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skelatal muscle in health and disease > Nutrition and starvation > Flashcards

Nutrition and starvation Flashcards

1
Q

What are the major nutrients ?

A
  • Fats
  • Carbohydrates
  • Proteins
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2
Q

What can carbohydrates and protein stimulate?

A
  • Stimulate insulin secretion
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2
Q

What role does insulin have in muscle protein breakdown?

A
  • inhibits muscle protein breakdown (MPB) to augment the anabolic effects of EAA on protein turnover
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3
Q

Explain the dynamic between muscle protein synthesis and muscle protein breakdown

A
  • In healthy weight-bearing humans, muscle mass remains constant
  • virtue of a dynamic equilibrium in protein turnover
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4
Q

Whata are glucose-dependent organs?

A

Brain, blood cells, renal medulla
- brain uses 50% of available glucose
- Preferential users of glucose :
- heart renal cortex (white skeletal muscle)

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5
Q

What organs use fatty acids as fuel?

A

Liver, red skeletal muscle
Protein/AA : NOT USED AS DUEL UNLESS EXCESSIVE INTAKE

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6
Q

Give a brief review of fed state

A
  • Exogenous fuel utilisation
  • Absorption of glucose and amino acids stimulates insulin secretion from pancreatic beta-cells
  • Deposition of nutrients in tissue
  • Glucose : glycogen, triglyceride synthesis
  • Amino Acids : protein synthesis, mainly in skeletal muscle
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7
Q

What is protein-calorie malnutrition?

A
  • Affects ~ 1 billion ppl ww
  • US - 30-50% of patients will be malnourished at admission to the hospital
  • 69% will have a decline in nutrition status during hospitlisation
  • 25-30% will become malnourished during hospitalisation
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8
Q

What are consequences of malnutrition in hospitilised patients?

A
  • Poor wound healing
  • Higher rate of infections
  • Greater length of stay
  • Greater costs
  • Increased morbidity and mortality
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9
Q

What is a fast?

A

-Exclusion of all food energy

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10
Q

What is starvation?

A
  • Prolonged inadequate intake of protein and/or energy
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11
Q

What is Cachexia?

A
  • Wasting induced by metabolic stress
  • diseases e.g. cancer
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12
Q

What is a fasted postabsorptive state?

A
  • Fed state ends when last nutrient is absorbed, body switches once again to endogenous fuel utilisatuon - constant cycling
  • Decrease level of insulin, increase in glucagon
  • Release, transfer and oxidation of fatty acids
  • Release of glucose from liver glycogen
  • Release of amino acids (stored as proteins) from muscle as a source of fuel
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13
Q

What is the progression of fasting?

A
  • Normal post absorptive state : ~ 12 hours
  • Release and oxidation of fatty acids from adipose tissue/ectopic stores
  • Release of glucose from liver glycogen
  • Liver glycogen capacity : approx 1000 kcal
  • Equivalent to ~ 250 g carbohydrate/glucose
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14
Q

What happens when you fast longer than 24 hours?

A
  • Further decrease in insulin, increase in glucagon
  • Proteolysis and release of AA from muscle as a source of fuel
  • Activation of hormone sensitive lipase
  • Increase in lipolysis
  • Increase in circulating FFA and tg
  • Gluconeogenesis
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15
Q

What is gluconeogenesis?

A

Cori cycle in Liver- Muscle:
- glucose - converted to lactate/pyruvate in skeletal muscle (anaerobic) - travels back to liver for conversion to glucose
- Glucose- alanine (cahill cycle)
- AA deaminated in muscle
- C skeleton used for energy – pyruvate and NH2 – alanaine
- Alanine returns to liver for deamination
- NH2 - urea for excretion
- Pyruvate - glucose via GNG

16
Q

Explain the glutamine cycle in the kidneys

A
  • Muscle glutamine - kidney - glutamate + NH3- A-ketoglutarate – glucose
  • Kidney is initially a minor source, increases to supply up to 50% of glucose over time
17
Q

What is ketosis?

A
  • Characterised by presence of ketone bodies (acetoacetate, acteonem b-hydroxybutyrate)
  • Bi-products of fatty acid oxidation in liver
  • Can be used by all tissues with mitochondria
  • Utilized by brain, decreasing glucose consumption by 25%
  • Can be prevented by providing 150 g glucose per day
18
Q

What occurs when a fast is around 7-10 days?

A

-significant musce protein loss
10-12 g urinary N/day
- 360g LBM per day initally
- 1-2 kg LBM over first 7 days
- Lethal depletion after 3 weeks if no adaptation occurs - by the end of 2-3 weeks , decrease muscle protein catbolism

19
Q

What occurs during long-term starvation?

A
  • Decreased metabolic rate
  • decreased actvity, body temp
  • Conservation of protein
  • decrease in muscle protein breakdown 64g to 30g / day
  • Increased fatty acid oxidation
  • Liver , heart and muscle use ketone bodies
  • Decrease glucose availability
20
Q

What happens to the brain during long term starvation?

A
  • Decreased glucose availability
  • Fed state uses 75%, completeluy oxidised
  • 50% of glucose with ketones
  • Decreased complete oxidation, recycles via GNG

In blood cells/ renal medulla
- Anaerobic glycolysis to pyruvate and lactate

21
Q

What are some changes in organ function during starvation?

A

Liver : loss of mass
- Decreased protein synthesis
- Peri-portal fat accumulation (fattu liver)
- Hepatic insufficiency
- Skeletal muscle:
- catabolised for GNG - decreased mass
- utilisation of ketones : slower contractions
- Diminished function: intercostal muscles - decreased resp function
-imparied digestion

22
Q

What can cause a decreased protein concentration?

A

1.) Reduction in protein synthesis
2.Increase in protein breakdown
3.Reduction in protein synthesis and increase in protein breakdwon
4.Increase in protein synthesis and even higher increase in protein breakdown

23
Q

What can cause skeletal muscle atrophy?

A
  • Immobilisation (Space flight, cast immobilisation, physical inactivity)
  • Disease-related (cancer, HIV, rheumatoid arthritis, renal failure, burns,sepsis)
  • Drug - related (glucocorticoids)
  • Inadequate nutritional intake or digestion ( starvation, protein malnurtrition, impaired digestion )
  • Ageing
24
Q

Describe the process of muscle sarcomere degradation

A
  1. Calpins disassemble the sarcomere at the Z-line (by digesting Z-line proteins such as nebulin and fodrin), break it up into smaller pieced
  2. Myosin, actin and other proteins are then digested by the ATP-ubiquitin -dependent 26S proteasome which cannot digest connected proteins
  3. Some proteins are also degraded by cathepsins, which are located in lysosomes.
25
Q

What does insulin supress?

A
  • Inhibits muscle protein breakdown to augment the anabolic effects of EAA on protein turnover
26
Q

What is the effect on nutrition on Muscle Protein Turnover?

A
  • In healthy weight-bearing humans, muscle mass remains constant by virtue of a dynamic equillibrium in protein turnover
  • MPB> MPS [fasted], MPS>MPB [fed]
27
Q

Compare starvation in a lean and obese individual

A
  • Lean 70kg man (13% fat) survival ~ 64 days at 1500 kcal/day
  • Obese - 242-302 at 2000-2500 kcal/day
28
Q

What is gene regulation during starvation?

A
  • Decrease in totala RNA (decrease in ribosome content)
  • Ubiquitin-proteasome mRNA increases : greater capacity for muscle protein breakdown
  • Carbohydrate- catabolism enzymes decrease but no upregulation of fat metabolism enzymes : Preservation of the limited glycogen reserves
  • Myosin heavy chain anf collagen expression goes down
  • Apoptosis markers increase
  • 4E-BP1 Increases : Increased inhibition of translation
29
Q

What are some key factors in regulating muscle atrophy?

A
  • E3 ubiquitin ligases such as MADbx and Murf1
  • determine the protein breakdown rare and net protein changes
  • measured with RT-PCR to confirm microarray
30
Q

What is cathepsin L?

A
  • protease
  • located in lysosomes
  • mRNA and protein induced in muscle wasting conditions (Sepsis, cancer, dexamethasone treatment)
  • Induced by dexamethasone ( synthetic glucocorticoid that induces muscle atrophy)
  • CL mRNA increases in response to unloading

skelatal muscle in health and disease (16 decks)

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