Lecture 34: Absorptive and Postabsorptive Nutrient Utilization-2 Flashcards

1
Q

What happens to glucose and glucagon during the postabsorptive phase

A

Blood glucose decreases, stimulates glucagon and inhibits insulin secretion

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2
Q

Describe the liver transition from absorptive to postabsorptive phase

A

Liver switches from glucose utilization to glucose production by glycogen and gluconeogenesis

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3
Q

What tissues are using glucose during postabsorptive phase

A

All tissues, including brain. Muscle and adipose tissue at a diminished rate

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4
Q

How does the liver mobilize its stores during postabsorptive phase

A

Decrease glucose stimulates glucagon secretion

Glucagon stimulated glycogenolysis and gluconeogenesis

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5
Q

How long does glycogen depot last during rest/moderate ecercise

A

8-12 hrs

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6
Q

How long does glycogen depot last during high demand/severe exercise

A

30 minutes

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7
Q

How does glucagon act on adipose tissues

A

Stimulates lipolysis

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8
Q

__ and ___ stimulate lipolysis and FA release through B-adrenoreceptors

A

Epi and NE

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9
Q

___ peptide from the heart stimulate lipolysis during exercise

A

Natriuretic

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10
Q

__ and ___ reinforce increased lipolysis during and after prolonged exercise

A

Growth hormone and cortisol

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11
Q

How are FA mobilized and released from adipose tissue

A
  1. Epi or Glucagon bind B-adrenergic receptor
  2. Activate hormone sensitive lipase
  3. NEFA are transported out as free FA, bound to albumin or VLDL
  4. Taken up by liver and skeletal muscle
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12
Q

NEFA’s are used for synthesis of ___ and ___

A

Ketones and VLDL

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13
Q

Why are there multiple transport mechanisms for NEFA’s

A

Albumin decreases during long phases of nutrient deficiency. VLDL’s are independent of AA availability

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14
Q

What transporters FA into cells

A

CD36

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15
Q

Describe the steps in transportation of FA into cells—> kreb cycle

A
  1. NEFA’s bind albumin and are transported
  2. CD36 transporters NEFA’s into cell
  3. After absorption enter B-oxidation in Krebs cycle
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16
Q

How does the absorption of fatty acids and glucose in the absorptive phase vs postabsorptive (what receptors are used)

A

Absorptive: GLUT4
Post-absorptive: CD36

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17
Q

How are muscle stores/proteins utilized during postabsorptive phase

A
  1. Decrease AA entry into AA pool
  2. Degrade and use AA pool for energy
18
Q

During the postabsorptive phase what enzymes does glucagon activate and deactivate

A

Deactivate: glycogensynthase and phosphofructokinase
Activate: fructose-1,6 biphosphate and glycogenophosphorylase

19
Q

Without food for 24 hrs or more the body forms ___

A

Ketone bodies

20
Q

After 24 hours without food all glycogen stores are exhausted and the body utilized ___ for energy

A

FA (which get converted to ketones)

21
Q

Brain can’t use __ too large so for first 48hrs without food the brain uses ___

A

FA, glucose

22
Q

> 48hrs without food the liver metabolizes FA to ___ which can be used by the brain

A

Ketone bodies

23
Q

How does the fuel oxidation shift in prolonged energy deficiency

A

Carbs to mainly lipids as oxidative source

24
Q

During prolonged energy deficiency what happens to lipolysis

A

Increases to provide body with FA—> TG and ketone bodies

25
Q

during prolonged energy deficiency __ are released from adipose tissue

A

NEFA’s

26
Q

What are the three mechanisms by which liver utilizations NEFA’s

A
  1. Oxidation
  2. Triglycerides
  3. Ketones
27
Q

During the prolonged energy deficiency phase, the goal is to preserve ___ and ___ and utilize ___

A

Glucose, AA and utilize fat

28
Q

Liver can produce FA from glucose and AA during absorptive phase or consume fatty acids and channel them to krebs or into ketogenesis. What determines pathway to use

A

Levels of malonyl Co-A, decreased levels enter ketogenesis

29
Q

During the absorptive phase (insulin high) malonyl CoA suppresses ___

A

CPT-1

30
Q

During postabsorptive phase and prolonged deficiency malonyl-CoA is __ because glugacon inhibits glycolysis

A

Low

31
Q

When malonyl CoA is low what happens to FA

A
  1. FA are released from adipose tissues and transported to mitochondria via CPT-1
  2. FA into mitochondria-> B oxidation and ketone body synthesis
32
Q

What is happening during hepatic lipodosis

A

Can’t convert NEFA to VLDL because hepatocytes become overwhelmed by NEFA

33
Q

Hepatic lipodosis leads to build up of TG’s which results in ___

A

Fatty liver

34
Q

What diseases are associated with hepatic lipodosis

A

Old age, obesity, DM, pancreatitis, DKA, IBD, cholangitis, hepatitis, cancer

35
Q

What are some symptoms of hepatic lipodosis in cats

A

Anorexia, obesity, icterus, liver enlargement, vomiting

36
Q

What is the treatment for H. Lipodosis

A

High protein diet

37
Q

How doe s a ruminant maintain glucose homeostasis

A

Production of propionate which results in gluconeogenesis

38
Q

What is negative energy balance in dairy cows

A

Usually occurs post calving and during lactation when they start spending lots of energy to produce milk and not gaining enough energy via feed3

39
Q

What happens to electrolytes during starvation (clinical correlation: refeeding)

A

Shift from intracellular space to extra cellular space

40
Q

What causes refeeding syndrome

A

Surge of insulin movement of electrolytes back to intracellular space and overwhelm, leading to severe hypokalemia

41
Q

What effect does insulin play in electrolyte homeostasis in regards to refeeding syndrome

A

Activates Na/K+ pump, movement of K+ to intracellular space—> hypokalemia—> effects on membrane potential for nervous tissue and cardiac muscle

42
Q

What is the therapy strategy for refeeding syndrome

A

Low carb/high fat diet
Adequate K, PO4, MG