q

What is Hepatic Steatosis?

A

Fatty Liver

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2
Q

What is the effect of insulin resistance on…

Muscle?
Adipose?
Liver?

A

Muscles – less glucose up-take (less GLUT4 on surface)

Adipose:

- less TG synthesis (less LPL, GLUT4 on surface)
- more FA released (less HSL inhibition)

Liver – “selective” insulin resistance:

- FA synthesis still up-regulated by insulin
- gluconeogenesis not inhibited by insulin
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3
Q

What are the two theories on insulin resistance?

A

1) Intramuscular fat inhibits IRS phosphorylation

2) Inflammatory cytokines cause inhibitory IRS phosphorylation

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4
Q

What is the intramuscular fat inhibits IRS phosphorylation theory of insulin resistance?

A
  • Excess TG in muscle
    • Leads to excess of other lipids in muscle (DG, other lipids)
    • these lipids activate serine/threonine kinases
    • these kinases phosphorylate IRS-1
    • this S/T phosphorylation inhibits insulin receptor phosphorylation of IRS-1
    • insulin signaling is reduced
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5
Q

What is the Inflammatory cytokines cause inhibitory IRS phosphorylation theory of insulin resistance?

A

Adipose tissue contains resident immune cells (macrophages, others)

  • Increased adipose and/or adipocyte stress increases immune cells (especially visceral fat)
  • Inflammatory cytokine secretion (TNF-a and others) increases
  • cytokine signaling increases S/T phosphorylation of IRS-1
  • this S/T phosphorylation inhibits insulin receptor phosphorylation of IRS-1
  • insulin signaling is reduced
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6
Q

What are the three sources of FA intake for the LV?

What are the two sources of FA disposal for the liver?

A

3 sources of FA for liver:
Chylomicrons (diet)
Serum FA (adipose)
Endogenous synthesis

2 sinks for FA:
Oxidation
VLDL export

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7
Q 
How are each affected by insulin?
3 sources of FA for liver:
Chylomicrons (diet)?
Serum FA (adipose)?
Endogenous synthesis?

2 sinks for FA:
Oxidation?
VLDL export?

A

3 sources of FA for liver:
Chylomicrons (diet) increased by positive energy balance
Serum FA (adipose) not decreased, due to insulin resistance (Adipocytes are insulin resistant and therefore adipocyte HSL is still active, in spite of insulin)
Endogenous synthesis high, due to selective hepatic insulin resistance (Ie insulin still activates FA synthesis)

2 sinks for FA:
Oxidation low, due to selective hepatic insulin resistance
VLDL export overwhelmed

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8
Q

What effect does increased pancreatic TG have on insulin release?

A

Higher expression of Uncoupling Proteins (UCP2)
Higher activity of UCP2
Therefore, less ATP
Therefore, less glucose-induced insulin secretion

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9
Q

What is Orlistat?

A

binds to Lipase in the intestines and leaks undigested fat out of the butt

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10
Q

What is Rimonabant?

A

New Anti-Obesity Drug

-CB1R antagonist
-inhibits endocannabinoid signaling
-strong appetite suppressant
-also considered for smoking cessation
But… psychiatric side-effects
-taken off market in Europe,
never approved in US

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11
Q

What is Sibutramine?

A

appetite suppressant with CV side effects

Removed from market

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12
Q

FYI: Rimonabant (endocannabinoid antagonist). Withdrawn.
Sibutramine (serotonin/noradrenaline re-uptake inhibitor). Withdrawn.
Fenfluramine (serotonin enhancer). Withdrawn.
Phentermine (noradrenaline, serotonin, dopamine enhancer). Short-term.
Lorcaserin/Belviq (specific serotonin receptor agonist). Recently approved.
Contrave (combo therapy: noradrenaline re-uptake, opioid antagonist). Recently approved.
Qsymia (combo therapy: phentermine, and anti-epilepsy med). Recently approved.

A

Rimonabant (endocannabinoid antagonist). Withdrawn.
Sibutramine (serotonin/noradrenaline re-uptake inhibitor). Withdrawn.
Fenfluramine (serotonin enhancer). Withdrawn.
Phentermine (noradrenaline, serotonin, dopamine enhancer). Short-term.
Lorcaserin/Belviq (specific serotonin receptor agonist). Recently approved.
Contrave (combo therapy: noradrenaline re-uptake, opioid antagonist). Recently approved.
Qsymia (combo therapy: phentermine, and anti-epilepsy med). Recently approved.

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13
Q

Prior treatment plan for diabetes in 2006

A

Keep A1C levels re less aggressive)
Order of treatment:
a) Lifestyle changes/metformin
b) insulin (now with caution)
c) Sulfonoureas (incretin therapy has replaced)
d) Thiazolidinediones (not used much anymore)

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14
Q

What are the effects of metformin?

A

In liver:

a) decreases gluconeogenesis
b) decreases FA synthesis
c) increases FA oxidation 2. In muscle - Increases GLUT4 on PM/glucose up-take
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15
Q

Don’t need to know the mechanism for Metformin

A

Don’t need to know the mechanism for Metformin

Probably inhibits Adenyl cyclase and counters the counterregulatory compounds of insulin

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16
Q

What are the effects of insulin?

A

Increased muscle glucose up-take

Decreased liver gluconeogenesis

Decreased FA oxidation

Increased fat storage

17
Q

What are sulfononoureas?

A

Inhibit the ATP-inhibted K channel in Pancreas beta cells.
This means that the channel is inhibited even without ATP.
Therefore, there is more stimulation of insulin release. (cell depolarizes and releases insulin)

18
Q

What are incretins?

exp: GLP-1, GIP

A

Released by intestines
Increases insulin release
Decreases glucacon release

19
Q

Where is GLP transcribed from?

A

from the same peptide chain as glucagon.
However it is antagonistic to glucagon.
Note: which protein is released glucagon vs GLP depends on which cell the chain is transcribed from.

20
Q

What cells produce glucacgon? When?

What cells produce GLP-1? When?

A

Glucagon: alpha pancreas cells
released in times of need
increases plasma glucose

GLP-1: Produced in Intestinal L cells
released after a meal
Increases insulin secretion and decreases glucagon secretion

21
Q

What enzyme degrades GLP-1 and incretins?

How fast are they degraded?

A

DPP4

degraded very fast (within minutes)

22
Q

What are 2 incretin therapies?

A 
DPP4 inhibitor (sitaglipin): extends life of GLP-1
GLP-1 analogue (Exenatide/Byetta)
23
Q

Why are Incretin therapies preferrable to Sulfonoureas?

A

Lower chance of hypo-glycemia. Incretins sensitize the beta cell RESPONSE to blood glucose (sulfonureas do regardless of glucose)

Lower weight gain. Effects on appetite

Hypothesis – do not induce beta cell “exhaustion”

24
Q

Incretins may delay the transition from early to late stage diabetes

A

Incretins may delay the transition from early to late stage diabetes

25
Q

How do Thiazolinediones work?

A

Synthetic PPAR-gamma ligands used therapeutically (decrease FA from muscles, but increase FA in fat cells. Cause problems)

Biochem Quiz 4 Winter (6 decks)

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