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38 Cards in this Set
- Front
- Back
1. In the fed state, what is the fate of dietary carbohydrates?
Three steps... |
1. Cleaved during digestion
2. Form monosaccharides and absorbed into blood 3. Glucose may be oxidized for energy or stored as glycogen in liver/muscles |
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2. What happens to excess glucose in liver during the fed state?
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Converted to triglycerides
Triglycerides are are packaged in very-low density lipoproteins (VLDL) and released into blood VLDL are mainly stored in adipose tissue |
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3. What is the fate of dietary fats (triglycerides) in the fed state?
Three steps... |
1. Digested to fatty acids and 2-monoglycerides
2. Intestinal epithelial cells resynthesize 2-monoglycerides to triglycerides 3. Packaged into chlyomicrons and secreted into blood *FA in chlyomicrons are mainly stored in adipose tissue |
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4. What is the fate of dietary proteins in the fed state?
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1. Digested to amino acids
2. AA used to synthesize new proteins and N-containing compounds |
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5. In the fed state, what does the rapid rise in glucose stimulate?
What does this inturn stimulate? |
Release of insulin from β-cells of pancreas
1. Stimulate uptake of glucose by responsive tissues (skeletal and adipose cells) 2. Storage of glucose as glycogen in liver/muscles 3. Synthesis and storage of FA in adipose cells 4. Synthesis of proteins |
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6. In the fed state which hormone levels is decreased?
What signals to the brain to end a meal? |
Glucagon
Neuroendocrine cells in intestine feed back to brain to slow down digestions |
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7. Where does absorption mainly occur?
What is each dietary component broken down into? |
Intestine
Carbs -> glucose Fat -> chylomicrons *lipase breaks down fats Protein -> AA |
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8. How does the glucose affect hormone levels in the blood?
Where does the glucose go? |
Increase Insulin
Decrease Glucogon 1. Liver -store as glycogen -acetyl CoA 2. Brain -acetyl CoA for TCA cycle -brain primarily depends on glucose for energy 3. RBC -pyruvate 4. Muscle -store as glycogen -acetyl CoA into TCA cycle 5. Adipose -TG |
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9. What can happen to the glucose in the liver once it become acetyl CoA?
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1. Enter TCA cycle
-produce ATP 2. Convert to TG -absorbed in blood as VLDL -VLDL combine w/ FA and glycerol to reform TG stored in adipose tissue |
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10. When will you store glucose as glycogen?
What is chylomicrons and when are they elevated? When is VLDL formed? |
Only in presence of high insulin levels
Dietary fats and elevated if had high fat diet VLDL comes from high levels of carbs |
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11. What happens to the AA from protein?
To form TG what is needed? |
Travel to tissues where can..
-resynthesize proteins -incorporate into important compounds -enter TCA cycle Need glucose and insulin present Also need glycerol C backbone which comes from glucose |
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12. What is hypoglycemia?
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Low blood glucose
Go unconscious |
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13. Following a meal, what happens to blood glucose levels?
What happens to insulin and glucagon levels? What does this result in? |
Decrease
-2 hrs after eating these levels return near the fasting range Serum levels of insuling fall and levels of glucagon rise Glucagon stimulates release of stored fuels *liver supplies glucose and ketone bodies |
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14. How are blood glucose levels maintained?
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By liver
Initially by breaking down glycogen (glycogenolysis) Then by gluconeogensis -glucose is synthesized from non carbohydrate compounds |
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15. How are ketone bodies synthesized?
What happens to adipose triglycerides (TG) during the basal state? |
In liver from FA
Metabolized to free FA and glycerol in fat cells *glycerol serves as source of C from gluconeogensis |
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16. What happens to muscles in the basal state?
What happens to the AA? What happens to released N? |
Proteolyzed resulting in release of AA
Used as carbon source for gluconeogensis Released N is converted into urea |
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17. How can tissues reproduce glucose?
Where does the glucose from the liver go? What happens to the lactate produced via RBC? |
Cori cycle
1. Brain (still uses glucose as main energy source) 2. RBC (still need glucose to derive energy) Go back to liver where used to remake glucose |
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18. What happens to adipose tissue during the fasting state?
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Break down stored TG into FA
*Derive more energy from FA than from glycerol FA can go to.... 1. Liver -acetyl CoA into KB which go to muscles to regenerate acetyl CoA for TCA cycle 2. Muscle -FA into acetyl CoA for TCA cycle |
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19. What does low levels of glucose increase?
What happens first when glucose levels drop? When does gluconeogensis occur? |
Epinephrine, growth hormone, cortisol, and glucagon
Glycogenolysis 6 hrs after eating |
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20. When does the starved state occur?
What happens in the starved state? |
When fasting occurs for 3 or more days
Body undergoes changes in fuel utilization and mobilization |
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21. In the starved state, what happens to muscles?
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Continues to oxidize FA, which remain elevated
Decreases it utilization of ketone bodies -rise in ketone body concentration in blood |
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22. What does the rise in ketone body concentration result in?
What happens as a result of the brain reducing its glucose requirement? |
Reaches a level where brain can reduce requirement for glucose and oxidize ketones for energy
Slows the rate gluconeogensis and reduces need to break down protein supply to AA **spares muscles and reduce urea production |
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23. What is the initial source of AA for gluconeogensis during the starved state?
How is the BMR during the first few days of starvation? What is this a result of? As starvation continues what happens to the BMR and why? |
Protein in liver and other visceral tissues (not skeletal muscles)
Increased Due to increased release of catecholamines and high rate of gluconeogensis Drops due to declining levels of thyroid hormone (T3) |
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24. What is an important pro-survival hormone during starvation?
What does it play a critical role in preventing? |
Glucocorticoid cortisol
Hypoglycemia-induced death |
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25. Do you still break down fat in the starved state?
Does muscle demand energy in the starved state? How is proteolysis affected in the starved state? What does this result in? |
Yes, esp b/c want to increase KB concentration
No b/c not exercising Decreases b/c brain requires less energy from glucose (use KB) Less urea (so can save water as well) |
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26. There is a strong relationship between obesity and what 15 medical conditions?
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1. Arthritis
2. Birth defects 3. Cancer 4. Cardiovascular disease 5. Carpal tunnel syndrome 6. Hypertension 7. Gall Bladder disease |
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27. There is a strong relationship between obesity and what 15 medical conditions?
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8. Obstetric and Gyno complications
9. Lower back pain 10. Pancreatitis 11. Sleep apnea 12. Stroke 13. Urinary stress incontinence |
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28. What characterized metabolic syndrome?
Four things... |
1. Hypertension
2. Central obesity 3. Insulin resistance 4. Dyslipidemia |
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29. Weight loss of about what percent can reduce which obesity related medical conditions?
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10% of body weight
Diabetes and hypertensions |
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30. What are 3 things that adipose cells are responsible for?
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1. Secretion of polypeptide hormones that participate in maintenance of body weight
2. Regulation of metabolism 3. Appetite |
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31. What is visceral fat deposits highly correlated with?
Six things.... |
1. Metabolic syndrome
2. Insulin resistance 3. Glucose tolerance 4. Dyslipidemia 5. Hypertension 6. Coronary artery disease *biochemical characteristics of visceral obesity and subcutaneous obesity differ |
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32. Hormones released from where play a role in maintaining appetite/homeostasis?
How do they do this? |
GI tract and adipose tissue
Signal to different neurons in brain These neurons regulate food intake and energy expenditure Hormones signal... -when it's time to eat -when consumed enough food -when feeding should cease |
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33. What produces leptin?
What does it regulate? What does leptin levels correlate with? How does this work? |
Adipsoe cells
Signals to brain to regulate food intake *how regulate weight over life span Correlates with body fat mass Decrease in body fat --> decrease in leptin levels --> stimulate food intake |
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34. What are leptin levels like in an obese individual?
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They are leptin resistant
*similar to type II insulin resistance diabetes Have higher than normal circulating levels of the hormone |
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35. Where is ghrelin released from?
What does it signal the body to do? When do they rise? What do they stimulate? |
Stomach
Eat Rise immediately before a meal Signal hypothalamic appeptite-stimulating neurons |
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36. Where is peptide YY released from and what does it do?
Where is cholecytokin release from and what does it do? |
Small bowel and colon
-signal satiety Small intestine -slows down digestion and release of stomach content -stimulated by fat and protein -short term appetite depressor |
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37. What appetite regulatory hormones does the hypothalamus release?
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1. NPY/AGrb
-stimulate appetite 2. POMC -decrease appetite **both affected by adiposity signals |
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38. To loos 1 lbs how many more kcal must you expend than you consume?
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3500 kcal
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