Biochem Qcom 2014 Test # 3

Front 1

METABOLICALLY, insulin increases these 5 processes:

Back 1

1) increases transport
(incr # of glucose transporters in p.m. to facilitate more glucose uptake. also, increases a.a. uptake, K+ uptake, Na+ efflux)

2) Glycogen synthesis

3) Fatty Acid Synthesis (in liver)

4) Triacylglycerol Synthesis (in adipose tissue & liver. notes say "f.a. exported from liver as ____"?)

5) glycolysis (conversion on glucose to acetyl coA in liver)

Front 2

METABOLICALLY, insulin DECREASES these 4 processes:

Back 2

1)glycogen breakdown (muscles & liver)

2) f.a. oxidation

3) triacylglycerol hydrolysis and subsequent release of f.a. from adipose tissues

4) gluconeogenesis (in liver)

Front 3

name 2 effects of insulin on GROWTH:

Back 3

1) increases DNA synthesis

2) increases cell growth and division

Front 4

Insulin is involved in biosynthesis and is therefore a(n) _____ hormone. It is released when an individual is in the (fed/fasting) state.

Back 4

anabolic

fed

Front 5

The METABOLIC effects of insulin occur very (rapidly/slowly) and require a (small/large) dose.

vs...

The GROWTH promoting effects (ie stimulating cell growth and division) of insulin, which occur much _____, and require a much _____ dose.

Back 5

rapidly
small

slowly
larger

Front 6

mechanism of depolarization in Beta cells of pancreas:

Back 6

beta cells transport in glucose via GLUT 2 transporter, it is immediately phosphorylated by glucokinase (hexokinase?) and glycolysis is carried out, which produces ATP. norm K+ is pumped out (?), this is blocked by incr. of ATP, cell depolarizes, causing Ca++ to rush into cell, stimulation of release of insulin via exocytosis from insulin containing granules.

Front 7

Fructose... what is it's effect on insulin release and why?

Back 7

Fructose does not stimulate insulin release from beta cells of pancreas. Most likely due to low concentration of GLUT 5 transporters on Beta cells

Front 8

Glucagon lowers the level of _________, thus inhibiting _____ and activating ______

Back 8

lowers FRUCTOSE-2,6-BISPHOSPH

inhibits PFK1

activates FRUCTOSE-1,6-BISPHOSPHATASE

Front 9

Glucagon also stimulates ATP to turn into _____ and PPi, thus activating ____ _____ ____ _____. (phosph pyruvate kinase --> inactivates?)

Back 9

cyclic AMP (cAMP)

cAMP dependent protein kinases

Front 10

also, Glucagon increases the transcription of ____ _____, which is helpful in cases of long term fasting.

Back 10

PEP carboxylase

Front 11

name 5 factors affecting insulin release:

Back 11

1) glucose levels- incr. blood plasma level --> insulin release. (most impt)

2) GI hormones- stimulate

3) Epi/Norepi - decrease/inhibit (?)

4) Pharm drugs- sulfonureas stimulate

5) A.A.s- stimulate

Front 12

Detemir insulin: marketed as _____. It has a f.a. (myristic acid 14:0) attached to ___ @ B29, causing it to bind to ____ in the blood and therefore it is released more _____.

Back 12

levemir
lysine
albumin
slowly

Front 13

Glargine is a ___ acting insulin. It adds 3 ++ charged ____ residues to the ___terminus of the B chain of insulin, thus increasing the pH and making it (more/less) soluble @ physiological pH.

Also, it replaces aspargine @ A21 with _____, to prevent _____ and _______

Back 13

slow
arginines
C terminus

GLYCINE
prevents DEAMINATION and DIMERIZATION

Front 14

Glulisine Insulin: (aka ______), is a ____ acting insulin, often used with insulin pumps. It has a ___ onset and a ____ duration. A.A asparagine (N) is replaced by _____ @ B3 and A.A. lysine (L) is replaced by ______ _____

Back 14

apidra
fast
rapid onset, short duration

Lysine (L)
Glutamic acid
(probably accounts for the name: "glu" "lysine")

Front 15

Aspart insulin (aka ____ and _____), is a ____ acting insulin. A.A. Proline is replaced by ____ @ B28. This results in a steric hindrance and charge repulsion due to the local conformational change at the C terminus of the B chain. This prevents the formation of _____.

Back 15

Novolog Novorapid

Rapid acting

Aspartic Acid ("probably reason for the name")

Hexamers

Front 16

Lisopro insulin (aka _____), is a ____ acting insulin which functions by reversing the order of the penultimate ______ and ____ residues on the C terminal end of the B chain, thus blocking the formation of ___ and ____. It is taken ______

Back 16

Humalog

rapid acting

Lysine and Proline ("hence the name")

blocks formation of dimers and hexamers

postparndial (after meal)

Front 17

Natural Insulin forms _____ with atom of _____. In this form, it (can/cannot) bind to the receptor. Thus this form is useful for the _____ (fast/slow) release of "____ ____" by dissociation from the ____ to the ______.

Back 17

Hexamer
Zinc
does not
slow
basal insulin
hexamer --> monomer

Front 18

Insulin secretion is primarily regulated by _____

Back 18

plasma glucose levels

Front 19

Proinsulin is packaged in ____ ____ and further processed by cleaving the __-_____. Upon stimulation, the granules/secretory vesicles fuse with the _____ _____ and release insulin into blood via ______.

Back 19

secretory vesicles
C-peptide

plasma membrane
exocytosis

Front 20

How Insulin is Made (overview): Insulin is synthesized as _______ in the ____ _____ of the _____ cells in the ____ of _____ in the pancreas. Then the ____ ____ is removed from the ____ terminus to form _______.

Back 20

preproinsulin
endoplasmic reticulum
Beta cells
islets of langerhorn

signal sequence
N terminus
proinsulin

Front 21

Glucagon= ____# A.A.s.
It functions to (incr/decre) blood glucose and (incr/decr) gluconeogenolysis

Back 21

29 A.A.s
INCREASES blood glucose
INCREASES glycogenolysis

Front 22

Name some organs that play a dominant role in fuel metabolism.

Back 22

liver, adipose tissue, mm (muscle?), brain (?)

Front 23

Pramlintide reduces ____ & improves _____ w/o ______ & increase risk of _______ (?)

Back 23

post prandial glycemic excrsions
A1c
weight gain
hypoglycemia

Front 24

____ & ____ injected seperately, but _____ a meal, work to control ________ (?). _____ reduces ____ by regulating _____ and reducing ______by action on _____ (?)

Back 24

Insulin and pramlintide
postprandial blood glucose levels
amylin, post prandial hyperglycemia
gastric emptying & food uptake
glucose sensitive part of brain stem= area postrema (?)

Front 25

Amylin (aka ____) has __# A.A.s. It is secreted by _____ @ same time as ____ in ___:___ ratio. Used to treat _____. It is a synergistic partner to ___ and reduces_____

Back 25

Islet Amlyoid Polypeptide (IAPP)
37 Beta cells pancreas
insulin (100:1)
pramlintide, SYMLIN
DM 1 & 2
insulin (meaning, you only give this to patients if they are on insulin. If they are not on insulin, a similar medicine you could give them is Byetta)

-rise in glucose in blood after a meal

Front 26

Exenatide= ____ agonist. Used as therapy for _____. Approved in ____ by _____. Synthetic version of ______, a hormone in the ____ ______ of _____. Has similar properties as ______.

Back 26

GLP-1
DM (diabetes mellitus) type 2
2005 by FDA
Exendrin-4, saliva, gila monster
human GLP-1

Front 27

GLP-1 enhances ____ in response to ______. It suppresses the secretion of _____. The result is ____ blood glucose.

Back 27

insulin
glucose
glucagon
decrease/lowering

Front 28

Insulin: _____ bond between A & B. # A.A.s in A= _____. # A.A. in B= ____. Increases glucose intake and lipogenesis.

Back 28

2 disulfide bond between chains
(A7<-->B7, and A20<-->B19, also, A6<--->A11)
21 A.A.
30 A.A.