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Final

NUTR 4210 Final: NUTR Final Notes
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by Emily
20 Pages
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Department
Nutrition
Course Code
NUTR 4210
Professor
Lindsay Robinson

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NUTR*4210
Nutrition, Exercise and Energy Metabolism
Table of Contents
Obesity 2
Insulin Resistance & Type II Diabetes 2
1. Uptake 3
2. Storage of Lipids 4
Weight Loss 5
What happens to adipose tissue in obesity? 7
Leptin = “thin” in Greek 7
Adiponectin 8
TNF-alpha 9
IL-6 10
Aging 11
Sarcopenia 11
Sarcopenic Obesity 13
Implicated Factors 13
Summary: 14
Treatment 14
Cancer 15
Cancer Cachexia 16
TX Strategies 18
Physical Activity & Cancer 19
Cancer-Related Fatigue 20
PUFA n-3 20
1
Obesity
Peripheral Obesity: SubQ fat; excess below the waist; not a major health risk factor"
Central (Abdominal) Obesity: Excess visceral fat around stomach & waist; very strong
indicator of health risk! "
Visceral Fat
-visceral fat is best quantified by MRI, CT scans, but $$$"
-waist circumference = easiest clinical measure to predict visceral fat stores"
-independent predictor of all-cause mortality in men"
-associated with insulin resistance"
a consequence of defects in insulin signalling that leads to impaired GLUT4
translocation to the membrane"
leads to reduced insulin-stimulated glucose uptake into skeletal muscle"
Insulin Resistance & Type II Diabetes
-Fasting hyperglycaemia: >7 mM (indicative of type II diabetes)"
-Increased, normal or low [ ] of insulin — depending on stage of development"
-Insulin resistance & type II diabetes can be assessed by:"
Oral Glucose Tolerance Test (OGTT)"
Euglycemic/Hyperinsulinemic Clamp "
OGTT
-measures acute metabolic response to glucose ingesting at the whole body level "
-Method: 75g oral glucose test"
-Diagnostic Criteria at2 hours after the drink:"
7.8 mM = impaired glucose tolerance 11.1 mM = type II diabetes "
However, with this test, both lean and obese
individuals respond in the same way! The
glucose data looks pretty good and are not in
the range of impaired glucose tolerance or type
II diabetes"
This test is done clinically and often only
glucose is measured - the doctor has no idea
that the insulin response levels are much
greater (compared to a lean individual) in order
to have a similar glucose curve"
the pancreas secretes a lot of insulin into the
blood and are nowhere close to returning to
baseline at the end of the test"
Hyperinsulinemic Euglycemic Clamp
-the “gold standard” to measure whole body
insulin sensitivity; measures responsiveness to
insulin but used in research ($$$)"
2
Time (min)
-30 060 75 90 120 150 180
Glucose (mM)
3
4
5
6
7
8
Lean
Obese
Diagnostic criteria at 2 hours
after glucose drink:
Ø7.8 mM = impaired glucose tolerance
Ø11.1 mM = type 2 diabetes
Time (min)
-30 060 75 90 120 150 180
Insulin (uIU/ml)
0
20
40
60
80
100
120
140 Lean
Obese
What about insulin?
Which insulin response
would you rather have?
-Raise insulin levels via infusion to supra-physiological levels"
-monitor glucose infusion required to maintain normal/steady blood glucose levels;
check blood glucose every 5-10 minutes"
-High glucose infusion rate (GIR) 7.5 mg/min = insulin sensitive "
-Low GIR: 4.0 mg/min = insulin resistance "
But contraction-stimulated glucose uptake is perfectly fine in obese rats! "
-contraction pool of GLUT-4 is still responsive"
-ATP turnover to induce AMPK activation can still
promote GLUT-4 translocated in obesity/diabetes'
Insulin stimulated glucose transport is impaired, but
contraction simulated glucose transport is not! "
-Fat cells secrete adipokines that induce insulin resistance"
-increased lipolysis leads to increased plasma free fatty acids "
-elevated plasma free fatty acids —> can induce insulin resistance in only 4-6 hours!"
1. Uptake
-Increased fatty acid uptake in type II diabetes! "
-due to redistribution of FAT/CD36 to the plasma membrane"
there is MORE FAT/CD36 on the plasma membrane'
Note: there is the same amount of FAT/CD36 content "
3
BUT contraction-stimulated glucose uptake is
perfectly fine in obese rats!
Contraction pool of GLUT-4 is still responsive!
ATP turnover to induce AMPK activation can still promote GLUT-4
translocation in obesity/diabetes
Solid black bars
= lean
Brozinick et al. JAP 1985
Different muscle types
Take home point: insulin stimulated glucose transport
is impaired, but contraction stimulated is not!
Plasma membrane GLUT-4
A measure
of plasma
membrane
GLUT-4
J
L
LJ
FAT/CD36 re-distribution to the plasma
membrane seems to be largest player
MORE
FAT/CD36 on
plasma
membrane
(corresponds
with large
increase in
uptake on the
previous slide)
Despite little to no
difference in
content of
FAT/CD36...
FAT/CD36 re-distribution to the plasma
membrane seems to be largest player
MORE
FAT/CD36 on
plasma
membrane
(corresponds
with large
increase in
uptake on the
previous slide)
Despite little to no
difference in
content of
FAT/CD36...

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Description
NUTR*4210 Nutrition, Exercise and Energy Metabolism Table of Contents Obesity 2 Insulin Resistance Type II Diabetes 2 1. Uptake 3 2. Storage of Lipids 4 Weight Loss 5 What happens to adipose tissue in obesity? 7 Leptin = thin in Greek 7 Adiponectin 8 TNFalpha 9 IL6 10 Aging 11 Sarcopenia 11 Sarcopenic Obesity 13 Implicated Factors 13 Summary: 14 Treatment 14 Cancer 15 Cancer Cachexia 16 TX Strategies 18 Physical Activity Cancer 19 CancerRelated Fatigue 20 PUFA n3 20 1
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