Nutrition Metabolism Review - Skildum Flashcards

1
Q

What accounts fro the majority of the chemical energy in your body?

A

Triacylglycerol

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2
Q

What is the brain’s primary energy sources?

A

Glucose and ketone bodies

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3
Q

What is the storage form for glucose, AA, and fats?

A
Glucose = glycogen, TAG
AA = protein
Fats = TAG
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4
Q

How long is the fed state? What is the hypercatabolic state?

A

Fed: Lasts 2-4 hours after a meal

Fasted: Overnight without eating

Starved: Prolonged fasting

Hypercatabolic: Trauma, sepsis, etc.; not related to meals

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5
Q

What process dominates the starvation state?

A

Fatty acid metabolism

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6
Q

Insulin is released from what type of cell?

A

Pancreatic beta cells

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7
Q

(T/F) The relative amount of carbohydrates in the meal doesn’t determine the ratio of insulin to glucagon.

A

The relative amount of carbohydrates in the meal determines the ratio of insulin to glucagon.

High carbs  More insulin

High protein  Less insulin, more glucagon

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8
Q

After feeding, what does the liver do?

A

The liver is the primary organ responsible for maintaining glucose homeostasis. After eating a carbohydrate rich meal, . . .

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

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

After eating a protein rich meal, 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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9
Q

After feeding, what is the function of these organs?

Brain:

RBCs:

White adipose cells:

A

Brain:
Oxidizes glucose to CO2 to make ATP through oxidative phosphorylation.

Red blood cells:
Ferments glucose to pyruvate; exports lactate.

White adipose cells:
Ferments glucose to glycerol 3-phosphate, the backbone for triacylglycerol synthesis.

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10
Q

Fed or fasted state?

Skeletal muscle
Glycolysis, fatty acid beta oxidation, glycogenogenesis, protein synthesis

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

A

Fed

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11
Q

What is the function of these cells during the fed state?

Intestinal epithelial cells:
.
Colonocytes:

A

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

Colonocytes (gut epithelial cells of colon)
Use short chain fatty acids produced by gut bacteria.

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12
Q

What cells produce glucagon and what are its downstream effects?

A

The glucagon receptor is a seven transmembrane domain heterotrimeric G protein coupled receptor.

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

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13
Q

During the fed state, what does the liver do with respect to glycogenolysis, gluconeopgenesis, ATP, and acetyl CoA?

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, lactate, and glycerol to produce glucose.

The ATP to power gluconeogenesis comes from the FAD(2H) and NADH reduced by fatty acid beta oxidation.

The acetyl CoA produced by fatty acid beta oxidation is a substrate for ketone body synthesis.

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14
Q

After an overnight fast, what’s happening in these organs?

Skeletal muscle

Cardiac muscle

A

Skeletal muscle:
Proteolysis produces free amino acids. Branched chain amino acids are used by the muscle as fuel. 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.

Cardiac muscle:
Fatty acid beta oxidation increases; glycolysis decreases.

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15
Q

Do gut epithelial cells still use glutamine as their primary fuel in the fasted state?

A

Yes. Gut epithelial cells still use glutamine as their primary fuel in the fasted state, but it comes from the blood, not the lumen of the gut.

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16
Q

Fed or fasted?
White adipose tissue:
Lipolysis of triacylglycerol produces fatty acids (used as fuel by heart, liver) and glycerol (used for gluconeogenesis by liver).

A

Fasted

17
Q

What is the primary AA used but gut epithelial cells?

A

Glutamine

18
Q

During starvation (prolonged fasting), what happens to:

Liver’s production of KBs

Ketone body utilization

Cardiac fuel source

Skeletal muscle structure

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.

19
Q

During starvation what are the plasma levels of glucose, KB, and FA?

A

Glucose > KB > FA

20
Q

What happens to the urea cycle during starvation?

A

It decreases its activity. No Nitrogen in FA so less need to excrete urea.

21
Q

[ ] is the rapid mobilization of stored fuels to provide energy for wound repair and immune system function.

When can this occur?

A

Hypercatabolism

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

Hypercatabolism is characterized by sustained muscle and organ protein breakdown.

22
Q

What mediates these processes?

  • Fatty acids moblized from adipose
  • Amino acids mobilized from muscle
  • Activates hepatic glycogenolysis and gluconeogenesis
A

EPINEPHRINE activates hormone sensitive lipase –> fatty acids moblized from adipose

CORTISOL activates muscle proteolysis  amino acids mobilized from muscle

GLUCAGON activates hepatic glycogenolysis and gluconeogenesis

23
Q

What promotes the flow phase of hypercatabolism?

A

Cortisol and glucagon

24
Q

Nitrogen balance is important for recovering patients. How do you measure Nitrogen balance?
How is it different pediatric patients?

A

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

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