Lecture 14.5 - Fuel Sources Flashcards
What are some type of fuel sources normally available and available under special conditions?
Normal:
- Glucose: Little free glucose, More stored as glycogen
- F.A: Stored as TAG
Special:
- A.a: Muscle protein broken down–>ketone bodies
- Ketone bodies: From F.A
- Lactate: Anaerobic respiration –> converted back to glucose via Cori Cycle
What are the 3 diff. types of A.a that can be metabolised under special conditions?
- Glucogenic= Ala & Val
- Ketogenic = Lys & Leu
- Both = Tyr & Phe
What happens immediately after feeding (~2 hours)?
[Glucose & Fat available in gut]
- Immediate glucose metabolism for growth processes
- Glycogenesis, Lipogenesis
What happens when glucose & fats X longer absorbed in gut (~2-10 hours)?
- B.G maintained by breakdown of glycogen
- F.A released from stores
- Preserve glucose requirement for brain
What happens when X consume food for 8-10 hours/glycogen stores depleted?
- Gluconeogenesis –> glucose for brain
- F.A metabolism
What happens in starvation?
- F.A metabolism produces ketone bodies
- Brains become able to metabolise ketone bodies (⬇️need for glucose)
What are some anabolic hormones (build)?
- Insulin, GH (increase protein synthesis)
- Promote fuel storage
What are some catabolic hormones (destroy)?
- Promote release from stores and utilisation
- Glucagon, Adrenaline, Cortisol, GH (increase lipolysis & gluconeogenesis), T3,T4
What are the effects of feeding?
- Increase in BG –> pancreas secrete insulin
- Increase glucose uptake/storage/utilisation
- Promote a.a uptake + protein synthesis in liver
- Promote lipogenesis and storage
What are the effects of fasting?
- 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)
What are the effects of starvation?
- ⬆️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]
What is the net weight gain of mother by end of pregnancy?
8kg
Describe the two phases of metabolic adaptation during pregnancy.
- 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) - Catabolic state: Maternal metabolism adapts to meet increase fetal-placental unit
- ⬇️insulin sensitivity
- ⬆️maternal glucose and free F.A
How is glucose transported to fetus? Which carrier?
- Simple diffusion
- Through GLUT 1
*GLUT 2- Pancreas, GLUT 4- S.M
What is the new endocrine unit during pregnancy and what does it secrete?
*they have anti-insulin effects
- Foetal-placental unit
- CRH, Progesterone, Human placental lactogen
What happens to maternal metabolism during first ~20 weeks of pregnancy?
- 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
How are conc. of nutrients kept high in maternal blood in 2nd phase of pregnancy?
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
What do the anti-insulin hormones from fetal-placenta unit result in?
- Transient (short-term) hyperglycaemia after meals due to insulin resistance
- Hypoglycaemia can occur btw. meals
What does insulin secretion in pregnancy cause?
- ⬆️appetite –> ⬆️ glucose ingested
- Oestrogen and progesterone ⬆️ sensitivity of B-cells to insulin –> hypertrophy & hyperplasia
When does gestational diabetes occur? State some causes.
- 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]
What are some clinical implications of gestational diabetes?
N.B Risk of complications ⬇️ if managed and diagnosed
- ⬆️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
What are factors that increase risk of gestational diabetes?
- 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
What is the management of gestational diabetes?
- Dietary modification: ⬇️calories
- Insulin injection
- Regular ultrasound scans: assess fetal growth
What is the importance of the metabolic response during exercise?
- Meet increase energy demands by mobilisation of energy stores
- ⬇️disturbance to metabolic homeostasis: utilisation=mobilisation
- Brain supplied w glucose
- End products removed quickly
What are some factors that influence metabolic reponse to exercise?
- Type of exercise
- Intensity and duration of exercise
- Physical condition + nutritional state of individual
What are some sources of ATP for muscles during exercise?
- ATP (~2 secs)
- Creatine phosphate: rapidly replenish ATP (~5secs)
- ATP supplied thru glycolysis + oxidative phosphorylation
Sources of fuel during exercise
- 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
Desc. energy metabolism in 100m sprint
(short high intensity)
- X deliver suff. O2 to muscles
- After creatine phosphate depleted–> anaerobic respiration –> lactate –> build up in H+ –> fatigue
- Glycogen
Desc. energy metabolism in 1500m sprint
medium intensity
- 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
Desc. energy metabolism in marathons
low intensity, long duration
- 95% aerobic
- Liver glycogen
- Muscle glycogen (deplete in a few mins)
- F.A (utilisation rise steadily)
What is the effect of prolonged exercise to hormones?
- 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
What are some benefits of exercise?
- *Body comp. change (⬆️muscle, ⬇️fat)
- *Glucose tolerance ⬆️
- *Insulin sensitivity ⬆️
- *TAG ⬇️ (HDL⬆️, VLDL &LDL ⬇️)
- *BP ⬇️
- Feel good
- important for D.M
Where and why is vitamin D converted to 25-hydroxyvitamin D?
Extra: Half life of calcitriol?
- Liver
- Has longer half life (2 weeks)
- Calcitriol is a few hours
