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Emma > Biochem - E4 Review Slides > Flashcards

Biochem - E4 Review Slides Flashcards

1
Q

Liver/Kidney carry out…

A

gluconeogenesis

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2
Q

Liver is primary home of…

A

urea cycle

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3
Q

Muscle/liver metabolize…

A

glycogen (glycogenolysis, glycogenesis)

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4
Q

rbc lack malic enzyme

A

When oxidant encountered and NADP+/NADPH ratio increases, can’t generate NADPH through malic enzyme.. severe oxidative damage and red cell destruction can ensue

rbc use g6p dehydrogenase to regen NADPH

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5
Q

Glucokinase vs. hexokinase

A

Glucokinase (liver/b cell) - high Km for glucose

hexokinase (ubiquitous) - low Km

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6
Q

Examples of allosteric inhibition/stimulation

A

PFK1 stim via F2,6BP (glycolysis)
AcetylCoA Carboxylase stim via citrate (FAS)
Carbamoylphosphate synthetase II inhib via UDP (pyrimidine synthesis)
Glutamate dehydrogenase inhib ATP (rxn prod alpha-ketoglutarate)
Carnitine acyl transferase 1 inhib via MalonylCoA (1st prod of FAS inhibits beta-oxidation)

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7
Q

Examples regulation of the amount of enzyme

A

Glucokinase increases with high CHO (glycolysis in liver)
Ornithine carbamoyl transferase increases with high protein (urea cycle)

PEPCK gene transcription increases with high cortisol (gluconeogenesis)

HMG-CoA reductase regulated by degradation/stabilization (CHL causes its degradation) (CHL synthesis)

peptidase in response to high protein diet

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8
Q

Examples of covalent modification - inhibition or activation (by phosphorylation)

A

Glycogen Phosphorylase stimu by phosphorylation (glycogenolysis)
Glycogen Synthase inhib by phosphorylation (glycogenesis)

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9
Q

Example of compartmental separation to regulate metabolism

A

Transport of FAs regulated by carnitine acyl transferase (CPT) 1 (beta oxidation)

Regulating acyl carnitine entering mitochondria where enzymes of beta oxidation are

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10
Q

Insulin (function and major metabolic path affected)

A
  • promotes fuel storage after a meal, promotes growth
  • stim glucose storage as glycogen (muscle and liver) (glycogenesis)
  • stim FAS and storage
  • stim aa uptake and protein synthesis
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11
Q

Glucagon (function and major metabolic path affected)

A
  • mobilizes fuels, maintains blood glucose levels during fasting
  • activates gluconeogenesis and glycogenolysis during fasting
  • activates FA release from adipose tissue (cAMP –> PKA –> TAG lipase aka hormone sensitive lipase)
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12
Q

Epinephrine

A
  • mobilizes fuels during acute stress
  • stim glucose prod from glycogen (glycogenolysis)
  • stim FA release from adipose
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13
Q

Cortisol

A
  • provides for changing requirements over long-term

Stimulates…

  • amino acid mobilization from muscle protein
  • gluconeogenesis
  • FA release from adipose
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14
Q

Adipose vs Heart lipoprotein lipase

A

Adipose LPL –> larger Km, storage repository, allows for removal when increased fat

Muscle LPL –> smaller Km, higher affinity allows heart for access to fat for fuel even when decreased fat levels

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15
Q

G-protein cycle

A
  • Activation of the G protein by GDP/GTP exchange –> release of GTP-bound Gs-alpha from G-beta-gamma –> activate adenylcyclase to synthesize cAMP
  • Hydrolysis allows return to inactive state (cholera toxin covalently modifies Gs-alpha to active state
  • Gs –> modified by cholera toxin to keep it in active state
  • Gi –> blocked by pertussis toxin to prevent inhib of adenyl cyclase (Gi –> normally inhibitory)
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16
Q

Cortisol Reacts with the Glucocorticoid Receptor Found in the _______

A

Cytoplasm

Cortisol binds to specific receptor in cytoplasm, conformational change takes place, releasing receptor from hsp (chaperone) so the receptor moves to the nucleus, binds DNA, activates transcription

Exp. gluconeogenic PEPCK

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17
Q

Stages of starvation (sources of glucose)

A

Absorptive (0-4 hrs): exogenous glucose

Postabsorptive (0-12hr): Glycogen, Hepatic gluconeogenesis

Early starv (16-30hr): Hepatic gluconeogen, Glycogen

Intermed starv: hepatic/renal gluconeogenesis

Prolong starv: hepatic/renal gluconeogenesis

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18
Q

Use of proteins during starvation

A

Early starvation - 75 g/day

Mid/late starvation - 20g/day (less)

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19
Q

Metabolite usage during fasting

A

Total amount of nitrogen excreted decreases (particularly urea).

N excreted as ammonia increases then stays higher than normal (partially to conserve cations that would be excreted along with xs KBs).

FA and KBs rise.

20
Q

Controlling Blood Glucose Levels

not dir connected to Insulin

A

a Glucosidase Inhibitors (Acarbose) Block Glucose Uptake

SGLT2 Inhibitors (Jardiance) Block Glucose Resorption in Kidney

Metformin Blocks Gluconeogenesis in Liver & Peripheral Uptake

21
Q

Controlling Blood Glucose Levels

connected to insulin secretion

A

Sulfonylureas (Glipizide) Inhibit ATP-Dependent K Channels, thus increasing insulin release from beta cells

Glinides (Replaginide) Inhibit ATP-Dependent K Channels

Incretin Analogs (Exenatide) With Extended life

DPIV Inhibitors (Sitagliptin) To Extend Incretin Life

22
Q

secretion of insulin from the pancreas

A

regulated by the ATP-sensitive potassium channel

High blood glucose and glucokinase in the cell
ATP production
closed K channels
depolarization
opening of voltage-activated calcium channels
Ca++ influx triggers exocytosis of secretory granules containing insulin

23
Q

sulfonylureas and meglitinides

A

target potassium channel of pancreatic cells

antidiabetic drugs (fo type 2)… act by increasing insulin release from the beta cells in the pancreas

24
Q

Hormones produced in the digestive tract that control insulin production/secretion

A

Incretins such as GLP-1 or GIP.
Released from cells in intestine in response to fed glucose

Close K channels via cAMP dependent signaling mechanism –> insulin release

25
Q

Type 1 DM

A 
loss of beta-cells
genetic susceptibility 
obsesity not usually
autoimmunity: +, GAD+ (Often)
Plasma insulin: little to none
Insulin response: normal
Fasting hyperglycemia: severe
Ketoacidosis: yes
Tx: insulin
26
Q

Type 2 DM

A 
beta-cells initially preserved
genetic susceptibility (IRS-1 mutations)
obsesity common
autoimmunity: usually no
Plasma insulin: low to high
Insulin response: usually reduced
Fasting hyperglycemia: variable
Ketoacidosis: not usually... Instead Hyperosmolar non-ketotic coma (HONK)
(Hyperglycemic hyperosmolar synd.(HHS)

Tx: Diet, oral antidiabetics, insulin

27
Q

Regulation of insulin secretion

A

ATP (ATP/ADP ratio) and GLP1/GIP are “natural” regulators of the K channel.

Sulfonylureas and meglitinides act on the potassium channels

GLP1/GIP incretin analogues

Inhibitors of DPP4 - blocks degradation of GLP1/GIP

28
Q

Insulin Signals Through a ________ Receptor

A

Insulin binds to insulin receptors on cell surface (Tyrosine Kinase receptor) –> these phosphorylate cellular targets …

  • activation of Ras –> phosph/transcrip
  • prod of lipid PIP3….
    1. relocalization of Glut4 to promote glucose uptake (adipose/muscle)
    2. activates protein phosphatase 1
29
Q

Insulin increases or decreases blood glucose?

A

decreases blood glucose by increasing glucose uptake in muscle and adipose cells.

30
Q

Insulin increases or decreases glycogen phosphorylase?

A

decreases

31
Q

Insulin increases or decreases glycogen synthase activity?

A

increases

32
Q

Insulin increases or decreases gluconeogenesis?

A

decreases, inhibits PEPCK

33
Q

Insulin increases or decreases glycolysis?

A

increases in the liver (PFK1 upregulated), so increasing acetyl CoA formation, increasing ketogeneis

34
Q

Insulin increases or decreases FAS in the liver?

A

increases (stim ACC)

35
Q

Insulin increases or decreases lipoprotein lipase?

A

increases, so increases lipid transfer to adipocytes

36
Q

Insulin increases or decreases glucose in adipocytes?

A

Increases, so increases TAG synthesis

37
Q

Insulin increases or decreases hormone-sensitive lipase?

A

Decreases, so increases lipid deposition

38
Q

Insulin increases or decreases amino acid uptake into cells?

A

Increases, so increases protein synthesis

39
Q

3 major ways that Insulin acts to reduce blood glucose

A
  1. promotes glucose uptake
  2. favors glycogen formation
  3. inhibits gluconeogenesis
40
Q

Hypertriacylglycerolemia

A

Loss of insulin –> the lipid triad

  1. elevated triglycerides
  2. low HDL
  3. small, dense LDL *atherogenic
41
Q

In obese people undergoing therapeutic starvation, daily excretion of urea is high in the first week and later declines. This is consistent with the fact that, as starvation continues,

A. carbohydrate demands of brain and muscle increase.
B. ketone body formation decreases.
C. the brain begins to use amino acids for gluconeogenesis.
D. the liver loses the ability to synthesize urea.
E. the rate of gluconeogenesis from amino acids decreases.

A

E.

42
Q

Which of the following is not true about Type II DM?

A. Most likely to be associated with adult onset
B. Does not require initial treatment with insulin for most cases
C. May be treated with a drug that sensitizes cells to insulin or increases insulin release
D. May result in hyperosmotic non-ketotic coma
E. Usually results in ketoacidosis

A

E.

43
Q

Diabetic Ketoacidosis (DKA)

A

No insulin leads to …
- uncontrolled lipolysis (hormone sensitive lipase)
- failure to take up FAs (LPL) in adipose tissue
Elevated FA –> synthesis of ketone bodies in liver

44
Q

hyperosmolar hyperglycemic state (HHS, HONK)

A

Type II DM

Non-ketotic, even more life-threateningly serious than DKA.

45
Q

glutamate dehydrogenase regulation

A

Inhibited by ATP/GTP, stimulated by ADP/GDP

46
Q

tx for hyperammonemia

A
  • supp. benzoate or phenylbutyrate
  • limit protein intake, have abundance of glucose (starch) to prevent gluconeogenesis
  • supply arginine
47
Q

Fates of arginine

A

creatine, nitric oxide

Emma (18 decks)

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