Physiology-Ingestive Behavior and Energy Balance

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Physiology-Ingestive Behavior and Energy Balance
2010-12-21 13:11:41

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  1. Glycogen
    • polysacchride stored in liver and muscle, part of the short term reserve
    • liver converts glucose into glycogen and stores it
  2. Glucagon
    • hormone secreted by the pancreas that promotes glycogen in the liver to convert to glucose
    • secreted when cells in the pancreas and brain detect a fall of glucose in the blood
  3. Ghrelin
    • peptide hormone released by the stomach that increases eating
    • also produced by neurons in the brain
    • activates orexigenic NPY neurons
    • dopaminergic neurons in the VTA contain ghrelin receptors
    • administration of ghrelin in rats increased activity of DA neurons and triggered release of activity in the NAc
  4. Hepatic Portal Vein
    brings blood from the intestines to the liver
  5. Vagus Nerve
    • connects the liver with the brain, brain recieves hunger signals via the vagus
    • makes its first central synapse in the medulla

    • dorsal= vagal afference
    • ventral= vagal efference

    • cut of dorsal root= 50% efference, NO afference
    • afferent lesion= no CCK detected
  6. Brown Adipose Tissue
    • Highly vascular
    • major contributor to heat production
    • innervated by the sympathetic nervous system
  7. Ways the body produces heat
    • Exercise associated thermogenesis (EAT)
    • non exercise (NEAT)
    • diet induced thermogenesis (DIT)
    • non shivering thermogenesis ex. BAT thermogenesis
    • shivering
  8. Uncoupling Protein
    • facilitates the conversion of nutrients into heat
    • expressed in brown adipose sites
    • may determine metabolic efficiency
  9. BLOT
    • enables scientist to know weight of a protein
    • each black blob is representative of the presence of a protein
  10. Bachman article
    • created a mouse with no beta-adrenergic receptor
    • when put into cold environment animals with no BAR has rapid decline in core temp.
    • uncoupling protein activity is dependent on beta receptor
  11. Nautiyal Paper
    • forebrain is surgically seperated= decerberate animal
    • animal and control are subjected to 3 ambient temps.
    • data supports: can adequately regulate core temp without forebrain
  12. Diet Induced Thermogenesis
    coined by Stock and Rothwell

    • experiment:
    • genetically lean and obese mice (hyperphagic)

    • lean mice:
    • -fed mouse chow
    • -fed cafeteria food= +food intake, + energy expenditure, no weight gain*

    • obese mice:
    • -fed mouse chow, intake amount is larger than lean mice
    • -fed caferia food= +intake, +weight, slight increase in energy expenditure
  13. GI signals
    preabsorptive: distention of stomach, nutrient detectors in upper intestine

    post absorptive: absorbed nutrients themselves or signals related to them

    • stomach= conveys volume
    • intestine= detects calories and nutrients
  14. Duodenum
    first part of the intestines

    • -contains afferent axons sensitive to presence of glucose, amino acids, and fatty acids
    • -contains chemoreceptors that transmit satiety signals
    • -secretes cholecystokinin (CCK) in the presence of fats
  15. PYY (peptide YY)
    • -produced by cells in the GI tract, released after a meal in amounts proportional to the amount of calories consumed
    • -satiety signal
  16. Leptin
    • a hormone secreted by adipose tissue
    • decreases food intake and increases metabolic rate
    • primarily inhibits NPY-secreting neurons in the arcuate nucleus of the hypothalamus
  17. NPY (neuropeptide Y)
    • a neurotransmitter that is part of the pathway activating MCH and orexin neurons of the lateral hypothalamus
    • extremely potent stimulator of food intake
    • neurons that secrete NPY are mainly found in the arcuate nucleus of the hypothalamus
    • activated by glucoprivation and ghrelin
  18. Cano Paper
    • BAT injected with virus
    • infected neurons identified with histochemistry
    • method highlighted the pathway of BAT output neurons
    • black, grey, white= 1st, 2nd, 3rd stage of infection
    • Raphe Palladus (RP) is one of the first to be infected
  19. White adipose tissue
    • storage depot
    • endrocrine organs- makes hormones, insulin and leptin
  20. Bachman paper
    • BAR (beta adrenergic receptor)
    • corresponding increase in leptin
    • metabolic rate evaluated by oxygen intake
    • no BAR= same cell shape of WAT and BAT
    • beta receptors are needed to have uncoupling protein
  21. Nautiyal Paper
    animals can control temp. from caudal regions

    • methods:
    • -control rats=sham surgery
    • -full decerberate rats
    • -both groups implanted with transponder to take
    • measurements
    • -used histology to verify complete transection in decerberate rats

    • Both groups exposed to temps:
    • -4C
    • -8C
    • -12C
    • HR, core temp., activity, and NE turn over were measured
  22. Nautiyal Paper Results
    • Core temp:
    • -control rats maintained 37C core temp during exposure
    • -CD rats showed gradual decrease in core temp. during 4C exposure
    • *did NOT show significant difference in 8C, 12C exposure

    • Heart Rate:
    • -control rats elevation during cold exposure correlated with the reduction in ambient temp
    • -CD rats not correlated with decreasing temp., HR elevation was equivalent in magnitude for each temp.
  23. NETO in Nautiyal Paper
    NETO in 4C: -CD rats showed significant increase in IWAT, RWAT, and IBAT but not heart in comparison to sham rats -this shows an overall increase in total body fat

    • Heart NETO- indicative of general sympathetic activity
    • -significantly increased by cold exposure in both groups to the same extent

    • IBAT NETO: increased in both groups
    • CD rats- increased 4x compared to sham group
  24. Conclusions for Nautiyal Paper
    • contributors of heat production and stability of core temp. by CD rats included:
    • -increased sympathetic drives to heart and IBAT
    • -elevated heart rate= increased IBAT blood flow that would facilitate the distribution of heat from IBAT thermogenesis

    • -reveals a range of energetic response compentencies and local caudal brain stem control of sympathetic outflows
    • -differences between CD and sham rats= thermoregulatory competence of the neutrally isolated brain stem is somewhat imcomplete
  25. Nakamura Paper
    • examined involvement of autonomic brain regions in sympathetic thermogenic responses in BAT to skin cooling in rats monitored by:
    • -BAT sympathetic nerve activity (SNA)
    • -BAT temp.
    • -metabolism (expired CO2)
    • -blood pressure
    • -heart rate
    • Examined the effect of chemical modulation of neurons with electrophysical activity
  26. Nakamura Paper results
    • Skin cooling: increases in:
    • - SNA 660%
    • -Tbat =.9C
    • -expired CO2=.4%
    • -HR 49bpm

    BUT Trec and Tbrain remained stable

    altered neuronal discharge in POa, DMH, RPa showed significant change in Tbat, HR, and expired CO2
  27. Nakamura Paper Conclusions
    • POa- GABAnergic transmission is critical for skin cooling-evoked stimulation of BAT thermogenesis
    • DMH- probably candidate for regions receiving a tonic inhibitory input from POa in the regulation of BAT thermogenesis
    • -decrease in skin cooling-evoked activity= DMH neurons are involved in the central mechanism for skin cooling-evoked thermogenesis in BAT
    • RPa- critical role of medullary raphe neurons in thermogenic responses to cold environments
    • -neurons in this region express Fos in response to cold exposure
    • -suppression of neuronal activity in raphe palledus nucleus= hypothermia in rats under normothermic conditions
  28. Kaplan Paper
    • affecting drop size, calories, etc. rats compensate to get usual amount of calories
    • D-fen: appetite supressant, effect seratonin


    • Experiment 1: rats w/ surgically implanted intraoral cannulas
    • -ingested 12.5% glucose
    • -D-fen or saline injected prior to each test, 2 conditions:
    • -delivered continuously
    • -interrupted for 10 mins. after 6 mins of infusion onset

    • Experiment 2: no surgery on rats
    • 2 groups= drop size 4mL/lick and 3 tests of 8 mL/lick
    • -group 2 received drop size test blocks is reverse order

    • -saline vehicle injected before 1st and 3rd tests of each block
    • d-Fen injected before 2nd test of each block

    • evaluated each conditon with 5 behavioral measures:
    • -licks per sec.
    • -ingestion rate mL/min
    • -meal duration
    • -first min. ingestion rate
    • -first min. licks
  29. Kaplan Conclusions
    only saw significant differences in first min. ingestion rate and licks between d-Fen and saline

    adjustment of # of licks based on drop size= intake effect doesn't depend on d-Fen's action on general motor performance
  30. Moran Paper
    • preabsorptive vs. postabsorptive signals
    • Hypthesis: caloric ingestion is regulated through a satiety mechanism

    • rats given 4 hr. feeding sessions and preloads 15 before feeding
    • preloads:
    • -balanced nutrients
    • -carbs.
    • -lipids
    • -protein
    • -saline

    calculated difference between saline and nutrient preloads

    • Results: every nutrient preload inhibits ingestion during meal
    • dose response relationship to caloric content of preload
  31. Moran Conclusions
    • Conclusion: taste, olfaction, and swallowing are not required for satiety
    • -rise in glucose is sufficient but not required for satiety
    • -satiety is an integration of several mechanisms:
    • -capacity to monitor caloric concentration
    • -gastric distention
    • *Satiety is the behavioral outcome of monitoring and controlling caloric ingestion
  32. Le Roux Paper
    • gastric bypass efficacy
    • gut hormones measured:
    • -PYY
    • -GLP-1
    • -Ghrelin
    • 1st Study:
    • 16 patients recieved laproscopic gastric bypass
    • plasma levels of gut hormones measured preoperatively and 2,4,7 and 42 days post operatively
    • visual analog scales (VAS) used to meaures hunger and fullness efore and after meals

    • Study 2: Good or Poor responders
    • 20 subjects chosen and best or worst responders to gastric bypass
    • plasma levels of gut hormones measured before and after 400 mixed calorie meal

    • Study 3: Pharmacologic inhibition of gut hormones release
    • 13 subjects given bypass or laproscopic banding
    • given either saline or somatostatin (blocks release of gut hormones)
    • meal served 60 min. after injection
    • plasma levels measured before and after injection
    • VAS measured
  33. Le Roux Results
    • Study 1:
    • day 2- increase in PYY and GLP-1
    • VAS- hunger=1/2
    • satiety= 2x
    • results continued through day 42

    • Study 3:
    • gastric bypass showed much larger increase in gut hormones compared to banding
    • somatastatin= 2x food intake for bypass patients
  34. Le Roux conclusions
    • bypass- levels of PYY and GLP-1 increased as soon as day 2 after operation
    • caused by surgery on stomach
    • inhibition of hormones= appetite recovery and normal eating behavior
    • patients who lost weight successfully=higher levels of gut hormones than those who lost less weight
  35. Huo Paper
    • leptin and control of food intake
    • showed leptic receptors in medial NTS
    • gastric distention regulation distention and leptin work together to reduce food intake
    • Neurons in the NTS are activated by gastric distention
    • active form of leptin= ObRb
    • exogenous admin. of leptin= reduction in meal size NOT frequency, mechanism is to magnify satiation signal during each meal
    • leptin receptors are found on neurons of NTS caudal brain stem
    • ObRb signaling localized to the mNTS subnucleus

    • Hypothesis: The same mNTS neurons might be activated both by leptin and GI afferent input
    • leptin signaling could potentiate the effectiveness of GI signals in suppression of F.I.

    • Experiment 1: Anatomical mapping of leptin responsive neurons in caudal brain stem
    • -injected with leptin or vehicle, anaesthetized
    • brains removed and examined PSTAT3 staining

    • Experiment 2: antomical analysis of cells in caudal brain stem activated by gastric distention and leptin
    • rats implanted with cannula and seperated in 4 groups:
    • -balloon distention and leptin
    • -sham distention and leptin
    • -balloon distention and PBS (vehicle)
    • -sham distention and vehicle

    • Experiment 3: behavioral effects by gastric distention AND/OR leptin injection
    • fasted for 15-17 hrs then received conditons:
    • -distention= balloon inflated w/ saline OR sham
    • -injection= leptin or vehicle
    • measured cumulative intake of food 30, 60, 90 min and 24 hrs. after initial access to chow
  36. Huo Paper Results
    • Experiment 1: P-STAT3 IHC in the NTS during leptin or vehicle
    • -leptin can be seen as blue dots
    • primarily in mNTS subnucleus
    • P-STAT3 showed that leptin responsive neurons are exclusively located in the medial subnucleus of the NTS
    • used nissl staining to detect subnuclei

    • Experiment 2:
    • used c-Fos IR imaging to show affects of gastric distention on neurons in NTS
    • red dots= reactive neurons
    • -very few c-Fos cells found when given sham distention
    • Double fluorescence on NTS
    • green= leptin fluorescence
    • red= distention induced fluorescence

    • part a of figure shows that distention activated a significant amount of leptin responsive cells
    • double fluorescent cells= yellow dots

    • Experiment 3: amount the stomach was filled affected intake over a 60 min. period
    • 5mL of distention= decrease intake by 33%
    • >5mL of distention= no significant effect

    bar graph shows that neither leptin nor distention is significant to reduce food intake alone