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CH350 > Metabolic Integration > Flashcards

Metabolic Integration Flashcards

1
Q

What are the four things that Glucose-6-P can be converted to

A
  1. Glucose1-P for use in glycogen
  2. Glucose for release into the blood
  3. 6-phophogluconolactetone to generate NADPH by pentose phosphate pathway
  4. fructose-6-P, used in glycolytic pathway to produce pyruvate
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2
Q

What does creatine kinase do

A

catalyzes a reversible transfer reaction that generates ATP in muscle cells that is a source of energy for muscle contraction

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3
Q

What is resynthesized during the muscle recovery period

A

Phosphocreateine

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4
Q

The brain depends on ___ as its sole energy source

A

glucose

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5
Q

what is the function of astrocytes

A

in the brain transport glucose metabolites to surrounding neruons

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6
Q

what is hte main cite for PET imaging

A

Glucose in the brain

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7
Q

What is the main export in the liver

A

glucose and triaglycerols

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8
Q

triacylglycerols in the blood are hydrolyzed by what

A

LPL- lipoprotein lipase

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9
Q

T or F: amino acids, ketone and lactate are at high levels in the blood

A

F

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10
Q

what does the traicylglycerol cycle do

A

exchanges free fatty acids and triacylglycerols between adipose and liver cells

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11
Q

Where does the glycernogenic pathway function

A

apidoctes and hepatocyctes

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12
Q

Insulin and glucagon are ____ hormones produced in the ______ that control ______

A

peptide homrones produced in the pancreas and control glucose homeostasis

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13
Q

what secretes insulin in the pancreas

A

islets of Langerhans in beta cells

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14
Q

where is glucagon secreted

A

islets of langerhans in alpha cells

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15
Q

what do delta cells produce

A

somatostatin which controls the seceretory process

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16
Q

what do acinar cells synthesize

A

digestive enzymes

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17
Q

Insulin signaling in the brain activates signals that regulate ____

A

eating behaviour

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18
Q

what are the three key differences in insulin effects in lever vs muscle

A
  1. GLUT4 in skeletal, GLUT2 in pancreas
  2. skeletal muscles do not contain Glucose-6-p and fatty acid synthase so all glucose is used for metabolic fuel
  3. Mass of skeletal muscle 30x grater than liver, therefore insulin stimulation of glucose uptake in muscle is hte primary mechanism
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19
Q

activation of glucagon receptors in liver and adipose tissues incerases, what also increases to activate pKA

A

cAMP

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20
Q

pKA also phosphorylates what in liver cells

A

glycogen synthase and phosphoyrlase kinase

21
Q

glucagon signaling in adipose tissue activates _____ hydrolysis

A

triacylglycerool

22
Q

PPAR signaling medates long term control of ____ ______

A

lipid metabolism

23
Q

PPAR alpha function

A

fatty acid oxidation, fasting response

24
Q

PPAR y function

A

lipid synthesis, insulin sensitivity

25
Q

PPAR d function

A

pentose phosphate pathway

26
Q

ligand binding to the PPAR receptor leads to gene activation through ___ ____ ___

A

transcriptional initiation complex

27
Q

conformational changes in PPAR-RXR heterodimer stimulate polyubiquination of _____ proteins tha recruit ______

A

corepressor, RNA polymerase

28
Q

what are the four major changes in metabolic flux during starvation

A

1- increase release of fatty acids
2- increased gluconeogenesis in liver and kidney
3- increase ketogenesis in liver
4- protein degradation in skeletal muscle

29
Q

What is the primary source of metabolic fuel during starvation

A

adopose and skeletal muscle

30
Q

fatty acids regenerate _____ for citrate cycle and production of ketone bodies during starvation

A

actetyl-CoA

31
Q

genetic defects in __ gene in mice leads to obesity

A

ob

32
Q

injecting leptin leads to what

A

reduced food intake and body mass

33
Q

leptin signalin pathways in first order POMC and NPY/AGRP neurons leads to decreased __________

A

fat storage

34
Q

what is metabolic syndrome

A

a cluster of conditions that when put together can increase risk of heart attacks, diabetes, stroke etc

35
Q

what are some symptoms of metabolic syndrome

A

insulin resistance, abdominal obesity, hypertension, hyperlipidemia

36
Q

fatty acids lead to the activation of ____ _____ _

A

Protein kinase C

37
Q

what is inhibits phophornostide-3 kinase in the insulin signaling pathway in obese individuals

A

Serine

38
Q

What should normally be phosphorylated in insulin signaling pathway

A

Ter

39
Q

Serum levels of free fatty acids in obese idividuals could promote ____ resistance in ____ cells

A

insulin, muscle

40
Q

elevated levels of _____- __ leads to down regulation of gene expression and inhibition of insulin signaling

A

TNF-alpha

41
Q

reduced levels of adipenectin results in decrease activation of ____ signaling in muscle cells

A

AMPK

42
Q

what is hte most perscribed drug for treating type 2 diabetes

A

metformin

43
Q

what does metformin do

A

increases AMP levels and activates AMPK signaling to improve glucose and lipid metabolism

44
Q

AMPK plays a key role as a ____ ____

A

master regulator

45
Q

what is an example in which AMPK would be activated

A

stress responses like low glucose

46
Q

binding to AMPKy does what

A

activaetes the AMPK complex

47
Q

T or F: AMPK complex enhances both transcription and translocation in GLUT4

A

T

48
Q

What are thiazolidinediones

A

ligands for PPAR nuclear receptor proteins that when activating gene expression in adipose tissue it leads to increased insulin sensitivity

CH350 (12 decks)

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