Thom1-Carbohydrates Flashcards

1
Q

What do most carbons from our diet get converted into?

A

AcetylCoA (oxidized in the TCA cycle)

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2
Q

What causes ketoacidosis?

A
  • Excessive production of ketone bodies
  • Diabetes ketoacidosis symptoms include: polydipsia (excessive) thirst, polyuria, fatigue, & blurred vision
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3
Q

What is ATP & what is the structural basis of the its high phosphoryl transfer potential?

A
  • Universal currency of free energy
  • High phosphoryl transfer potential results from structural differences between ATP & its hydrolysis products: –> Hydrolysis products are more stable bc of electrostatic repulsion, resonance hybridization, and stabilization due to hydration
  • Energy is stored in phosphoanhydride bonds
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4
Q

How does ATP drive metabolism?

A
  • Phosphoryl transfer potential is an important form of cellular energy transformation (flow of phosphoryl groups from high-E phosphate donors to low-E phosphate acceptors)
  • ATP hydrolysis shifts equilibrium of coupled reactions
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5
Q

What are oxidants and reductants?

A

-Oxidant (oxidizing agent): become reduced, electron accepting molecule

-Reductant (reducing agent): become oxidized (dehydrogenated), electron-donating molecule -Transfer of: electrons, H-atoms, hydride ions

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6
Q

What is a reducing equivalent?

A

A single electron equivalent participating in an oxidation/reduction reaction

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7
Q

What are some major cofactors for redox reactions?

A

-Niacin (from vit-B3), nicotinamide, tryptophan

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8
Q

What is pellegra?

A
  • Niacin vitamin deficiency
  • Dementia, diarrhea, dermatitis
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9
Q

What are the 2 phases of respiration?

A

1) The oxidation of fuels
2) ATP generation from oxidative phosphorylation

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10
Q

What is the role of the respiratory chain?

A

It oxidizes reducning equivalents and acts as a proton pump.

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11
Q

How are metabolic pathways regulated (3 ways)?

A

1) Amounts of enzymes (protein synthesis, degradation)
2) Catalytic activity (feedback and allosteric inhibition)
3) Accessibility to substrate: hormonal control

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12
Q

Where do major metabolic pathways take place?

A

-Cytosol: glycolysis, pentose phosphate pathway, protein synthesis, FA synthesis, part of urea cycle, part of gluconeogenesis

-Mitochondria: krebs cycle, FA oxidation, acetylCoA formation, part of urea cycle, part of gluconeogenesis

-Lysosomes: degradation of complex macromolecules

-Nucleus: DNA & RNA synthesis

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13
Q

What are the major specialized functions of the liver?

A

1) FA synthesis (along w/fat cells)
2) Gluconeogenesis (along w/kidney)
3) HMP shunt (along with adrenal cortex, far cells)
4) AA synthesis & breakdown
5) Urea synthesis
6) Cholesterol synthesis

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14
Q

Where does FA oxidation not occur?

A

It does not occur in the brain and in RBCs

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15
Q

What are the types of receptors used for hormonal regulation?

A

1) Coupled to adenylate cyclase (2nd msn systems, glucagon, epinephrine)
2) With kinase activity (insulin-R)
3) Coupled to phosphatidyl inositol hydrolysis (epinephrine, GH)
4) Coupled to gated-ion channels (angiotensin II, GABA, acetylcholine)
5) Intracellular receptors (for transcription activation; steroids/Vit-D/retinoic acid/thyroxine)

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16
Q

What are glycans?

A

-Carbohydrates, compounds that usually contain and aldehyde or ketone group and hydroxyl groups.

17
Q

What are isomers, enantiomers, epimers, anomers?

A
  • Isomers: same chemical formula, different structure (glucose & fructose)
  • Enantiomers: mirror images of each other
  • Epimers: differ only in position of the hydroxyl group around asymmetric carbon (ex. glucose & mannose; glucose & galactose)
  • Anomers: differ only in configuration around new asymmetric carbon
18
Q

What is a reducing sugar?

A

-When oxygen on anomeric carbon is not attached to other structure, it can react with chemical reagents & become oxidized to carboxylic acid

19
Q

What is the importance of the anomeric carbon?

A
  • Cyclization of glucose produces a new asymmetric center at C1
  • Anomers have a different configuration at this new asymmetric carbon
  • alpha: OH below the ring
  • beta: OH above the ring
20
Q

What’s a glycosidic bond?

A
  • Hydroxyl group on anomeric carbon of monosaccaride reacts with hydroxyl or amino group of another compound.
  • N-glycosidic bond: sugar linked to N in asparagine side chain
  • O-glycosidic bond: sugar linekd to O in serine’s side chain
21
Q

What are some sugar derivatives?

A
  • Sugar alcohol: lacks an aldehyde or ketone (ribitol)
  • Sugar acid: aldehyde at C1 or OH at C6 is oxidized to carboxylic acic (gluconic acid)
  • Amino sugar: amino gorup substitutes for a hydroxyl (glucosamine, N-acetylglucosamine)
22
Q

How do plants and humans store glucose?

A
  • PLANTS: store glucose as amylose or amylopectin, collectively called starch. Polymeric storage minimized osmotic effects. Also, cellulose (beta-1–>4 linkages).
  • HUMANS: amylose is a glucose polymer with a(1–>4) linkages. Adopts helical conformation. the end wuth an anomeric C1 not involved in a bond is the reducing end.
23
Q

How are carbohydrates digested?

A

1) a-amylase in the mouth (low pH in stomach stops action)
2) Pancreatic a-amylase breaks a(1–>4) linkages in the small intestine
3) Mucosal cell membrane-bound enzymes break down small polymers

24
Q

How are simple CHOs transported across the intestinal epithelium?

A

-Several glucose transporters:

  • Glut 1: most cells
  • Glut 2: glucose, galactose, fructose (low affinity/high capacity)
  • Glut 3: high affinity, basal
  • Glut 4: muscle, adipose. Insulin dependent
  • Glut 5: fructose (high affinity
  • Faciitated diffusion (Glut 2/5)
  • Secondary active transport (SGLT1)
25
Q

How does SGLT1 work?

A

SGLT1 (sodium glucose transporter 1) uses secondary active transport:

1) Na/K ATpase in basolateral membrane uses ATP to pump out Na ions creating a low [Na] inside the cell
2) SGLT1 is a symporter of Na & glucose in the lumen membrane. Na is passively pumped into cell, and glucose takes advantage of the Na gradient to come inside along with Na.
3) Glucose travels down its [C] gradient to EC fluid through Glut2, and Na is pumped out with ATPase

–> Glut2 starts working until there is a strong [C] gradient, and it can trasnport a lot of glucose

26
Q

What happens in lactose intolerance?

A
  • Individuals have a lactase deficiency, so lactose is not broken down into galactose and glucose in the small intestines
  • Lactose is then used by bacteria in the large intestine, which produces acetic acid, CO2, lactic acid
  • It presents with bloating, diarrhea, dehydration
  • It can be genetic or acquired