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Endocrinology Final > Neuroendocrine Regulation of Metabolism > Flashcards

Neuroendocrine Regulation of Metabolism Flashcards

1
Q

Energy balance

A

Energy intake = energy expenditure

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2
Q

Where do we get energy from?

A

foods and beverages consumption

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3
Q

Hunger

A
  • Physiological drive to eat
  • Controlled by the body
  • Opposite of hunger is satiety
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4
Q

Appetite

A
  • Psychological drive to eat (external)
  • Appetitive behavior
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5
Q

How do we use or release energy?

A
  • BMR
  • Thermic effect of food (TEF)
  • Physical activity
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6
Q

What is the role of reward centers in energy?

A
  • Food consumption is rewarding (increase palatability)
  • Regulate food motivation and preferences
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7
Q

What is the role of the hypothalamus in energy?

A
  • Receives info via circulation hormones on available energy storage
  • Gut innervating neurons project directly to the hypothalamus, mainly to the arcuate (ARC) neurons
  • Anorexigenic (stops eating, ventromedial) and orexigenic centers (eats, lateral)
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8
Q

What is the role of the gut-brain axis in energy?

A
  • Signals released from the GI tract monitoring nutrients
  • Info conveyed by the vagus nerve to the NTS (brainstem)
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9
Q

Short-term regulation of intake

A
  • Peripheral
  • Within meal-to-meal basis
  • Info conveyed via nerve
  • Determines the quantity and quality of food eaten during meals/days
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10
Q

Long-term regulation of intake

A
  • Central
  • From days to weeks
  • Information conveyed circulating hormones
  • Set the tone (modulates short term signals, sensitivity, BMR)
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11
Q

Arcuate Nuclears

A
  • ARC is closed to the third ventricle
  • Responds to circulating signals (leptin)
  • Contains two populations of neurons (first-order neurons):
    1. POMC/CART
    2. NPY (neuropeptide Y) / AgRP (Agouti gene-related protein)
  • NPY neurons have a GABAergic inhibitory action on POMC neurons
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12
Q

How do first-order neurons project to the hypothalamus?

A
  • Second order neurons in the PVN (hypothalamus)
  • PVN is the satiety center
  • PVN neurons can secrete anorexigenic NTs such as:
    1. Corticotropin releasing factor (CRF)
    2. Thyrotropin-releasing hormone (TRH)
    3. Oxytocin
  • MC4-R activation by alpha-MSH stimulates CRF, TRH, and oxytocin release
  • AgRP is a melanocortin agonist
  • NPY binding to Y1R inhibits CRF, TRH, and oxytocin release
  • Melanocortin signaling: balance between alpha-MSH and melanocortin antagonist AgRP at the MC4R receptor
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13
Q

How do first-order neurons project to the lateral hypothalamic area (LHA)?

A
  • NPY/AgRP neurons project to the LHA
  • LHA is a hunger center
  • LHA neurons secrete orexigenic peptides (Orexin-A and MCH)
  • Y1R activation stimulates LHA neurons
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14
Q

Leptin Signaling

A
  • 16kDA hormone secreted by adipocytes, proportionally to fat mass
  • Feedback signal on available energy storage in adipose tissue
  • Levels decreases with fasting
  • Circulating leptin enter the brain in proportion to its plasma levels
  • Long form of the receptor (Ob-R: leptin receptor) serves as a transporter
  • Leptin reduces appetite
  • Leptin regulates POMC
  • Leptin acts at the level of the ARC
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15
Q

Explain the Leptin signaling pathway (receptor).

A
  1. Leptin binds to the receptor (dimer)
  2. JAK2 phosphorylation (both sides)
  3. Phosphorylation of STAT3
  4. Phosphorylated STAT3 are released from receptor and move to nucleus together
  5. Transcription of genes (ex: POMC)
  6. SOCS3 inhibits JAK2 phosphorylation
  • Box 1: JAK2 recruitment
  • Box 2: STAT3 recruitment
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16
Q

How does leptin impact POMC neurons?

A
  • Activates POMC neurons by direct depolarization
  • Increases POMC transduction
  • Increases alpha-MSH release
17
Q

How does leptin impact NPY/AgRP neurons?

A
  • Inhibits NPY/AgRP neurons via hyperpolarization
  • Decreases expression of neuropeptides
  • Decreases releasing activity
  • Decreases inhibitory feedback onto POMC/CART neurons
18
Q

How does leptic impact energy expenditure?

A
  1. Modulates activity
  2. Thermogenesis
19
Q

Insulin Signaling

A
  • Insulin secreted by pancreatic beta-cells
  • Carbs and protein consumption stimulate insulin secretion
  • Insulin release increases with body mass
  • Levels decrease with fasting
  • Insulin enters the brain proportionally to its circulating concentration by an IR-mediated mechanism (tyrosine kinase)
  • Transport into the brain can take hours following increase in circulating levels
  • Insulin stimulates anorexigenic neurons
20
Q

Insulin Receptor Function

A
  1. Insulin binds to receptor (dimer)
  2. Phosphorylation of IRS1
  3. Phosphorylation of PI3
  4. Phosphorylation of AKT
  5. Glucose transport, glucose utilization, neoglucogenesis
    - SOCS3: inhibits IRS1 phosphorylation
21
Q

Adipokine or Adipocytokines

A
  • Cytokines secreted by the adipose tissue (leptin, adiponectin)
22
Q

Adiponectin

A
  • Protein hormone (244-AA long)
  • High circulating levels
  • Acts via activation of GPCR (AdipoR1 and AdipoR2)
  • Participates in control of glucose and lipid metabolism
  • Increases tissue sensitivity to insulin= incretin
23
Q

Obesity

A
  • Disease: eating continues beyond satiety
  • Inflammation: normal body first response directed towards containment or elimination of microbial invaders (component of the innate/nonspecific immunity)
  • Cellular and humoral responses
  • As body weight increases, circulating leptin levels rise (high intake is maintained and no changes in energy expenditure are detected
24
Q

Acute Inflammatory Response

A
  • Series of tissue responses that occurred within the first few hours following injury (redness, heat, swelling, pain, loss of function)
  • Strong response that gradually declined until offending agent is undetectable
25
Q

Regulation of the inflammatory response

A
  • Resolution of inflammation is an active process
  • Several anti-inflammatory factors are being released during an acute inflammatory response
26
Q

Chronic inflammation

A
  • Response to persisting inflammatory triggers
  • Inflammation is a factor of pathologies and metabolic abnormalities associated with obesity (type 2 diabetes, atherosclerosis, CVD)
27
Q

Leptin resistance

A
  • Central leptin resistance developed
  • ARC neurons do not respond to leptin anymore
  • Leptin signals via induction of STAT3
  • SOCS3 is part of negative feedback loop regulating STAT3
  • SOCS3 blocks leptin signaling
  • When leptin levels rise, SOCS3 protein levels increase
  • Inflammation also induces SOCS3
  • Block leptin signaling
  • Transport to brain also altered
28
Q

Ob/ob and db/db receptors

A
  • Lacking leptin receptors
  • Ob: lacking leptin
  • Db: lacking receptor
  • Hyperphagia in ob/ob mice and Zucker rat is due to an increase in meal size
29
Q

MC4R

A
  • MC4R KO mice are hyperphagic and obese
  • Animals eat larger meals and have increase preference for fats
30
Q

Y1 agonist versus antagonist

A
  • Y1 agonist: increase in meal size
  • Y1 antagonist: reduces food intake
31
Q

Monogenic Obesity

A
  • Leptin-melanocortin pathways
  • Leptin deficiency (Ob/Ob) is a rare recessive genetic disorder
  • Leads to: hyperphagia, food seeking behavior, aggressive behavior when food restricted
32
Q

Effects of leptin therpy.

A
  • Reduced overall energy intake
  • Decreased meal size
  • Decreased motivation to eat
33
Q

Mutations in MC4R

A
  • More common than LEP
  • 2-3% of childhood and adult obesity cases
  • Hyperphagia
  • Complete or partial loss of function
34
Q

Loss of POMC

A
  • Results in: hypothyroidism, obesity, loss of hair pigmentation
  • Use of MC4R agonist was inefficient in impacting weight and. intake
  • Other mutations include beta-MSH, PC1 (POMC maturation)
35
Q

Prader-Willi Syndrome

A
  • 1 in 10,000 to 30,000 people worldwide
  • Loss of function of genes on chromosome 15
  • Segment of paternal gene is deleted
  • Hypothalamus does not develop properly
  • Infancy: hypotonia (poor muscle tone) and difficulty feeding
  • Childhood: insatiable appetite (hungry all the time), obesity

Endocrinology Final (13 decks)

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