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BioMedChem Midterm 1 > 3 - Hormones and Metabolism > Flashcards

3 - Hormones and Metabolism Flashcards

1
Q

Gluconeogenesis

A
  • Glycogen / Lactate / AA / Glycerol
    • ​–> Form Glucose in LIVER
  • 90% of all glucose (not from diet) is generated in the LIVER
  • Stimulated by decreasing blood glucose levels
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2
Q

Negative Feedback of Glucose

A
  • System senses Increase in Glucose
  • Pancreas releases Insulin
  • Insulin signals muscle/adipose tissue to intake glucose
    • ​-> Reduction in glucose in blood
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3
Q

Pancreas

A
  • Controls Metabolism by producing:
    • Digestive Enzymes (from acinar cells)
      • ​Trypsin
      • Chymotrypsin
      • Elastase
      • Amalase
    • 2 Endocrine Hormones
      • ​Insulin
      • Glucagon
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4
Q

Acinar Cells

A
  • Exocrine cells of the Pancreas that secrete digestive enzymes
    • ​Trypsin
    • Chymotrypsin
    • Elastase
    • Amalase
  • ​–> breakdown food in GI
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5
Q

Delta Cells

A

In Islets of Langerhans of Pancreas

Produce:

SOMATOSTATIN

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6
Q

Sigma Cells

A

In Islets of Langerhans of Pancreas

Produce:

GHRELIN

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7
Q

Insulin’s 5 Main Functions

A
  1. Prevents release of Fatty Acids from Adipose tissue
  2. Promotes synthesis of Glycogen
  3. Accelerates transport of Glucose -> Muscle
  4. Accelerates synthesis of Triglycerols
  5. Inhibits synthesis of Glucose by _liver_
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8
Q

Insulin

A
  • Peptide Hormone (Anabolic)
    • Pre-proinsulin -> ER
      • cleaved -> Proinsulin -> secretory vesicles
        • -> Insulin + C-Peptide
    • ​​Many of the AA’s are MUTATED
      • genetic mutations everywhere are what cause different diseases
  • ​​​Half life of insulin is about 5 minutes
    • _​_degraded by the liver + kidney
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9
Q

C-Peptide

A
  • @Secretory Vesicles
    • Proinsulin -> Insulin + C-Peptide
  • ​Biomarker for insulin levels
    • longer half life
    • useful for monitoring pancreatic B-cell activity
      • ​due to low rxn w/ insulin
      • absence in synthetic preparations
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10
Q

Pathway of Insulin Release

A
  • Glucose -> Pancreatic B-Cell via GLUT2
    • ​Glycolysis in Cytosol -> Mito
      • -> Increase in ATP/ADP ratio
        • ​modulation of K+ channels
        • ​Depolarization (more negative)
          • Ca2+ INFLUX
            • ​INSULIN RELEASE
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11
Q

GLUT2

A

Glucose Influx Transporter

Pancreatic Beta Cell

Liver

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12
Q

How does Insulin INCREASE Glucose absorption into the cell?

A
  • Insulin -> Insulin Tyrosine Receptor Kinase on Muscle + Adipocytes
    • ​IRS1 Phosphorylation -> P13Kinase
      • ​Phosphorylated AKT
        • Translocates GLUT4 to the membrane
          • ​MORE TRANSPORTERS TO BRING GLUCOSE INTO THE CELLS
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13
Q

GLUT4

A

Glucose Influx Transporter

Found on Muscle + Adipocytes

Upregulated by Insulin binding

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14
Q

Insulin action on the LIVER

A
  • Stimulates GLYCOLYSIS
    • ​GLUT2 brings glucose into liver
      • -> brings IN glucose -> glycogen
  • ​Inhibits Gluconeogenesis
    • ​inhibits formation of glucose
  • Blood flow goes from Pancreas to Liver
    • exposes Liver to large amounts of hormones
      • Stimulates GLUCAGON synthesis
    • major organ for pancreatic hormone inactivation
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15
Q

Insulin action on Adipocytes

A

Prevents release of

FREE FATTY ACIDS

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16
Q

Insulin action on Muscle

A
  • Accelerates influx of GLUCOSE into the muscle
    • ​via GLUT4
    • -> sets stage for glucose oxidation
17
Q

Glucagon

A
  • Produced by Alpha-Cells of Islets of langerhans
  • Part of Precursor w/ other peptide hormones
    • GLP-1 / GLP-2 / GRP
  • ​STIMULATED by Low plasma Glucose
  • Inhibited by Insulin & Somatostatin
  • Mostly impacts the LIVER and not other tissues
18
Q

Glucagon’s 5 Main Functions

A
  1. Stimulates Amino Acid uptake
  2. Gluconeogenesis
  3. Glucose release
  4. Inhibits Glycolysis
  5. Inhibits FFA synthesis
19
Q

Somatostatin Production

A
  • From Delta Cells of pancreatic islets
    • Stimulated by increase in Glucose
      • similar to insulin release
  • Produced as a larger precursor
    • cleaved in the ER to form a mature 14 AA product that is released
  • Inhibits Glucagon readily
  • Inhibits Insulin from rising too rapidly
20
Q

GLP / GIP Receptor

A
  • Found on Beta Cells of islet of langerhans
  • Sense Glucose levels
    • -> stimulate release of Insulin
    • Similar to UCN3 of Delta cells but secrete different hormones
21
Q

UCN3 Receptor

Urocortin3

A
  • Found on Delta Cell on islet of langerhans
  • Sense Glucose
    • Secrete SOMATOSTATIN
    • sense the SAME signal as GLP/GIP but have a diffrentiation in signal transduction
22
Q

Somatostatin Function

A

PARACRINE REGULATION

acts on alpha/beta cells locally

  • Inhibits* Glucagon Readily
  • Inhibits* Insulin from RAPIDLY RISING
23
Q

Priority for the disposal of Dietary Fuels

A
  • 1) Restore Glucose for Brain
    • ​brain can use glycerol from liver
    • while rest of body uses fatty acids
  • 2) Replenish Glycogen in the liver
24
Q

Leptin

A

Decreases Food Intake

  • Polypeptide hormone produced by ADIPOCYTES
    • Binds to LEPR-B in the BRAIN
      • ​​translation of neuropeptide POMC​
  • ​Links body energy (fat) to the central conrol of energy balance
    • Leptin action is key for energy stores to be sensed by the CNS
  • Does NOT benefit obesity due to
    • LEPTIN RESISTANCE
25
Q

Leptin Actions

A

binding to LEPR-B -> translation of neuropeptide POMC->

Increases Energy Expenditures (use storage)

  • Decreases Food Intake / Appetite*
  • Reduces Body Weight*
26
Q

Leptin Pathway

A
  • Increase in Intake = Energy Imbalance
    • Intake > Expendature
  • Adipocytes secrete Leptin
    • leptin binds to LEPR-B in BRAIN hypothalmus
      • _​_translation of neuropeptide POMC
        • _​_signal to Use Energy
        • decrease Food Intake
        • reduce Body Weight
27
Q

ob + db gene discovery

A
  • ob gene codes for LEPTIN
  • db gene codes for Leptin Receptor ( LEPR-B )
  • Cross between OBESE mice, each with each KO gene
    • ob KO mouse lost weight
      • leptin from db mouse transfered over and was able to bind to leptin receptors​
    • db KO mouse stayed obese
      • receptor can not transfer from one mouse to another so the db mouse stayed obese

BioMedChem Midterm 1 (9 decks)

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