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MEH Sem 1 > Lecture 14.5 - Fuel Sources > Flashcards

Lecture 14.5 - Fuel Sources Flashcards

1
Q

What are some type of fuel sources normally available and available under special conditions?

A

Normal:

  1. Glucose: Little free glucose, More stored as glycogen
  2. F.A: Stored as TAG

Special:

  1. A.a: Muscle protein broken down–>ketone bodies
  2. Ketone bodies: From F.A
  3. Lactate: Anaerobic respiration –> converted back to glucose via Cori Cycle
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2
Q

What are the 3 diff. types of A.a that can be metabolised under special conditions?

A
  1. Glucogenic= Ala & Val
  2. Ketogenic = Lys & Leu
  3. Both = Tyr & Phe
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3
Q

What happens immediately after feeding (~2 hours)?

[Glucose & Fat available in gut]

A
  • Immediate glucose metabolism for growth processes

- Glycogenesis, Lipogenesis

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4
Q

What happens when glucose & fats X longer absorbed in gut (~2-10 hours)?

A
  • B.G maintained by breakdown of glycogen
  • F.A released from stores
  • Preserve glucose requirement for brain
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5
Q

What happens when X consume food for 8-10 hours/glycogen stores depleted?

A
  • Gluconeogenesis –> glucose for brain

- F.A metabolism

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6
Q

What happens in starvation?

A
  • F.A metabolism produces ketone bodies

- Brains become able to metabolise ketone bodies (⬇️need for glucose)

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7
Q

What are some anabolic hormones (build)?

A
  • Insulin, GH (increase protein synthesis)

- Promote fuel storage

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8
Q

What are some catabolic hormones (destroy)?

A
  • Promote release from stores and utilisation

- Glucagon, Adrenaline, Cortisol, GH (increase lipolysis & gluconeogenesis), T3,T4

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9
Q

What are the effects of feeding?

A
  • Increase in BG –> pancreas secrete insulin
  • Increase glucose uptake/storage/utilisation
  • Promote a.a uptake + protein synthesis in liver
  • Promote lipogenesis and storage
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10
Q

What are the effects of fasting?

A
  • B.G falls and insulin is supressed–> glucagon secreted
  • Glycogenolysis (maintain blood glucose for brain and other dependant tissues)
  • Lipolysis (F.A for tissues)
  • Gluconeogenesis (maintain blood glucose for brain)
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11
Q

What are the effects of starvation?

A
  • ⬆️Cortisol from adrenal gland & glucagon from pancreas
  • Stimulate gluconeogenesis, proteolysis and lipolysis
  • Reduction in I/IA ratio –> F.A preferentially metabolised
  • Glycerol from fat –> gluconeogenesis
  • Liver produce ketone bodies –> brain use (reduce need for glucose)
  • Fat depleted –> proteins –> death due to loss of muscle mass [respiratory muscles]
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12
Q

What is the net weight gain of mother by end of pregnancy?

A

8kg

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13
Q

Describe the two phases of metabolic adaptation during pregnancy.

A
  1. Anabolic phase: Preparatory increase in maternal nutrient stores
    - ⬆️maternal fat stores
    - ⬆️insulin sensitivity
    - Nutrients stored to meet future demands of rapid fetal growth (2/3rd growth in last 1/3 of pregnancy)
  2. Catabolic state: Maternal metabolism adapts to meet increase fetal-placental unit
    - ⬇️insulin sensitivity
    - ⬆️maternal glucose and free F.A
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14
Q

How is glucose transported to fetus? Which carrier?

A
  • Simple diffusion
  • Through GLUT 1

*GLUT 2- Pancreas, GLUT 4- S.M

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15
Q

What is the new endocrine unit during pregnancy and what does it secrete?
*they have anti-insulin effects

A
  • Foetal-placental unit

- CRH, Progesterone, Human placental lactogen

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16
Q

What happens to maternal metabolism during first ~20 weeks of pregnancy?

A
  • Preparatory increase in maternal nutrient stores for:
    (i) Rapid growth rate of fetus
    (ii) Birth
    (iii) Lactation
  • Increase insulin sensitivity–> ⬆️anabolic state –> increase nutrient storage
  • Hyperplasia and hypertrophy of β-cells
17
Q

How are conc. of nutrients kept high in maternal blood in 2nd phase of pregnancy?

A

i) Reducing maternal utilisation of glucose by switching to use of F.A
ii) Delaying maternal disposal of nutrients after meals
iii) Release of F.A stores

  • Insulin still increase but anti-insulin hormones by fetal-placenta unit increase more –> I/IA falls
18
Q

What do the anti-insulin hormones from fetal-placenta unit result in?

A
  • Transient (short-term) hyperglycaemia after meals due to insulin resistance
  • Hypoglycaemia can occur btw. meals
19
Q

What does insulin secretion in pregnancy cause?

A
  • ⬆️appetite –> ⬆️ glucose ingested

- Oestrogen and progesterone ⬆️ sensitivity of B-cells to insulin –> hypertrophy & hyperplasia

20
Q

When does gestational diabetes occur? State some causes.

A
  • β-cells X suff. insulin to meet increase requirement in late pregnancy
  • Causes:
    i) Autoimmune disease –> autoantibodies (similar to D.M 1) [less than 10% cases]
    ii) Genetic susceptibility [rare]
    iii) Obesity and chronic insulin resistance [most common]
21
Q

What are some clinical implications of gestational diabetes?

N.B Risk of complications ⬇️ if managed and diagnosed

A
  • ⬆️risk of miscarriage
  • ⬆️congenital malformation
  • Fetal macrosomia (large body): Disproportionate adipose around shoulder –> shoulder dystocia (shoulder stuck during birth)
  • Preeclampsia: high BP/protein in urine
22
Q

What are factors that increase risk of gestational diabetes?

A
  • Maternal age (>25 years): fat/lean body mass ratio increase w age
  • BMI >25kg/m2
  • Race: more common in asian, black, hispanic
  • Fam. history of diabetes/ macrosomia
23
Q

What is the management of gestational diabetes?

A
  • Dietary modification: ⬇️calories
  • Insulin injection
  • Regular ultrasound scans: assess fetal growth
24
Q

What is the importance of the metabolic response during exercise?

A
  • Meet increase energy demands by mobilisation of energy stores
  • ⬇️disturbance to metabolic homeostasis: utilisation=mobilisation
  • Brain supplied w glucose
  • End products removed quickly
25
Q

What are some factors that influence metabolic reponse to exercise?

A
  • Type of exercise
  • Intensity and duration of exercise
  • Physical condition + nutritional state of individual
26
Q

What are some sources of ATP for muscles during exercise?

A
  • ATP (~2 secs)
  • Creatine phosphate: rapidly replenish ATP (~5secs)
  • ATP supplied thru glycolysis + oxidative phosphorylation
27
Q

Sources of fuel during exercise

A
  • Glycogen (intensive exercise last ~2mins)
  • Blood glucose: Increase in BG through glycogenolysis and gluconeogenesis
  • Lactate: recycled through Cori cycle in liver
  • F.A: only in aerobic condition
    i) slow release
    ii) limited carrying capacity due to mitochondrial membrane (carnitine shuttle)
    iii) Low rate of ATP production but sustained production
28
Q

Desc. energy metabolism in 100m sprint

(short high intensity)

A
  • X deliver suff. O2 to muscles
  • After creatine phosphate depleted–> anaerobic respiration –> lactate –> build up in H+ –> fatigue
  • Glycogen
29
Q

Desc. energy metabolism in 1500m sprint

medium intensity

A
  • Deliver some O2 to muscles (~40% anaerobic)
  • Initial phase: creatine phosphate and anaerobic glycogen metabolism
  • Long middle: ATP produced aerobically from glycogen
  • Final sprint: Anae. glycogen –> lactate
30
Q

Desc. energy metabolism in marathons

low intensity, long duration

A
  • 95% aerobic
  • Liver glycogen
  • Muscle glycogen (deplete in a few mins)
  • F.A (utilisation rise steadily)
31
Q

What is the effect of prolonged exercise to hormones?

A
  • Insulin falls slowly
  • Glucagon ⬆️:
    i) ⬆️glycogenolysis (glycogen phosphorylase)
    ii) ⬆️gluconeogenesis (PEPCK, fructose 1,6 bisphophatase)
    iii) ⬆️lipolysis (Lipase)
  • Adrenaline⬆️ :⬆️glycogenolysis, lipolysis,
  • GH ⬆️: ⬆️lipolysis, gluconeogenesis
  • Cortisol ⬆️: ⬆️lipolysis & gluconeogenesis
32
Q

What are some benefits of exercise?

A
  • *Body comp. change (⬆️muscle, ⬇️fat)
  • *Glucose tolerance ⬆️
  • *Insulin sensitivity ⬆️
  • *TAG ⬇️ (HDL⬆️, VLDL &LDL ⬇️)
  • *BP ⬇️
  • Feel good
  • important for D.M
33
Q

Where and why is vitamin D converted to 25-hydroxyvitamin D?
Extra: Half life of calcitriol?

A
  • Liver
  • Has longer half life (2 weeks)
  • Calcitriol is a few hours

MEH Sem 1 (18 decks)

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