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Behavioral Endocrinology > homeostasis > Flashcards

homeostasis Flashcards

1
Q

Walter Canon and homeostasis

A

named process by which body maintains a constant internal state

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2
Q

homeostasis

A

maintenance of an internal environment; tendency to keep the body variable within a set range

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3
Q

set point

A

single value body aims to maintain

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4
Q

allostasis

A

adaptive way body changes its set point depending on the situation; maintaining stability via physiological/behavioral processes

  • adaptive in short term, usually a reflection in food, water, and shelter availability
  • achieved through alterations in HPA axis hormones, ANS, cytokines, or other systems
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5
Q

hunger

A

motivation to find and inject food

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6
Q

satiety

A

cessation of eating

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7
Q

energy acquisition

A

feeding/eating

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8
Q

energy expenditure

A

burning calories via exercise/metabolism

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9
Q

adipose tissue

A

excess energy stored as fat

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10
Q

metabolism in a well fed state

A
  1. food is broken down into glucose, fatty acids, amino acids
  2. insulin released from the pancreas to facilitate the transport of glucose (lowers blood glucose levels and stores it)
  3. excess glucose is converted to glycogen and stored (process occurs in liver, glucose–> glycogen)
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11
Q

glycogen

A

stored form of sugar in the liver

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12
Q

lipogenesis

A

creation of fat

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13
Q

glucagon

A

released from the pancreas to facilitate release of glucose from the liver to increase blood sugar levels

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14
Q

how to raise blood sugar levels without eating

A
  1. decrease insulin, increase glucagon
  2. gluconogenesis: production of glucose from amino acids in the liver
  3. lipolysis: fat breakdown
  4. glycogenolysis: breakdown of stored glycogen in liver
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15
Q

type 1 diabetes

A

insulin dependent diabetes
**B cells of the pancreas are destroyed by the immune system–> no insulin produced at all, so no storage of glucose at all

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16
Q

type 2 diabetes

A

tissues develop an INSENSITIVITY to insulin (insulin is being produced, but not really doing its job anymore)

  • no glucose take-up–> hyperglycemia
  • cells insensitive to insulin–> energy deficit–> increase in insulin release
  • adipose tissue LAST to become insulin-resistant–> take-up of glucose–> lipogenesis
  • **with increasing energy deficit and lipogenesis–> increased appetite, increased food intake, and weight gain
17
Q

effects of type 1 and 2 diabetes

A

difficulty moving glucose out of the blood into the tissues

  • hyperphagia: elevated appetite
  • hyperglycemia: high blood glucose levels
  • increased thirst and urination
18
Q

hyperinsulinemia

A

too much insulin

  • increased glucose uptake, inhibited lipolysis–> decreased breakdown of fats, low blood sugar
  • obesity results, people hungry, cannot lose body fat, eating frequently
19
Q

orexigenic

A

increases food intake: ghrelin, NPY, AgRP,

20
Q

anorexigenic

A

decreases food intake: leptin, insulin, CCK, POMC/CART, a-MSH

21
Q

leptin

A

concentrations in proportion of body fat

  • elevated leptin: signals hypothalamus that fat stores are high, decreases eating
  • lower leptin: signals hypo that fat stores are low, increases eating
22
Q

anorexia

A

loss of appetite

23
Q

aphagia

A

absence of feeding

24
Q

high leptin and insulin

A

feeding inhibitory pathway–> stimulation of CATABOLIC pathway–> decreased eating, increased energy use

25
Q

low leptin and insulin

A

feeding stimulatory pathway–> ANABOLIC pathway–> increased eating, decreased energy use

26
Q

Hypothalamus, feeding stimulatory and inhibitory pathway, PVN/hypothalamic nuclei, hormones

A

hypothalamus has a feeding stimulatory and inhibitory circuit, both send signals to the PVN and other nuclei of the hypothalamus to modulate feeding behavior

  • feeding stimulatory and inhibitory circuits are modulated by hormonal signals that cross the BBB
  • leptin, insulin, ghrelin
27
Q

feeding stimulatory circuit: NPY and AgRP

A
  • NPY: stimulates PVN to evoke feeding behavior–> increased motivation to eat
  • AgRP: promotes feeding by BLOCKING melanocortin type 4 receptor (appetite inhibitor)

**under fed state: low levels of L and I–> activation of NPY and AGRP neurons–> increase food intake

once L and I levels are restored, NPY and AGRP inhibited

28
Q

feeding inhibitory circuit: POMC and CART

A

increased CART–> decreased food intake
-POMC–> produces a-MSH (acts through melanocortin type 4) to decrease appetite

**elevated leptin and insulin activates POMC/CART–> secrete products into PVN and LHA–> decrease food intake

29
Q

ghrelin

A

increases food intake

  • opposite effects of L and I
  • associated with NPY and AGRP (increase food intake)
30
Q

adiposity signals communicate with autonomic circuits to mediate food intake

A
  • stomach distention information

- CCK released from duodenum–> signals that food has been digested

Behavioral Endocrinology (12 decks)

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