11.2 - Metabolic And Endocrine Control During Special Circumstances Flashcards
What fuel sources are normally available in the blood and available under special conditions?
Normally
- glucose
- fatty acids (except in RBC, brain and CNS)
Special conditions
- amino acids from muscle mass, converted to glucose or ketone bodies
- ketone bodies from fatty acids, used when glucose short as brain can use it
- lactate, made in anaerobic metabolism in body
What happening 2 hours after feeding?
Immediate metabolism supported by glucose
Speed up growth and repair process
Make glycogen as rapidly as possible
Increase fat stores
What happens 2-10 hours after feeding?
Glucose and fats no longer being absorbed
Maintain blood glucose by drawing on glycogen stores
Support other metabolic activity with fatty acids released from stores
Preserve blood glucose for brain
What happens 8-10 hours after feeding?
Glycogen stores depleted = need to make more glucose
Continue to support metabolism with fatty acids
What happens during starvation?
Need to reduce protein breakdown
Fatty acid metabolism produces ketone bodies
Brain becomes able to metabolise ketone bodies = reduces need for glucose.
What do anabolic hormones do?
Promote fuel storage e.g insulin
Lack of insulin = catabolic state
What do catabolic hormones do?
Promote release from stores and utilisation
E.g glucagon, adrenaline, cortisol, growth hormone and thyroid hormone
What does insulin stop and promote?
Stop
- gluconeogenesis
- glycogenolysis
- lipolysis
- ketogenesis
- proteolysis
Go
- GLUT4 transporter for muscle uptake
- glycolysis
- glycogen synthesis
- protein synthesis
What does feeding promote?
Amino acid uptake and protein synthesis in liver and muscle
Promotes lipogenesis and storage. Of fatty acids as triacylglycerol in adipose
What do you get from fasting?
Glycogenolysis
Lipolysis
Gluconeogenesis - glycerol from fat provided. Kidney also starts doing this also.
Cortisol is released which prevents most cells from using glucose and fatty acids are preferentially metabolised.
Liver starts making ketone bodies and brain starts to utilise these sparing glucose requirement from protein
What are the two main phases of metabolic adaptation during pregnancy?
Anabolic
- early pregnancy
- increase in maternal fat stores and small increase in insulin sensitivity
- nutrients stored to meet futur demands of rapid foetal growth
Catabolic
- late pregnancy
- decreased insulin sensitivity (increased resistance)
- tissues use fatty acids to save glucose
- increased resistance to insulin = increase maternal glucose and free fatty acid conc
- allows greater substrate availability for foetal growth.
What’s the fetoplacental unit?
Placenta, fetal adrenal glands and fetal liver make an endocrine entity called the fetoplacental unit
What hormones does the placenta release to control the maternal hypothalamic pituitary axis?
Hypothalamic
- CRH
- GnRH
- TRH
- GHRH
Pituitary like
- ACTH
- Human chorionic gonadotropin
- human chorion thyrotropi
- human placental lactogen
What happens to insulin levels in the second half of pregnancy?
Maternal insulin increases
Anti insulin hormones increases at a faster rate
Therefore the insulin/anti insulin ratio falls
Cells therefore have decreased insulin sensitivity
What are anti insulin hormones?
cause transient hyperglycaemia after meals because Of increased insulin resistance
Hypoglycaemia can occur between meals and at night because of the continuous fetal draw of Glucose
NB: maternal ant pit becomes desensitised to CRH so more ACTH and cortisol is around
Whats insulin secretion like in pregnancy?
Increased appetite = more glucose in ingested
Oestrogen and progesterone increase sensitivity of maternal pancreatic B cells to blood glucose
- B cell hyperplasia
- B cell hypertrophy
Leads to increased insulin synthesis and secretion
If B cells don’t respond normally, blood glucose may become seriously high and gestational diabetes may develop
What are the underlying causes of gestational diabetes?
1) autoantibodies similar to those characteristic of type 1 DM
2) genetic susceptibility to maturity onset of diabeties
3) B cell dysfunction in setting of obesity and chronic insulin resistance
What are the clinical implications of gestational diabetes?
- Increased incidence of miscarriage
- Incidence of congenital malformation is 4x higher
- Fetal macrosomia (large body) = could get shoulder dystopia (shoulder gets stuck during birth)
- Associated with gestational hypertension and preeclampsia
- risk minimised if diagnosed and managed
What makes someone more at risk of gestational diabeties?
Higher insulin resistance before pregnancy
Also age as fat to lean body mass ratio increases and insulin resistance increases with age (over 25)
BMI over 25 kg/m2
More common in Asians, black and Hispanic groups
If you have gestational diabetes during pregnancy will probably develop type 2 later in life.
What’s the management for gestational diabeties?
Dietary modification
Insulin injections if persistent hyperglycaemia
Regular ultrasound scans to asses fetal growth
What metabolic responses occur during excersise?
Increased energy demands met by mobilisation of energy stores
Glucose supply to brain maintain
End products of metabolism are removed asap
How are atp stores replenished in exercise ?
Muscle creatine phosphate stores rapidly replenish
Glycolysis supplied atp - 2 per glucose
- using muscle glycogen in intensive excersise that’s anaerobic
- oxygen can be supplied from complete oxidation of glucose and glycogen stores from muscle and liver in long excersise e.g jogging
Oxidative phosphorylation - but needs oxygen
What’s the role of the liver in blood glucose conc?
Excersise increases hepatic blood glucose production through glycogenolysis and gluconeogenesis
Liver recycles lactate produced by anaerobic metabolism
Rate of glucose production from liver is insufficient to meet full demands,
Needs to be maintained for brain
EXTRA
Muscle takes glucose from GLUT4 from insulin and GLUT 1 (always active )
Excersise also have insulin independant process of glucose uptake
How are fatty acids used as fuel?
In aerobic conditions
- slow release from adipose tissue
- limited carrying capacity in blood
- capacity limited by uptake across mitochondrial membrane
Low rate of atp production but high capacity for sustained production
How is energy produced in a sprint?
Anaerobic respiration and muscle store of glycogen , helps to spare blood glucose for brain
How is energy used in 1500 m distance race?
Three phases
- initially creatine phosphate and anaerobic glycogen metabolism
- long middle phase in which ATP is made aerobically from muscle glycogen
- anaerobic metabolism of glycogen and produce lactate
How is energy made in a marathon?
Aerobic mainly, uses muscle and liver glycogen and fatty acids
Insulin levels slowly fall
Glucagon Levels rise and do their thing
Adrenaline for glycogenolysis and lipolysis and more growth hormone for lipolysis and gluconeogenesis
Cortisol rises slowly for lipolysis and gluconeogenesis
What are the benefits of excersise?
- less adipose more muscle
- glucose tolerance improves
- more insulin sensitive tissues
- less blood triglycerides
- blood pressure falls
- psychological effects
