Integration of Metabolism

Question 1

Postprandial hypoglycemia

Answer 1

exaggerated insulin release after meal
-cuz high glycemic index food
frequent small meals

Question 2

Alcohol hypoglycemia

Answer 2

elevated NADH-makes gluconeogenesis and TCA slow down

Question 3

insulin induced hypoglycemia trx

Answer 3

mild-give carbs orally

severe-adminster glucagon subcutaneously/intramuscularly

Question 4

Pathways for liver @ starvation

Answer 4

degrades glycogen to produce glucose for export
-after deplted-does gluconeogenesis from AA, glycerol ,adn lactate

recieves FA from adipose tissues-oxidizes them to produce energy and ketone bodies for export

Question 5

how does body recover for loss of liver glycogen

Answer 5

glocuoneogenic pathway in liver and kidenys
-glucose for brain and RBC

FA bbecome primary fuel
-large about of FFA to liver-high levels of acetyl Coa-TCA slows down and makes aceyl COA shift to ketogenesis to make ketone bodies

Question 6

Brain pathways under starvation

Answer 6

Use glucose normally

now use ketone bodies to get acetyl coa to run TCA cycle

Beta ox-makes NADH and hydroxy butyrate (main ketone body)-leads to acetoacetate

Question 7

DM criteria

Answer 7

Wait above 40 or 35 inches
TAgs over 150
HDL less than 40, 50mg  (woman)
BP over 130/85
fasting glucose over 110

need 3

Question 8

stims for glycogenolysis

Answer 8

stronger-epi/norepi

strong-glucagon

Question 9

stims for glucogenesis

Answer 9

stim by glucagon and cortisol

Question 10

DM metabolic tissue (in terms of insulin)

• subcat white adipose
• BAT
• visceral white

Answer 10

-insulin sensitive-can still store sugar

BAT-maks you more insulin sesntive

Visceral white-insulin resistant

Question 11

adipokines

Answer 11

signalling proteins secreted by adipose tissue

Question 12

intraabdominal adiposity results in

Answer 12

increase inflammatory marekrs, increased FFA, increased adipokines
-dyslipidemia, insulin resistance, inflammation

Question 13

Role of visceral adipose tissue in insulin resistance

Answer 13

FFA to liver, adipose as secretory organ, excess fat influences insulin signalling/secretion

Question 14

NEFA

Answer 14

nonesterified free FA-made by fat cells

inhibit inuslin secretion (turns off GLUT4)
-glucose taken up by muscle

more gluconeogenesis

Question 15

Adipocytic hormones

• resistin
• leptin
• adiponectin

Answer 15

resistin-pro hyperglycemic
-inhibits AMPK-gluconeogenesis activated

letpin and adiponectin-reduce hyperglycemia

• if problems with receptor/secretion=hyperglycemia
• activate AMPK

these affect CNS (change if hungry/want to excercise=@ hypothalamus)

Question 16

AMPK functions (6)

Answer 16

even in absence of glucose

• muscle glucose uptake
• muscle glycolysis
• beta ox
• decrease lipolysis in adipose tissue
• inhibit FA synthesis
• inhibit gluconeogenesis

Question 17

DM and starvation

Answer 17

DM is starvation in presence of high blood sugar

Question 18

CCK, GLP1, GIP

Answer 18

CCK-weaker than otehrs

bind to INCRETIN receptor

activate cAMP

• leas to secretion of insulin/ihibition of glucagon
• lwoers blood glucose

glucose independent insulin secretion

Question 19

Why clinical consequences in organs without inuslin depence

Answer 19

if has insulin depence-glucose doesnt go in here

• if doesnt have it-glucose can build up here
• aldose reductase to make sorbitol
• H2o difuses in

Question 20

chornic elevated glucose effects (2)

Answer 20

nonenzymatic glysoylation
-chagnes property of protein-reduces half life (but HbA1c lasts 120 days?)/enzymatic activity/binds to things should bind

Question 21

aldose reductase

-results in

Answer 21

glocuse adn NADPH to sorbitol

neprhopathy, neuropathy, lens problems

Question 22

DM 1 and autoimmune attack

Answer 22

Initating event-virus/toxin exposure starts B cell destruction

• starts slow and remains kinda slow
• see clinical disease only when 90% beta cells destroyed

Question 23

DM2 and weight loss

Answer 23

will occur cuz cant take glucose into cells

Question 24

Hyperglycemia Sx

Answer 24

3P

polyphagia, polyuria, polydipsia

Question 25

3P mechs

Answer 25

polyphagia-increased lipolysis and protein catabolism

polyuria-hyperglycemia and ketoacidosis=effecive osmoles

Polydipsia-volume depletion

Question 26

3 more bad thigns about DM

Answer 26

• hypertag-LPL low beucase less when insulin low
• ketoacidosis-increase FA mobilization from adipose, to liver beta ox-to syntehsis of ketone bodies
• overproduction of glucagon

Question 27

Ketoacidosis and DM1 or 2

Answer 27

Most likely in DM1

Question 28

Intensive vs standrard insulin therapy

Answer 28

Intensive therapy decrease HbA1C alot more than standard but its not good for small children since can result in hypoglyemia

Question 29

DM2

Answer 29

milder sx than type 1

• usually no ketoacidosos
• HYPERTAG-VLDL production
• more LDL since have some insulon
• usually dont need insulin trx-unless let it get really bad lol

Question 30

Adult onset DM2

Answer 30

gradual appearnce of insulin resistance

• often higher levels in begining but still no response of GLUT4
• highly genetic (DM1 not highly genetic)-polygenic

Question 31

insulin trx in DM1 vs 2

Answer 31

DM1 has high decrase of glucose

DM2 has no decrease in glucose (cuz receptors dont work)

Question 32

Insulin vs glucose

• normal
• DM 2

Answer 32

Blood glucose levels stay within narrow limitts

DM2 has to make alot more insulin to keep it wihin these narrow limits

Question 33

why insulin makes less ketogenesis

Answer 33

less lipolysis (ratio of glucagon to insulin isnt that bad)

• increased LPL
• less VLDL but still elevated

Question 34

glucose/FFA tox

Answer 34

changes activity of insulin and uptake of gluocse by muscle/adipose tissue

Question 35

Alpha glucosidase inhibs

Answer 35

Acarbose

slow absorption of carbs-reduce postprandial elevationsin plasma glucose

Question 36

sulfonylureas

Answer 36

gliuride

Cause depolarization of beta cell membrane-open Ca2+ channels-more Ca2+ into cell, stimulates insulin secretion

Question 37

Metoformin

Answer 37

inhibits gluconeogenesis
Inhibits Oxphos Complex I
-males AMP level increase
—-blocks glucagon-R
———-leads to glycolytic and gluconeogenesis
—-AMPK activates
———-Improved insulin-R funciton, improved Glut4, less FA syn

Question 38

DPP4 inhibitor

Answer 38

Januvia

DPP4 decreades incretins
-block this and have insulin secretion

Question 39

SGLT2 inhibs

Answer 39

block glusoe reabosption in distal kidney (90% resorpbtion)

SGLT1 in stomach and prox kidney (10% resoption)

Question 40

acute complicatns of DM1 vs 2

nutrtional status at disease onset

Answer 40

ketoacidosis-1, undernourished

2-hyperosmolar state, overnourished