Appetite and Weight Regulation

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Appetite and Weight Regulation
2013-12-19 08:16:23
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  1. 1. What % of people who lost weight eventually regain?

    2. define the short-term and long-term regulatory components of food intake?

    3. Draw model of short/long-term regulation of body weight (9)
    1. 90%

    2. Short-term signals stop and start of meal times. Long-term maintains body compartments over long intervals

  2. 1. What is ob protein? 

    2. Does it signal short-term or long-term?
    3. what experiment discovered its characteristics? 

    4. What were the characteristics? (2) Type of gene?

    5. What was missing in the ob/ob mouse that was in high amounts in the db/db mouse?

    6. What is activated by? (3)
    1. Weight regulatory protein secreted from adipocytes (leptin) cues satiety


    • 2. Long-term
    • 3. Parabiosis (sewing two mice together of diff phenotypes allowing them to share blood)
    • 4. Increased appetite + low energy expenditure --> obese. Autosomal recessive

    5. Ob protein aka satiety signal

    6. Activated by insulin, cortisol, and needs glucose as a substrate
  3. 1. Where is leptin expressed?
    2. When is it released?
    3. What accelerates its release from IC pool?
    4. What does it increase with? (2)
    5. What do the long-form and short-form receptors do?
    • 1. Adipose tissue
    • 2. Constituitively 
    • 3. Insulin
    • 4. Fat mass (number/size of adipocytes)
    • 5. Short-form mediates leptin transport in blood across tissue; long-form mediates weight regulatory influences (found exclusively hypothalamus)
  4. 1. What happens when you administer leptin to ob/ob mice? (3)

    2. WHat happens when you adminsiter leptin to humans?

    3. What is RQ? What does a higher number indicate?

    4. Where are leptin receptors located? (3) mainly where?

    5. What does lesioning lateral hypothalamus do? Why? (3) What does lesioning medial hypothalamus do?

    6. Where are energy expenditure and feeding signals received? What specifically signals it?

    7. Draw 2011 model of MCH, Orexin, Insulin/Leptin, etc. 

    Remember NPY/AgRP talk to Orexin and MCH too
    1. Decreased feeding in a dose-response manner both peripherally and centraly

    2. Nothing really

    3. RQ = respiratory quotient = carb oxidation/fat oxidation. Higher number means more carb oxidation

    4. Arcuate nucleus, PVN, and VMH. Mainly in ARC.

    5. Rapid onset of weight loss. Because Orexin A (intake) and B (sleep, arousal, reward) and MCH are released here. 

    Rapid onset of weight gain (destruction of satiety signals)

    6. PVN. ARC
  5. 1. What is NPY?
    2. Where is it expressed?
    3. What happens when you inject NPY into PVN?
    4. What is wrong with db/db mouse?
    • 1. Orexigenic neuropeptide 
    • 2. GGut, ARC, other areas
    • 3. Immediate hyperphagia --> obesity
    • 4. Mutated leptin receptor
  6. Draw feeding regulatory pathway of leptin and ghrelin
  7. 1. What do MC3R and MC4R do?

    2. What is an agonist for these receptors?
    3. What is the antagonist?
    4. What is the melanocortin feeding system a rare example of?
    5. What is the central regulator of feeding behavior in ARC?

    6. What is interesting about insulin?
    1. Activate EE and inhibit feeding

    • 2. A-MSH (increases it)
    • 3. AgRP (decreases it)
    • 4. Endogenous agonist and antagonist in same area
    • 5. Leptin

    6. Peripherally, insulin is an anabolic hormone. But centrally, it is catabolic (reduces food intake, stimulates thermogenesis)
  8. 1. What is leptin resistance?

    2. What can induce it? (2) Short-term? (1)

    3. Can leptin be used to control body weight?

    4. Where does leptin resistance occur? Why?

    1. Reduced responsiveness to the effects of leptin (feeding/EE) in comparison with lean controls 

    2. Increasing age and leptin system mutations; dietary obesity

    3. No, because obese people have high levels of leptin --> obese develop leptin resistance

    4. At BBB (1) leptin levels increase in response to high-fat diet but transport mechanisms are saturated - leptin levels in CNS of obese are same as those in lean (2) High-fat diet impairs transport mechanism

    (2) high-fat diet down-regulates long-form of leptin receptor 

    (3) Downregulation of receptor expression also inhibits secondary messenger signaling 

    All of this combines to form functional leptin resistance.
  9. 1. Does leptin resistance cause human obesity?

    2. What about administration of leptin to humans after weight loss? (5)
    1. Leptin has little/no weight regulatory function even at lean BW levels, so you can't claim that leptin resistance has anything to do with human obesity. Leptin resistance can occur at very low body weight level (humans' systems are more easily saturated)

    2. Improves satiation, EE with weight loss, neural activation to food stimuli, increase in skeletal muscle work efficiency, increase in Te and T4 hormone levels
  10. Short-term signals of satiety? 

    1. Preabsorptive? (1-2, 2-3)

    2. Absorptive? (1-2)
    3. Postabsorptive? (1-2)

    1. Direct vagal signals (stretch/nutrient receptors) and gut peptides acting locally/in brain (CCK, GLP-1, and PYY0

    2. Absorptive - nutrients to liver (glucoreceptors & energy receptors)

    3. Postabsorptive - nutrients to systemic tissues & brain (glucoreceptors/energy receptors)
  11. 1. What is CCK? Where is it from? What is it released into? What does it effect?

    2. What does it do? 

    3. What activates its release? What does it bind to? Where? 

    4. What does CCK signal to? 

    Draw CCK neural pathway
    1. Gut peptide released from mucosal cells lining doodenuma nd is released into enteric circulation. Neural.

    2. Releases pancreatic juice/bile, but also reduces feeding in rats in dose-response feeding. 

    3. By nutrients in the stomach. Binds to CCK-A receptors in pyloric sphincter. 

    4. Brainstem --< PVN --< VMH

  12. Describe regulation of CCK release (3)
    1. Food activates CCK - releasing factor, releasing CCK into enteric circulation

    2. Monitor peptide stimulates CCK-RF and pancreatic juice

    3. Pancreatic juice contains trypsin which digests monitor peptide and destroys CCK-RF simultaneously, shutting down CCk release
  13. 1. What is the glucostatic hypothesis?

    2. Does it explain why we initiate feeding? Why?

    3. What condition does glucoprivic feeding mimic?
    1. Significant hypoglycemia initiates feeding. 

    2. No ,because it only occurs when glucose levels are dangerously low. 

    3. Type 2 diabetes (insulin resistance)
  14. 1. What is ghrelin?

    2. Where is it expressed? Where was CCK expressed?

    3. What does it bind to? What inhibits its expression?

    4. What does it mainly do?

    5. What is the active form?
    1. Ghrelin is a circulating gastric peptide

    2. Expressed and secreted from gastric mucosa (stomach) whereas CCK was secreted from duodenum

    3. growth hormone secretagogue receptor (GHS-R) Nutrients in the stomach (opposite of CCK)

    4. Initiates feeding

    5. Acylated ghrelin
  15. 1. What happens to ghrelin after weight loss? What does this indicate?

    2. What happens after bypass surgery?

    3. How does ghrelin affect hunger? Neuro-wise

    4. What is unique about ghrelin?
    1. Increases, indicating that ghrelin adjusts to nutrient levels

    2. Leads to decreased circulating ghrelin despite weight loss

    3. Ghrelin activates NPY and AgRP release from those neurons in ARC (AgRP inhibits MC4 receptors) activating eating. 

    4. Ghrelin is one of the only GI peptides that stimulates feeding.
  16. 1. What happens when you give sucrose to rats long-term? 

    2. Can you reduce fat cell size?

    3. What is the usual role of LPL?

    4. What happens to LPL in weight loss? Conclusion?

    5. What happens when you treat rats with anti-adipocyte antibodies? 

    6. What do adipocytes do in response to calorie excess?
    • 1. Obesity via increased size & number of adipocytes
    • 2. Only surgically

    3. LDL hydrolyzes triglyercides in CM and VLDL allowing fatty acids to be stored in WAT.

    4. After weight loss, LPL levels have a huge increase (over 10x baseline levels) after a meal (same w/ response to insulin)

    During caloric restriction, LPL protects ability to store lipid in adipose tissue. Zucker rats actually sacrified lean mass to retain adipose tissue. 

    5. Increased lean mass while increasing body weight in general. 

    6. Enlarge then proliferate continuously
  17. 1. What is PKU caused by? (2)

    2. What does PKU cause? (2) Why?

    3. Treatment (2)

    4. What is the other defect? what can it lead to that's serious? What is the main organ affected? 

    5. Treatment? (3)
    1. Tyrosine hydroxylase def or tetrahydrobiopterine

    2. Neurological problems (bc low L-tyrosine, decreasing dopamine levels) and hypopigmentation - bc L-tyrosine is substrate for melanin. 

    3. B12 supplements decrease phenylalanine. Synthetic diet; low phenylalanine diet supplemented with tyrosine

    4. Tyrosinemia I/II (I is most common). Can lead to cancer. liver

    3. (1) Restriction of phenylalanine and tyrosine in diet but it's ineffective bc of buildup (2) liver transplant (3) NTBC - most effective
  18. 1. What regulates flux? (2)

    2. What can acetyl CoA be used for? (4)

    3. When do we want PDH to be on? (3)
    1. Substrate concentration (2) enzyme activity (allosteric, covalent, gene expression)

    2. Energy, cholesterol synthesis, ketone body synthesis, FA synthesis

    3. High energy (high NADH, ATP, and acetyl CoA)
  19. Good Summary
  20. 1. Where is MEOS located in cell? Organ?
    2. What kind of oxidase does it use?
    3. What does it upregulate?

    4. How does alcohol affect glucose metabolism? 

    5. symptoms of consuming alcohol? (2)

    6. Can RBCs do PPP? What can it do? (3)
    1. Smooth ER in liver

    2. Mixed function oxidase

    3. Ability to metabolize alcohol and other drugs. 

    4. Metabolism of alcohol greatly increases NADH in cell, causing pyruvate --> lactate and malate. Reduces GNG. Decreased OAA: acetyl CoA --> ketones. 

    5. Hypoglycemic and ketoacidotic. 

    6. yes, important for creating reduced glutathione to combat oxidative stress. (1) uses glucose only (2) non-oxidative (3) uses PPP to reduce glutathione.
  21. 1. Where are insulin receptors? (5)
    2. Where are glucagon receptors? (2)

    3. Where are epinephrine receptors? (5)

    4. Where are glucocorticoid receptors? (1)
    1. Liver, muscle, adipose, pancreas, others

    2. Liver, kidney

    3. Liver, muscle, heart, adipose tissue, brain

    4. Most tissues.
  22. 1. What is the precursor for catecholamines? (1)

    2. Name the catecholamines? (3)
    3. Where are they secreted from? Stimulated by? (5)

    4. Which affects insulin secretion? Why?

    5. What else do stressors activate? How is this regulated?
    1. Tyrosine

    2. Epinephrine, norepinephrine, dopamine

    3. Adrenal gland. Stimulated by stress, hypoxia, exercise, hypoglycemia, pain

    4. epinephrine bc it wants to increase glucose levels in the blood

    5. Stressors stimulate hypothalamus to release CRH (cortisol releasing hormone) --> pituitary gland (releases ACTH adrenal gland) --> release of cortisol.

    Cortisol feeds back to pituitary gland and hypothalamus to reduce CRH and ACTH release.
  23. 1. What effect do catecholamines have? (3)

    2. What do glucocorticoids do? (3)

    How are the following affected by insulin, glucagon? 

    1. Cell permeability to glucose
    2. Glycolysis
    3. Glycogen synthesis
    4. TG synthesis
    5. GNG
    6. Protein degradation
    7. Protein, DNA, RNA synthesis?

    What does epinephrine do? (7)
    1. (1) epinephrine decreases insulin secretion (2) increase of glucose secretion via GNG, glycogenolysis, HSL), (3) increases FA/glucose absorption by muscle

    2. Increase lipolysis, activate GNG/glycogen breakdown, and increase muscle breakdown

    Epinephrine increases cAMP levels, TG mobilization, glycogenolysis (decreases glycogen synthesis), increases glucose release from liver, increases blood glucose level, decreases glucose use by muscle). 

    Glucagon also activates cAMP levels
  24. 1. Why is WAT white?
    2. Roles? (2)
    3. Does gluacagon mediate metabolism in fat tissue?
    4. describe mechanism of fat breakdown
    • 1. Lack of mitochondria. 
    • 2. Stores excess energy, endocrine organ releasing adipokines
    • 3. Not really bc there aren't any glucagon receptors there. 

    • 4. 1. Epinephrine binds to B-adrenergic receptor
    • 2. Activates cAMP --> activates PKA
    • 3. PKA p'lates hormone sensitive lipase (HSL - DG) and Perilipin 1 releasing CGI58 --> ATGL (TG), MGL: MG --> glycerol + FA
  25. 1. Best way to produce weight loss?

    2. What does mit look like in WAT? Where else is this?

    3. Does BAT have fat?

    4. Describe process of activating BAT? (5)

    5. Where is smooth muscle used?
    1. Exercising at low temperatures. 

    2. Reticulum. Muscle. 

    3. Not really, mostly mitochondria. 

    4. Cold temp --> sympathetic nervous system --> adrenaline --> B-adrenergic receptor --> increased expression of UCP

    5. Mostly gastric motility
  26. 1. What is exercise essentially?

    2. Describe slow-twitch fibers? (5)

    3. Describe fast-twitch fibers? (5)

    4. Which would you use during sprinting vs. marathons?

    5. What is the only form of energy that muscle can use? 

    6. What does heart muscle generally use as fuel source?
    1. Skeletal muscle contractions - repeated formation of cross-bridges between myosin (thick) and actin (thin) filaments. 

    2. Slow-twitch: (1) type 1- slow oxidative fibers (2) lots of mitochondria (fat use) (3) enriched in myoglobin for oxygen (4) low glycogen content (5) develop force slowly but low fatigability

    3. OPPOSITE DONT GO OVER Fast-twitch (1) type2a/x - fast glycolytic fibers (2) few mitochondria (3) low myoglobin (4) high glycogen (5) develop force quickly but high fatiguability

    4. Type2 for sprinting, type 1 for marathons. 

    5. ATP

    6. Mostly fatty acids, but some glucose.
  27. 1. What controls CPT-1?

    2. What are the two different types of ACC and what do they do? 

    3. How does AMP affect glycogenolysis and glycolysis?

    4. What are 3 immediate energy sources?
    1. AMP activates it. High Ma CoA inhibits it

    High AMP --> activates AMPK --> inhibits malonyl CoA decarboxylase (MA CoA --> AC CoA) and ACC-2. No malonyl CoA means CPT-1 can run free. 

    2. ACC-1 (cytosol for fatty acid synthesis) and ACC-2 (close to mit membrane)  for inhibiting B-oxidation via CPT-1

    3.Adenylate kinase produces AMP (+ATP) --> activates AMP-dependent PK --> inhibiting ACC-2 and activating MCoA DC (to produce less malonyl). AMP also activates phosphorylase b in glycogenolysis and PFK-1

    4. Muscle ATP, muscle creatinine phosphate and muscle glycogen stores.