MEH: Metabolic & Endocrine Control During Special Circumstances Flashcards
(31 cards)
What are the major metabolic fuels and their sources in the normal individual
Normally available in the blood:
- glucose (preferred fuel source)
- fatty acids
Fatty acids are an example of a metabolic fuel normally available in the blood. Which cells can use
Can be used as fuel by most cells except red blood cells, brain and CNS
Which fuel sources are available under special conditions
Amino acids: converted to glucose or ketone bodies
Ketone bodies: mainly from fatty acids, used when glucose is critically short
Lactate: liver can convert back to glucose via the Cori Cycle or can be utilised as fuel source for TCA cycle in other tissues
What are the main energy stores
Glycogen (about 400g stored in liver and muscle)
Fat (TAG in adipose tissue, about 10-15 kg)
Muscle protein (about 6 kg, used in emergency)
Describe the process of feeding to starvation
1) feeding
2) glucose available from the gut for up to 2 hours. Immediate metabolism supported by glucose, making glycogen as quickly as possible and increasing fat stores.
3) from 2-10 hours, glucose and fats are no longer being absorbed. Blood glucose maintained by glycogen and fatty acids support other metabolic activity
4) no food for 8-10 hours, glycogen stores are depleted. Need to make more glucose for the brain via gluconeogenesis
5) starvation: fatty acid metabolism produces ketone bodies and brain becomes able to metabolise ketone bodies
What are the 2 anabolic hormones
Promotes fuel and storage
- insulin
- growth hormone
Give 2 catabolic hormones
Promotes release from stores and utilisation
- glucagon
- adrenaline
- cortisol
- GH
- thyroid hormones
Insulin. What processes are inhibited (5) and what processes are stimulated. (4)?
Inhibited: gluconeogenesis, glycogenolysis, lipolysis, ketogenesis, proteolysis
Stimulated: glucose uptake in muscle and adipose via GLUT 4, glycolysis, glycogen synthesis, protein synthesis
Effects of feeding (4)
Increase in blood glucose
Pancreatic beta cells release insulin
Promote glucose uptake (GLUT4)
Promotes storage of glucose as glycogen in liver and muscle
Promotes amino acid uptake and protein synthesis in liver and muscle
Promotes lipogenesis and storage of fatty acids as TAG in adipose tissue
Effects of fasting (5)
Blood glucose falls and insulin secretion depressed
Reduces uptake of glucose by adipose and muscle
Glucagon released which stimulates: glycogenolysis in liver, lipolysis in adipose tissue & gluconeogenesis
Effects of energy starvation (6)
Reduction of blood glucose stimulates release of cortisol in adrenal glands and glucagon from pancreas
Stimulates gluconeogenesis and breakdown of protein and fat
Reduction in insulin and anti-insulin effects of cortisol prevent most cells from using glucose and fatty acids are preferentially metabolised
Ketone bodies produced by liver
Kidneys contribute to gluconeogenesis,
Deplete fat stores, protein used as fuel
Complications of refereeing syndrome
Urea cycle has been down regulated so if you give lots of protein, ammonia toxicity will occur
Hypophosphataemia (rapid kickstart of metabolic pathways… needs phosphate… low phosphate already due to starvation)
When does 2/3rds of fetal growth occur
Last trimester
Mother’s net weight gain by end of pregnancy
8kg
Out of the 8kg weight gain, how much is maternal fuel stores and how much is foetus
Maternal fuel stores: 3kg
Foetus: 3.5 kg
Two main phases of pregnancy
1) anabolic phase: increase in maternal fat stores, increase in insulin sensitivity, nutrients stored
2) catabolic phase: decreased insulin sensitivity (maternal insulin levels continue to increase but the production of anti insulin hormones by fetal placental unit increases at an even faster rate and the insulin/anti-insulin ratio therefore falls), increase in maternal glucose and free fatty acid concentration therefore allows for greater substrate availability for foetus. Transient hyperglycaemia after meals due to anti insulin hormones (corticotropin releasing hormones), reducing maternal utilisation of glucose by switching tissues to use of fatty acids
Placental transfer
Most substances transfer by simple diffusion down concentration gradient
Glucose in principal fuel for fetus and transfer facilitated by transporters (GLUT1)
The placenta, fetal adrenal glands and fetal liver constitute a new endocrine entity known as
Fetoplacental unit
Placenta secretes a wide range of proteins that can control the maternal hypothalamic pituitary axis
HYPOTHALAMIC LIKE RELEASING HORMONES:
CRH, GnRH, TRH, GHRH
Pituitary like hormones: ACTH, hCG, cCT, hPL
Important placental steroid hormones include:
Progesterone and oestriol
What are the anti insulin hormones produced in placenta
Corticotropin releasing hormone resulting in increased in ACTH and cortisol
Results in transient hyperglycaemia after meals because of increased insulin resistance
Also, human placental lactose and progesterone
How does gestational diabetes occur
Oestrogens and progesterone increase sensitivity of maternal pancreatic beta cells to blood glucose therefore increased insulin synthesis and secretion
If beta cells do not respond normally, blood glucose elevates and it occurs
gestational diabetes: pancreatic beta cells do not produce sufficient insulin to meet increased requirement in late pregnancy.
Give 3 known underlying causes and 3 complications
Autoantibodies similar to those of Type 1 DM, genetic susceptibility, in setting of obesity and chronic insulin resistance
Increased risk of miscarriage, congenital malformation, fetal macrosomia (—> shoulder dystocia), gestational hypertension, pre-eclampsia
Risk factors of gestational diabetes
Family history of gestational diabetes Family history of macrosomia Race/ethnicity: more common in Asian, black and Hispanic ethnic groups Maternal age of older than 25 BMI higher than 25
How to manage gestational diabetes
Diet modification, maybe caloric reduction in obese patients
Insulin injections if persistent hyperglycaemia
Regular ultrasounds to check fetal growth and wellbeing
