Integration of Metabolism

Question 1

Possible fates of G6P?

Answer 1

1.Stored as glycogen
2.converted via glycolysis anf PDH to acetyl COA –>ATP
2 . precursor for FA and cholesterol synthesis
3. enter PPP to make NADPH and ribose 5 phosphate

Question 2

fates of Amino acids

Answer 2

(1) protein synthesis-liver and plasma proteins
(2) enter bloodstream to be used by other tissues to make proteins
(3) used as precursors for biosynthesis of nucleotides, hormones, other compounds
(4) yield products that enter TCA cycle; ammonia converted to urea and excreted
(5) Pyruvate converted to glucose and glycogen
(6) converted to acetyl-CoA, then oxidized via (7) the TCA cycle and (8) OXPHOS to produce ATP
(9) used to make lipids for storage
(10) TCA cycle intermediates make glucose
(11) muscle proteins converted to alanine, which is can be used to make glucose in liver via the glucose-alanine cycle

Question 3

F.A Metabolism in Liver fates ?

Answer 3

converted to liver lipids;

(2) oxidized to give acetyl-CoA and NADH;
(3) acetyl-CoA further oxidized via TCA cycle and (4) used to make ATP via OXPHOS;
(5) excess acetyl-CoA is converted to ketone bodies (fuel for heart, and for brain during prolonged fasting)
(6) some acetyl-CoA used for synthesis of cholesterol;
(7) fatty acids can be converted to the TAGs and the phospholipids of plasma lipoproteins;
(8) and some is bound to serum albumin and carried to heart and skeletal muscle for use as fuel

Question 4

Metabolism in Adipose Tissue

Answer 4

in notes

Question 5

__+__=energy consumed

Answer 5

energy expended + energy stored

Question 6

Short-term biochemical signals (all are peptides)

Originate from ?

Answer 6

GI tract, beta cells of pancreas, and fat cells

Question 7

Short-term biochemical signals target ?

Answer 7

arcuate nucleus of the hypothalamus

Question 8

What are Two signals relay feelings of satiety?

Answer 8

1. chloesystokin- secreted by the SI

2. glucagon like peptide 1

Question 9

Ghrelin?

Answer 9

Ghrelin: secreted by stomach, stimulates appetite

Question 10

when leptin binds to its receptor it __?

Answer 10

Binding to its receptor increases sensitivity of muscle and liver to insulin, stimulates b-oxidation of FAs, and decreases TAG synthesis

Question 11

orexigenic

Answer 11

appetite stimulating

Question 12

neurons in the arcuate nucleus inhibit __

Answer 12

Neurons in arcuate nucleus: inhibits production of appetite-stimulating (orexigenic) peptides Neuropeptide Y (NPY) and agouti-related peptide (AgRP)

Question 13

Insulin inhibits ______, thereby inhibiting food consumption.

Answer 13

NPY/AgRP-producing neurons,

Question 14

describe the process of the insulin signaling

Answer 14

in notes

Question 15

Most obese people have high blood levels of leptin.

But they have leptin resistance. Why?

Answer 15

Because of overactivity of Suppressors of Cytokine Signaling (SOCS) proteins
Disrupt interactions among components of insulin (& leptin?) signaling pathway, inhibiting it

Question 16

1921: __ and __ discovered insulin is produced in the pancreas (dogs).

Answer 16

Frederick Banting and medical student Charles H. Best

Question 17

type 1 diabetes is insulin dependent caused by?

Answer 17

destruction of pancreatic Beta cells

Question 18

Type II (NIDDM) is characterized by?

Answer 18

insulin resistance

Question 19

dyslipidemia?

Answer 19

—called metabolic syndrome, a precursor to diabetes

Question 20

in the pricess on secteting insulin , high ATP/ADP ratio will cause ?

Answer 20

K+ channels to close, Ca2 channels to open, influx of Ca2+ and release of insulin

Question 21

How does insulin resistance cause pancreatic failure?

Answer 21

Normally, ER in b-cells processes proinsulin to mature insulin
As insulin resistance develops, ER ramps up effort to process insulin, but becomes overwhelmed,
ER is stresssed and caused B cell apoptosis

Question 22

in Type 1 Diabetes Patient is in a biochemical fasting mode despite high blood concentration of glucose causing ?

Answer 22

cells to be starved and Liver is “stuck” in ketogenic and gluconeogenic mode

Question 23

High glucagon/insulin ratio

causes

Answer 23

inhibition of glycolysis
promotes glycogen breakdown in liver—excessive amount of glucose produced by and released from liver
Result: glucosuria, polydypsia

Question 24

Uncontrolled breakdown of lipids and proteins yields high levels of ___?

Answer 24

ketone bodies (ketogenic state)

Question 25

in the fed state Glucose and amino acids transported from __ into blood

Answer 25

intesine

Question 26

in the fed state lipids are packaged into __ and tranported into the blood via ___ system

Answer 26

chylomicrons

lymphatic

Question 27

the fed state stimulates ?

Answer 27

storage of fuels and synthesis of proteins
Stimulates glycogen synthesis in muscle and liver; suppresses gluconeogenesis; stimulates glycolysis in liver, which, in turn, increases fatty acid synthesis

Question 28

How is excess blood glucose after a meal removed?

Answer 28

Glucokinase: acts to trap large quantities of glucose in the liver as Glu6P
Rise of Glu6P, together with insulin action, leads to the buildup of glycogen
entry of glucose into muscle and adipose tissue

Question 29

stage two of the starved fed cycle

Answer 29

early fasting or postabsorbative
Stimulates glycogen breakdown and inhibits glycogen synthesis
inhibit FA synthesis; stimulate gluconeogenesis

Question 30

in the early fasting stage Entry of glucose into muscle and adipose tissues __ as insulin level declines

Answer 30

decreases

Question 31

What is result of liver glycogen depletion?

Answer 31

Gluconeogenesis from lactate and alanine continues, but this just replaces glucose used

Question 32

stage 3 of starved fed state?

Answer 32

refed stage

Liver remains in gluconeogenic mode, but glucose used to replenish glycogen; and FA synthesis

Question 33

what is Priority #1 during fasting?

Answer 33

Provide sufficient glucose for brain and other tissues (RBCs) that are dependent on it

Question 34

what is Priority #2 during fasting?

Answer 34

to preserve protein by shifting fuel source to fatty acids and ketone bodies

Question 35

Metabolic Changes during Day #1 of Starvation?

Answer 35

liver uses mainly fatty acids for fuel

Question 36

In Metabolic Changes during Day #1 of Starvation what causes inhibition of glycolysis?

Answer 36

b-oxidation of fatty acids produces acetyl-CoA, which stimulates phosphorylation and inhibition of PDH
Increase of Acetyl CoA and citrate

Question 37

by day 3 of starvation __ is secreted by liver

Answer 37

ketone bodies

Question 38

3 stages of liver damage

Answer 38

) Fatty liver stage

(2) alcoholic hepatitis: groups of cells die and inflammation results
(3) cirrhosis of the liver:

Question 39

: ethanol consumption leads to accumulation of?

Answer 39

NADH

Question 40

microsomal ethanol-oxidizing system (MEOS)?

Answer 40

Cytochrome P-450-dependent; generates acetaldehyde, then acetate; also NAPD+

Question 41

What causes oxidative stress in MEOS

Answer 41

P-450 enzyme uses O2 and consumes the NADPH needed to form GSH; free radicals are produced and not adequately removed,

Question 42

Excess alcohol disrupts vitamin _ metabolism

Answer 42

A

Question 43

Other disruptions due to alcoholic malnutrition?

Answer 43

Wernicke-Korsakoff syndrome due to thiamine insufficiency, and (2) alcoholic scurvy due to vitamin C insufficiency

Question 44

leptin ?

Answer 44

Binding to its receptor increases sensitivity of muscle and liver to insulin, stimulates b-oxidation of FAs, and decreases TAG synthesis