Metabolism And Lipid Membranes Flashcards

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1
Q

What is Kwaashiorkor?

A

Condition that is characterized by protein deficiency.

Symptoms include Edema, Fatty lover, muscle wasting, skin lesions, hypoptoteinemia (obv)

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2
Q

What is the end process that all macronutrients enter to produce ATP?

A

All Become Acetyl Coa —> TCA

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3
Q

What are the three “hubs” of metabolic systems?

A
  1. Glucose-6-Phosphate
  2. Pyruvate
  3. Acetyl-CoA
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4
Q

Besides glycolysis, what other pathways use G6P?

A
  • Converted to G1P to become glycogen

- Forms precursors for pentose phosphate pathway to form nucleotides and NADP

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5
Q

What is Von Gierke Disease?

A

Type I GSD

  • Autosomal recessive
  • deficiency of Glucose-6-phosphatase
  • Have fasting hypoglycemia and accumulation of glycogen, siezures, hepatomegaly, hypertiglyceridemia
  • Lactic Acidosis: Impairment of gluconeogenesis leads to accumulation of Pyruvate which impairs conversion of lactate
  • Build up of Lactic acid competes with Uric Acid —> Gout
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6
Q

How is pyruvate generated from different metabolic pathways?

A
  • Muscle cell fermentation through Cory cycle from lactate in Liver
  • Deamination/transamination to/from alanine (gluconeogenesis)
  • Pyruvate to Acetyl-CoA
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7
Q

What are the two main sources of Acetyl-CoA?

A

Pyruvate and Fatty Acids

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8
Q

What metabolic pathways are connected to acetyl-CoA?

A
  • Ketone Bodies are converted to Acetyl-CoA in brain and Cholesterol
  • Acetyl-CoA is made from amino acids produced from G6P

*** Acetyl-CoA cannot make Pyruvate!

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9
Q

What may be produced from FAs?

A
  • Full Oxidized to CO2/H2O
  • Serve as precursors of cholesterol and steroids
  • Transformed to ketone bodies
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10
Q

What can happen to the Carbon skeleton after AA transamination?

A
  • Become fully oxidized
  • Used in gluconeogenesis
  • Form ketone bodies or Acetyl-Coa for FA synthesis
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11
Q

How does stress and the CNS affect metabolism?

A
  • Adrenaline activates Liver (similar to glucagon)

- Adrenaline activates muscle -> Glycogen production of G1P -> G6P -> ATP

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12
Q

What part of the brain is involved in the anorexigenic affect of acute stress?

A

Hypothalamic-pituitary-adrenal axis

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13
Q

What are the major metabolic affects of stress?

A
  • Increase in Glucagon
  • INC Cortisol -> Gluconeogenesis and FA mobilization
  • INC EP/NE
  • Hyperglycemia and insulin resistance
  • Catabolism of skeletal muscle and inflammation
  • Reliance on proteins for source of glucose
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14
Q

What percent of the pancreases are islets of langerhans?

A

1-2%

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15
Q

What cell make up the islets of langerhans?

A
Beta - Insuln
Alpha - Glucagon
Delta - Somatostatin
Gamma - Pancreatic polypeptide
Epsilon - ghrelin
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16
Q

What affect does glycogen have in the liver?

A

Inhibits glycogen synthase

17
Q

What are the main affects of glucagon across the body?

A
  • Activates glycogen phosphorylase
  • Activate lipid catabolism
  • activate AA catabolism
18
Q

What process allows G6P to leave the Liver?

A

Glucose-6-phosphatase hydrolyzes it to glucose which can leave

19
Q

What are the fat-soluble vitamins?

A

VitamiNs A K E D

20
Q

How do normal capillaries differ from ones in the BBB?

A
  • No fenestrae
  • BBB capillaries are surrounded by astrocytes and pericytes
  • Contain Tight junctions, so only H2O, CO2, and O2 can pass freely
21
Q

What is the MCT1?

A

Transporter of Monocarboxylic acids

22
Q

what are the main transporters in the BBB?

A
  • GLUT1
  • MCT1
  • Essential AA transporters

*nonessential are blocked from transport

23
Q

What are the pathways that can result in brain damage from metabolic dysfunction?

A

Hypoglycemia -> INC MCT1 -> Slowing of energy supply —> DEC NT synthesis —> No ATP —> Brain damage

Hypoxia —> No O2 for ETC -> anaerobic fermentation. —> Dec in pH —> Brain damage

24
Q

What is the skeletal muscle’s main source of energy during rest, moderate activity, and burst of heavy activity?

A

At Rest: Mainly FAs through Beta oxidation.

Moderate: Uses FAs and glucose from liver

Heavy: Uses FAs, Glucose, and Phosphcreatine

25
Q

What advantage is there for muscle to use glycogen?

A

When the source is glycogen breakdown, there is a net gain of 3 ATP due to the lack of investment needed to produce G6P from glucose

26
Q

How does cardiac muscle use of energy differ from skeletal muscle?

A
  • Mainly uses FAs all the time
  • Always needs O2 (No anaerobic Respiration)
  • VERY sensitive to pH
27
Q

Describe McArdle Disease.

A
  • Type V GSD
  • Inability to break down glycogen in muscle
  • Deficiency of Glycogen phosphorylase
  • Symptoms include exercise intolerance on initial start, however will get “Second wind phenomenon”
28
Q

Describe Cory/Forbes Disease

A
  • GSD Type III
  • Autosomal recessive
  • Deficiency in glycogen debranching enzyme alpha-1,6-glucosidase
  • Symptoms include hepatomegaly and hypoglycemia
29
Q

How does cytoplasmic calcium affect skeletal muscle?

A

Causes fusion of GLUT4 independent of Insulin

30
Q

Where is the TCA located?

A

Mitochondria

31
Q

Where do PPP and FA synthesis occur?

A

Cytosol