Metabolism of Weight Loss #2 Flashcards
Ketone bodies types, why they are made and how they are excreted
Acetoacetate and β-hydroxybutyrate
Produced due to overwhelming fatty acid oxidation
Used as brain fuel to reduce gluconeogenesis need (even after an overnight fast can read positive on a ketone stick and reduce appetite)
Excreted in urine and lungs as acetone
Health implications of ketone excretion
Requires “salting” by kidneys which involves loss of Na, K, H or NH4 (ideal loss)
K is the preferred ion excreted which increases risk of hypokalemia
Patterns for insulin, glucagon, I:G ratio, glucose, FA, ketones, lactate and alanine from fed state, post absorption (12hr), 3 day fast and 5 week starvation
Insulin rapid ↓ and then slow decrease
Glucagon steady increase and slight decrease in longterm starvation
I:G steady decrease from .5–.05
Glucose: steady decrease to half starting amount
FA: steady increase
Ketones: steady increase especially longer term
Lactate: rapid decrease then steady
Alanine: steady decrease
Why is weight loss faster at first?
Due to water loss which is bound with glycogen and LBM
Weight loss from fat is linear and cannot go faster
Urinary nitrogen constituents from normal to starving condition
Normal: High urea nitrogen, small amount of ammonia and other products
Starvation: minimal urea N, ammonia increases due to salting of ketone bodies and production of simultaneous bicarbonate
Acid-base balance changes during starvation due to ammonia production and requires more water for excretion
Relationship between energy intake and N balance
If you consume a diet below energy requirements the N balance will always be negative
If you consume adequate or above adequate energy intake, it was take less g of N to reach N balance
Ex. At 1.5x EI only require 4g of N intake to reach N balance, whereas 1x EI might require 7g N intake to reach N balance
Takeaway #1: difficult to maintain N balance during weight loss
Takeaway #2: weight loss should be accompanied by high protein consumption to reach N balance
Forbes equation
Shows change in LBM per change in weight (y axis) by body fat in kg (x axis)
Prediction I: during fast individuals with more fat mass will lose less N/LBM than thin people
Prediction II: The more fat mass the less LBM contribution to total weight loss during energy restriction
Physiological changes to severe weight loss
↓ CO/HR/BP (dehydration) and ↑ tachycardia (compensatory)
↑ stress on kidneys to maintain pH
↓ T-cell function
↓ lipid absorption/steatorrhea
↓ gastric/pancreatic/bile secretion/production
↓ villous SA
K loss due to LBM and intracellular loss
Change in CNS function
What is the cause and symptoms of refeeding syndrome?
Physiological response?
Cause: rapid flux of insulin in response to glucose availability, shift of intracellular electrolytes (PO4, K, Mg), sodium and water retention
Symptoms: fatigue, lethargy, dizziness, muscle weakness, arrhythmia (most dangerous), hemolysis and edema
Physiological response occurs rapidly:
ECF expansion (edema from ↑ Na)
Glycogen synthesis (lowers serum PO4/K)
↑ REE (LBM build)
↑ insulin (N retention), synthesis signals in fed state
Steps to refeeding properly
Go SLOW
1) Normalize fluid/electrolytes w/ PO4, K and Mg supplementation while limiting Na and fluid
2) Aim for 100-150g glucose but start at 25% of that to stop LBM ↓ + B1/multivitamin
3) Provide 1.5-2 g/kg current BW protein starting with 20g/day (adaptation period for urea cycle enzymes)
4) Monitor serum electrolytes, weight, intake and output
Physiological changes after diet-induced weight loss
Increase energy storage: ↓ EE, fat oxidation, thyroid hormones and ↑ cortisol
Increase food intake: ↓ leptin, PPY, amylin, insulin and ↑ ghrelin, appetite and altered neural activation
How much does energy expenditure change during weight loss?
REE ↓ ~15% per kg lost –> more than expected from changes in body weight/composition
PA usually decreases, as does TEF from lower EI
Appetite increases with hormonal adaptations (high ghrelin, low PPY), and improved food reward/palatability/olfaction
Very persistent adaptation 1+ years
Obesity energetics
More LBM in a more obese individual - weight loss lowers LBM and PA output
Measured RE is less than predicted REE leads to an energy gap of 200-250 kcal - likely from reduced sympathetic drive/thyroid/↓leptin
Response to exercise decreases as well - no ↑ in EE despite increased volume/intensity of training due to biomechanical efficiency
The biggest loser follow-up study
Metabolic adaptation increased from the end of the competition to 6 years later while RMR remained reduced (more than predicted) by 500 kcal
Increase adaptation not related to weight regain with no correlate between hormones/fasting metabolites and adaptation
Overall mean 12% weight loss and 57% maintain >10% weight loss
Macronutrient composition of weight loss diet
Excess energy intake, not macronutrient comp is main driver of weight gain
Low fat or low CHO makes no different (stat significant lower in low fat but not clinically relevant)
Higher protein diets offset REE by +150 kcal
Helps to maintain LBM and weight after loss
