Starvation and Metabolic Syndrome Flashcards

1
Q

What combination of hormones leads to the largest rise in blood glucose?

A
  • glucagon, epinephrine, and cortisol.
    • synergistic effect.
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2
Q

Main hormonal activators of glycogenolysis:

A
  • norepinephrine and epinephrine.
    • glucagon too, but not as strongly.
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3
Q

Main hormonal activators of gluconeogenesis:

A
  • cortisol and glucagon.
  • norepi/epi do not trigger gluconeogenesis.
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4
Q

What hormone stimulates both liver glycogenolysis and gluconeogenesis?

A

glucagon.

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5
Q

The 4 types of hypoglycemia:

A
  1. Insulin induced.
  2. Postprandial.
  3. Fasting.
  4. Alcohol.
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6
Q

Treatment for mild and severe insulin induced hypoglycemia:

A
  • mild: oral carbohydrates.
  • severe: glucagon shot.
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7
Q

Main glucose sources during starvation (time 0 to weeks):

A
  • ingested glucose (4 hours).
  • glycogen stores (4-18 hours).
  • gluconeogenesis.
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8
Q

Once liver glycogen stores are depleted in starvation, what two important changes in body metabolism occur?

A
  1. gluconeogenesis in liver and kidneys increases.
  2. fatty acids/ketones become primary metabolic fuel; spares glucose for brain and RBCs.
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9
Q

When do ketone bodies become the primary source of metabolic fuel?

A

14-21 days of starvation.

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10
Q

What is the primary ketone body produced during starvation?

A
  • beta-hydroxybutyrate.
    • results from NADH and acetyl CoA produced by FA beta-oxidation.
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11
Q

Brain fuel source during fed state:

A

100% glucose.

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12
Q

Brain fuel source during starvation state:

A
  • 60% beta-hydroxybutyrate.
  • 30% glucose.
  • 10% acetoacetate.
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13
Q

Metabolic syndrome is defined as meeting three or more of the following criteria (5):

A
  1. central obesity
  2. high fasting triglycerides
  3. low HDL
  4. hypertension
  5. hyperglycemia
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14
Q

Which two types of fat are insulin sensitive and aid in maintaining/lowering blood glucose?

A
  1. Brown fat.
  2. Subcutaneous white fat.
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15
Q

Which type of fat is insulin resistant?

A

visceral white fat.

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16
Q

What three things does visceral fat secrete in excess, which promote dyslipidemia, insulin resistance and inflammation?

A
  1. inflammatory markers (C-reactive protein).
  2. free fatty acids.
  3. adipokines (cytokines).
17
Q

What is hypothesized to be the main cause of T2 diabetes due to visceral fat/metabolic syndrome?

A

increased FFA secretion from visceral fat.

18
Q

Effects of increased FFA secretion from visceral fat on metabolism:

A
  1. inhibits insulin secretion.
  2. decrease glucose uptake in muscle and adipose tissue (insulin activates GLUT4).
  3. increase gluconeogenesis (increase glucagon/insulin ratio by lowering insulin).

HYPERGLYCEMIA / T2 DIABETES

19
Q

The three hormones secreted from adipocytes affecting blood glucose (and their classification):

A
  1. Resistin (pro-hyperglycemic).
  2. Leptin (anti-hyperglycemic).
  3. Adiponectin (anti-hyperglycemic).
20
Q

The main downstream molecule of resistin, leptin, and adiponectin is:

A

AMPK

21
Q

How does resistin released from adipocytes promote hyperglycemia?

A
  • resistin inhibits AMPK and activates gluconeogenesis.
    • AMPK promotes glucose uptake (GLUT4) and glycolysis.
22
Q

How do leptin and adiponectin released from adipocytes promote glucose uptake?

A
  • leptin and adiponectin activate AMPK.
    • AMPK promotes glucose uptake (GLUT4) and glycolysis.
23
Q

What changes in adiponectin, leptin, and resistin will cause obesity?

A
  1. adiponectin and leptin deficiency.
  2. adiponectin and leptin receptor defects.
  3. resistin levels are high.
24
Q

What hormone released from adipocytes interacts with the CNS, and how?

A
  • leptin; reduces food intake and increases energy expenditure via hypothalamus.