metabolism GI Flashcards

1
Q

How many kcal is glucose?

A

4

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2
Q

How many kcal/gram are fatty acids?

A

9

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3
Q

how many kcal/gram are protien?

A

4kcal/gram

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4
Q

What are the major breakdown products of glucose?

A

pyruvate to Acetyl Coa (or lactate

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5
Q

What are FA broken down into

A

Actyle CoA

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6
Q

What metabolic functions are performed by the liver?

A

storage of glycogen and TAG, protien synthese, and fats-storage and TAG

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7
Q

What is the Teleological statement (what the body wants) of the fed state?

A

After eating, the body wants to store calories that exceed its immediate energy needs, so that it can withstand periods of nutrient unavailability. The body stores excess calories as carbohydrate, fat, and protein.

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8
Q

what is the xMechanistic statement (how it happens) of fed state

A

After eating, nutrients stimulate the release of specific hormones, such as insulin, that upregulate biosynthetic pathways in different tissues.

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9
Q

What hormones rise after feeding? what falls?

A

insulin (in response to glucose), glucagon falls

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10
Q

what is glucagon function? what is it inhibited by?

A

Insulin inhibits the release of glucagon, the major regulator of catabolism in the fasted state.

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11
Q

What does a high protein meal release in terms of hormones?

A

more glucagon, not as much insulin, if you have a bunch of insulin around you wont be able to turn amino acids into glucose (aka gluconeogensis)

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12
Q

What kind of receptor does insulin bind to?

A

tyrosine kinase, a peptide horomone

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13
Q

What are the two pathways we need to know that insulin activates?

A

Map kinase that leads to transctiption, and PKB which activates PP1 and inactiviatesGSK3

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14
Q

What PP1 do when activated?

A

it dephosphorylates glycogen sunchinate? kinase and glycogen phosphorylase inactivating them and promoting sythensis of glyocgen

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15
Q

What does the liver do after each a carb rich meal?

A

biosynthetic pathways that produce glucose (glycogenolysis, gluconeogenesis) are inhibited.

metabolic pathways that store glucose (fatty acid biosynthesis, cholesterol biosynthesis, protein synthesis, glycogenogenesis) are activated.

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16
Q

What does the liver do after eating a protein rich meal

A

elevated amino acids in the blood increase the secretion of glucagon by pancreatic alpha cells. In this case, excess amino acids are used by the liver for gluconeogenesis.

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17
Q

What does the brain do in repsonse to eating?

A

Oxidizes glucose to CO2 to make ATP through oxidative phosphorylation.

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18
Q

What does the RBC do in reponse to eating

A

Ferments glucose to pyruvate; exports lactate.

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19
Q

What does the

White adipose cells do in repsonse to eatng

A

Ferments glucose to glycerol 3-phosphate, the backbone for triacylglycerol synthesis.

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20
Q

What does Skeletal muscle

do in response to eating

A

Glycolysis, fatty acid beta oxidation, glycogenogenesis, protein synthesis

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21
Q

what does Cardiac muscle

do in response to eating

A

Fatty acid beta oxidation (60-80%); Oxidation of glucose and lactate (20-40%).

22
Q

What do the intestinal epithelia cells do in response to feeding

A

Convert glutamine, glutamate and aspartate from the diet to a-ketoglutarate.

23
Q

What is the Teleological statement regarding fasting

A

In between meals, the body wants to mobilize stored energy so that it can continue to perform work.

24
Q

What is the mechanistic statement regarding fasting

A

Low carbohydrates in the blood promote the release of glucagon, a major regulator of hepatic fuel mobilization, from pancreatic alpha cells. Furthermore, intracellular enzymes that activate fuel mobilization pathways are directly regulated by energetic imbalance. E.g., AMP-K.

25
Q

What is the glucagon receptor?

A

is a seven transmembrane domain heterotrimeric G protein coupled receptor.

26
Q

What does the binding of glucagon to its receptor activate

A

Ligand binding causes activation of adenylate cyclase, production of cAMP, and activation of PKA.

27
Q

in the fed state, what is the status/function of Glycogen synthase

A

phosphorylated and inactive

28
Q

in the fed state, what is the status/function Glycogen phosphorylase kinase

A

phosphorylated and active.

29
Q

What is the liver’s response to fasting?

A

The liver increases production and export of glucose for use by other tissues.
Glycogenolysis uses hepatic glycogen stores.
Gluconeogenesis uses carbon skeletons from amino acids(MOST IMPRTANT SOURCE), lactate (RBC fermentation of glucose), and glycerol to produce glucose.

30
Q

Where does the ATP to power gluconeogenesis come from

A

FAD(2H) and NADH reduced by fatty acid beta oxidation

31
Q

THe acetyl CoA produced by fatty acid beta oxidation is a substrate for what?

A

ketone body synthesis

32
Q

What is the skeletal muscle response to fasting

A

Proteolysis produces free amino acids( due to cortosl). Branched chain amino acids are used by the muscle as fuel used within the muscle cell, . Alanine and glutamine are exported for use as gluconeogenic substrates by the liver.
As the fast prolongs, skeletal muscle can use ketone bodies for energy.

33
Q

What does cardiac muscle do in response to fasting

A

Fatty acid beta oxidation increases; glycolysis decreases.

34
Q

In a fasted state, where does glutamine come from?

A

the blood!

35
Q

How does White adipose tissue respond to fasting

A

Lipolysis of triacylglycerol produces fatty acids (used as fuel by heart, liver) and glycerol (used for gluconeogenesis by liver).

36
Q

What is the Teleological statement to starvation

A

the body preserves body structure by degrading only tissue with the most caloric density (fat) to provide energy.

37
Q

what is the Mechanistic statement regarding fasting

A

Adipose triacylglycerol is mobilized for fuel and to synthesize ketone bodies; muscle protein breakdown is minimized; glucose is spared for red blood cells.

38
Q

what are some body changes in response to prolonged fasting

A

Lipolysis of adipose triacylglycerol increases; the liver increases its production of ketone bodies.

Ketone body utilization by skeletal muscle decreases, and ketone body utilization by the brain increases.

Cardiac muscle continues to use fatty acids; the heart does not like to use ketone bodies.

Skeletal muscle breakdown decreases; the liver decreases gluconeogenesis.

39
Q

what happens to the urea cycle with starvation?

A

it decreases

40
Q

What happens to the urea cycle overnight?

A

it increases, since metabolism is dominated by amino acids

41
Q

What is hypercatabolism?

A

Hypercatabolism is the rapid mobilization of stored fuels to provide energy for wound repair and immune system function-sustained muscle and organ breakdown

It can occur after surgery, trauma, burns, or sepsis.

42
Q

In the first day of hypercatabolism, what hormone peaks right away and then decreases?

A

catechoalimes-epinephrine activates hormone sensitive lipase -> fatty acids moblized from adipose

43
Q

In the hypercatabolism state, what takes longer to increase but stays high? What does it do?

A

cortisol-activates muscle proteolysis ->amino acids mobilized from muscle

44
Q

What peaks right away and has a slowly decreasingduring hypercatabolism? What its function?

A

glucagon activates hepatic glycogenolysis and gluconeogenesis

45
Q

what is the goal in all recovering hypercatabolic patients

A

maintain pos nitrogen balance

46
Q

what is the equation for determining nitrogen balance

A

Nitrogen balance = nitrogen intake – (urinary urea nitrogen + 2)

47
Q

Whats the nitrogen/protein ration?

A

.16g nitogen/1 gram protien

48
Q

in the nitrogen balance equation, what does the two stand for

A

The “2” accounts for nitrogen lost in sweat, sloughed skin and intestinal cells. This number varies– in pediatric patients eating normally, this value is increased to 4. For pediatric patients receiving total parenteral nutrition, the value is 3.

49
Q

Where is creatine made? what is its use?

A

synthesized in the kidney and liver, and serves as a buffer of high energy phosphate bonds to replenish ATP in skeletal muscle, cardiac muscle and brain.

50
Q

Whats a way to measure nutrional status?

A

creatine-height ratio, meausred over 24 hours

51
Q

Other ways to asses nutrional status?

A
Physical appearance:
Muscle mass in fingers, face
Cheilosis, allopecia
Hepatomegaly
Body mass index (BMI)

Radiology findings:
For scurvy, vitamin C deficiency

Laboratory results:
Creatinine Height Index
Serum creatinine (normal 0.6-1.6 mg/dL)
24 hour urinary urea nitrogen (nitrogen balance)
Serum albumin (normal 3.5 – 5.5 g/dL)
Serum pre-albumin / transthyretin (normal 20-40 mg/dL