Metabolism of Weight loss and Adaptations Flashcards
at rest which organs have the greatest % energy expenditure
brain, liver, skeletal muscle
fuels in a 75-kg man
adipose - 110,000
protein - 25,000 other + 25,000 muscle
carb- 2,000 muscle glycogen
liver glycogen - 400
free glucose - 80
weight of using 100 kcal of glycogen, protein and adipose tissue (explain the differences)
The main principle here is that glycogen is hydrophilic and therefore when 100kcal glycogen is spent, water is also lost ( so on the scale it will look like 100g is lost) whereas when 100kcal of adipose is used, 10 g will be lost- bc no water weight is lost (where does the water go?)
what are the 3 phases of blood glucose curve
uptake slope (1 hour), decay slope (1.5-3 hours) and steady phase (34 hours after)
lower insulin: glucagon is going to trigger?
steady phase in which increased glycogenolysis and gluconeogenesis
why do TG take longer to increase than glucose after a mixed meal ?
must be packed into CM, enter lymphatic system, give off TG into tissues, go to liver, repacked as VLDL- whereas glucose absorbed right into bloodstream from the gut
difference between FFA and TG response after a meal
TG slowly increase from the meal, FFA raise from lipolysis during higher glucagon and less insulin, when FA need to be used for gluconeogenesis ( they are NOT from meal )
why does glycerol decrease after a meal
bc lipolysis is decreased in response to insulin
- same kinda thing as FFA, we do not need gluconeogenesis with high insulin
- we see a slow increase after glycogen in excreted and insulin is lowered which will induce lipolysis
what happens to total amino acids after a meal
they are going to increase as they get transported into the blood, then insulin has a profound impact on the uptake of AA into tissues which will prompt protein synthesis, later once glucagon is secreted, and insulin is lowered, the proteolysis is no lower restricted and so AA would increase later on - gluconeogenesis
what happens to urea nitrogen after a meal
it will decrease, this is because the increase in amino acids result in protein synthesis and not the breakdown. may not nessasarily be a positive N balance bu the influx of aa will at least create a zero N balance
- later we see it may increase as proteolysis is induced
why do pre-diabetic/insulin resistance lead to hypoglycaemia
insulin resistance means insulin is still excreted in large amounts, just the cells are unresponsive. Therefore there is dysregulation of the negative feedback mechanisms, where the excess insulin secretion will promote smaller amounts of glucagon. so now less gluconeogenesis, glycogenolysis and lower blood glucose levels
is there such thing as glycogen resistance
yes
what dictates energy storage
insulin: glucagon storage
what causes fat storage
excess carbs + excess fat ( excess energy causes fat storage - not necessarily a function of high GI foods alone
- what about excess protein ??
what are the goals of adapting to fasting?
- reduce LBM breakdown ( spare protien)
- meet energy needs (REE will lower, become more efficient, less movement)
- glucose requirements
alanine cycle
pyruvate in muscle turns to alanine, gets transported in blood to liver, turned back to pyruvate–> gluconeogenesis
early fasting
2000kcal/24h
- gluconeogenesis
- glycogenolysis
- lipolyis (constant rate )
prolonged fasting
decrease EE by 500kcal
- 1500kcal/24 h
- liplysis (constant rate)
- no glycogen
- sparing effect - less gluconeogeneis from proteins - ketone bodies switch to being main fuel
- cori/alanine continues at the same rate
prolonged fasting
decrease EE by 500kcal
- 1500kcal/24 h
- lipolysis ( constant rate)
- no glycogen
- sparing effect - less glujconeogeneis from proteins - ketone bodies switch to being main fuel
- cori/alanine continues at the same rate
before ketones can be excreted they ned to be?
salted out which involves the loss of NA, K H, orNH4
what cation is preferred for ketone excretion
K , which can lead to hypokalemia
pro requirement
- 0 healthy
1. 0-1.2 for elderly adult
fluid requirements
100 ml/kg 1st 10
50ml/kg 2nd 10
20ml for ever kg after that
ex. 70 kg man
(10 x 100) + (50 x 10) + (20 x 50) = 2500ml
fluid based on energy
1ml/kcal
fluid balance based on urine output
urine output + 500mL/d
describe the prolonged total fasting weight loss curve
rapid weight loss at the beginning bc glycogen and protein stores are being used
- over time switch to fat ( no water, so less weight seen) lipolysis at a steady state
why does urea decrease with prolonged starvation and ammonia increase?
more ketone bodies are being excreted in the body , get salted out with ammonia. protein sparing effect, so less catabolism of protein, less proteolysis which means less urea
- overall less g of nitrogen are excreted bc less overall breakdown and intake of protein
- increase in ammonia also from gluconeogenesis in the kidneys
- glutamine into glucose
renal consequences of starving
- need normal kidney function
- ammonia is toxic so need more water
- acid/base balance changes in response to starvation need to be controlled by the kidney
describe the main idea behind the N intake, EE and N balance graph
This graph shows that for someone who EI=EE (1.0), as N intake increases, N retention increase and you will reach zero, you can see that it is possible to go into a positive nitrogen balance for a short time but it will eventually balance out to zero as body adjusts. we see that when someone is not meeting energy needs it takes longer for them to reach zero ( if ever) bc so much protein catabolism is taking place ( so much N excretion). in the same sense someone eating above E requirement, can reach a N balance faster ( with less pro intake) so a positive N balance can be seen even with low intake ( less excretion )
why in graph with reduction diets was N balance initially negative ?
on a energy restriction diet, the body was needing to use some protein so excreting a lot of N , and are not able to reach zero until body adjusts ( relies less on protein )
describe Forbes equation
relationship between the amount of body fat and the loss of LBM during dieting
- with higher body fat initially, we see less LBM loss: total weight
- whereas, if low body fat, will have more LBM loss
Forbes predictions 1:
during fast, obese individuals will lose less nitrogen ( hence less LBM) than thin ppl
Forbes prediction 2:
the fatter the subject the less LBM to Toal weight loss
what happens to the cardiovascular system with severe weight loss?
less cardio output, HR, BP increased tachycardia ( fast heart beat to compensate for low BP and low BV)
what happens to the immune system with severe weight loss?
less T-cell function/lympocytes
less cytokines
what happens to the renal system with severe weight loss?
acid/base stress on the kidneys
what happens to the GI system with severe weight loss?
less lipid absorption- ste-at-orr-hea (fatty stools)
what happens to the electrolytes with severe weight loss?
potassium losses - hypokalemia
why does steatorrhea occur during starvation?
decrease in villous SA due to atrophy ( gradually decline in effectiveness or vigor due to underuse or neglect ) - bc eating less, using system less - so less lipid absorption
why is there potassium loss with severe weight loss?
potassium is the main buffering agents during the excretion of ketoacids
- this casues hypokalemia
why would we never advise someone with impaired kidney function a severe weight loss diet
acid/base balance changes in response to starvation need to be controlled by the kidney
if not properly functioning - build up of keto acids, not properly excreted - toxic
acid/base stress on the kidneys
refeeding syndrome
metabolic complication associated with nutritional repletion
cause of referring syndrome
shift back to glucose instead of ketoacids
what does the shift back to glucose cause
rapid fluxes of insulin
rapid shift of electrolytes and anions and cations into intracellular space ( think sodium glucose linked transporters that are needed for uptake of glucose into the cells) so when lots of insulin - lots of glucose moving into the cell - lots of anions and cations moving into the cell
- this casues sodium and water retention ( anions moving into cell- water following )
which anion/cation is the biggest issue during the referring syndrome?
The hallmark biochemical feature of refeeding syndrome is hypophosphatemia, also referred to as refeeding hypophosphatemia (RH). … The combination of cellular uptake of phosphorus together with depletion of total body stores during starvation causes extracellular hypophosphatemia.
symptoms of referring syndrome ( mostly due to hypophosphatemia )
fatigue, weakness, arrhythmia, hemolysis, edema, dizziness, lethargy
how fast is onset of referring syndrome
fast ( first day of repletion )
what changes physiologically during repletion
ECF expansion - deem from increased Na intake and electrolyte imbalances ( this is why want to limit water and salt intake during referring )
ECF expansion
The sodium retention and extracellular fluid expansion together with thiamine deficiency can lead to congestive cardiac failure. excess carbs lead to the retention of sodium and water
glycogen synthesis during refeeding
may lower serum Po4 and K concentration
increased REE during refeeding
due to the reversal of starvation and LBM rebuilding and thermogenic effects of metabolizing food
physiological changes during repletion
- glycogen synth
- insuring secretion
- ECF expansion
- increased REE
steps in refeeding
- normalize fluid balance and electrolytes - PO4, K and Mg with supplements ( seperatee from food)
- limit sodium and water intake
- mixed diet- aim for 100-150g glucose to stop LB breakdown but start with 25% dose
- thaimine supplement
protein at 1.5-2 ( but start at 20g/day) - monster
why is thiamine so important in refeeding syndrome
cofactor for many anabolism mechanism - for production of ATP
PRO for refeeding
start with 20g/day but gradually increase to 1.5-2 g/kg/d
glucose for refeeding
aim for 150-200g/d but start with 25% dose
important supplements during refeeding
K, PO4, Mg, thiamine
physiological changes after diet induced weight loss that lead to increased energy storage
lowered FA oxidation, EE, thyroid hormones, increased cortisol
physiological changes after diet induced weight loss that lead to increased food intake
low leptin, PYY, amylin, insulin and raised gherkin and altered neural activity
how much does REE decrease per kg lost
15%
what lead to a decrease in EE during weight loss
15% REE
less PA
decrease in TEF
PYY _____ after weight loss
decreased ( it is an anorexigenic hormone that decreases hunger)
what did high fat/low carb diet resemble
metabolically similar to “fasting state”
describe high Fat vs high carb diet results
more severe weight loss initially with high fat (more water loss?), but net result was only a slight weight difference ( < 1kg)
effect of insulin on low fat vs low carb?
no effect- didn’t prevent baseline insulin
short term effects of keto
halitosis, muscle cramps, headache, weakness, rash,
long term effects of keto
ketoacidosis ( if illness also) elevated LDL renal stones thiamine def carotene def water sol vitamin def
