Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FHB Block 4 > Metabolic Homeostasis > Flashcards

Metabolic Homeostasis Flashcards

1
Q

What is wasting?

A

A prolonged fasted state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What type of cytokines are prevalent in pathology that leads to wasting?

A

Pro-inflammatory cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What axis is activated during times of wasting?

A

HPA axis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are growth hormone (and consequently IGF-1) affected by wasting?

A

They are dysregulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the “metabolic switch” that occurs after prolonged fasting

A

Protective mechanism against a prolonged state of fasting - helps your brain get enough nutrients/survive and protects protein breakdown

Ketone body production are now used as a source of energy in the brain. This reduces the demand on the body to use protein for fuel (protein catabolism drops from 300g to 20g a day of break down)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the definition of obesity?

A

BMI >30, waist: hip ratio is greater than 0.95 in men and 0.85 in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the definition of syndrome X (metabolic syndrome)

A

Visceral obesity (waist >40 inches for men, 35 for women)
Insulin resistance
Dyslipidemia (high TAGs, low HDL)
Hypertension

Metabolic syndrome puts you at risk for developing Type II diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the primary hormone produced by adipose tissue?

A

Leptin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the role of the transcription factor Sterol regulatory binding protein 1C (SREBP 1C)?

A

Promotes TG synthesis and increases glucose “trapping” in cells by upregulating synthesis of glucokinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What type of receptor is PPARgamma?

A

nuclear steroid hormone receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is PPARgamma responsible for?

A

Regulation of TG storage and adipocyte differentiation - makes new adipocytes and makes them bigger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are thiazolidinediones (TZDs)?

A

They are PPARgamma agonists used to treat insulin resistance and Type II diabetes mellitus

This works by increasing the storage of fatty acids in adipocytes, thereby decreasing the amount of fatty acids in circulation. As a result cells become more dependent on the oxidation of carbohydrates (glucose) as a source of energy - increase peripheral sensitivity to insulin actions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the relationship between the amount of fat someone has and the amount of leptin?

A

Directly relationship - more fat = more leptin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does leptin affect appetite?

A

Leptin stimulates the inhibitors of appetite, and inhibits the stimulators of appetite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name two stimulators of appetite

A

Neuropeptide Y
Agouti-related peptide (AGRP)

-Both are from the hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name two inhibitors of appetite

A

alpha-MSH (cleaved from POMC)

Cocaine-amphetamine regulated transcript (CART)

17
Q

Discuss the reversibility of insulin-resistances

A

Insulin-resistance (pre-diabetes) is reversible

Once the diagnosis of type II diabetes has been made, you can’t reverse the resistance, because beta-cells are damaged.

18
Q

What does insulin resistance refer to?

A

Insulin resistance –> GLUT4 is not transported to the cell membrane –> glucose is not effectively taken up into the skeletal and adipose tissue –> high blood plasma levels –> hyperinsulinemia –> downregulation of insulin receptors

Over time, pancreas reduces insulin output.

Eventually Type II diabetes mellitus –> type I as beta cells die

19
Q

How does obesity affect C-peptide and insulin output to the same amount of glucose when compared to a normal person?

A

An obese person pumps out more insulin and c-peptide in response to the same amount of glucose as a C-peptide

20
Q

What is HbA1C?

A

Glycosylated hemoglobin- good indicator of average blood glucose levels over a longer period of time

Anything over 6.5% is considered diabetic

21
Q

What is polyphagia and why does it occur with diabetes?

A

Polyphagia = excessive hunger due to inability of cells to utilize glucose “cellular starvation”

You don’t get this with diabetes insipidus, but you do get it with diabetes mellitus

22
Q

What is polyuria and why is it bad?

A

Polyuria= excessive glucose in blood- leads to increased plasma osmolality and excessive water and sodium loss

23
Q

What is polydipsia and why does it occur?

A

Polydipsia= excessive thirst due to severe dehydration

24
Q

How do sulfonylurea drugs work to treat Type 2 DM?

A

They close the K+ ATP-dependent channel in beta cells –> depolarization –> Ca2+ release –> insulin release

25
Q

How do biguanides (metformin) work to treat type II DM?

A

Inhibits hepatic gluconeogenesis
Increases activity of the insulin receptors making them more sensitive to insulin –> increased glucose uptake from the blood

26
Q

How do alpha-glucosidase inhibitors work to treat Type II DM?

A

They delay intestinal absorption of carbohydrates

27
Q

Is insulin required for type I DM?

A

YES- insulin is absolutely required. Insulin type I = autoimmune destruction of pancreatic beta cells

28
Q

What causes a diabetic coma?

A

Severe dehydration (due to osmotic diuresis) and metabolic acidosis (due to increased ketone production)

29
Q

Do you get ketogenesis with type II DM? Type I DM? If not, why?

A

No, not in type II DM because there is some insulin being made- which allows for glucose uptake into the cells

You do get acidosis with type I DM

30
Q

What is DKA?

A

Diabetic ketoacidosis - found in patients with Type I DM. There is no insulin to take up glucose into the cells via GLUT4 transporter, therefore ketone bodies are produced for a source of energy to the brain. Ketone production leads to H+ release in the cells.

31
Q

How does mental status relate to osmolality of the blood?

A

The higher osmolality leads to worse and worse mental state (until coma)

32
Q

Compare type I DM to starvation state

A

All of the hormones are the same, except there is high blood glucose

33
Q

GWAS studies on type II DM showed that genes mainly affecting what are associated with DM?

A

Most genes identified affect beta cell development, proliferation, survival and function

34
Q

Which is the most highly associated genetic polymorphism in type II DM? What is it important for?

A

TCF7L2- important for the WNT signaling pathway; a coactivator for beta catenin

35
Q

Islet neogenesis occurs during embryonic development. When does beta cell proliferation really take off?

A

1st year of life

36
Q

What is the role of PDX-1?

A

PDX-1 is important for islet neogenesis and beta cell proliferation

Defects lead to an inability to make islet cells

37
Q

What is neurogenin 3 important for?

A

Key protein for endocrine cell development

38
Q

How do beta cells respond to an increased need in insulin, due to a increased resistance towards insulin?

A

Beta cells proliferate.

FHB Block 4 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions