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Biochem 385 Unit 2 > Lecture 27: Metabolic Integration: Health and Disease > Flashcards

Lecture 27: Metabolic Integration: Health and Disease Flashcards

1
Q

thrifty gene hypothesis

A

ppl genetically program to store fat in times of plentiful food

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2
Q

leptin

A

nrg metabolism

neuro control of eating behavior

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3
Q

genetics… and weigh

A

40%-70% of weight due to genetics

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4
Q

Energy balance

A

amount of food consuming=amount of calories spending
can be in nrg balance and be unhealthy
all this means is that your weight is staying the same

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5
Q

positive energy balance

A

consume more cals than spending

weight gain

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6
Q

negative energy balance

A

consume fewer cals than spending
weight los
but you eventually have to reach nrg balance

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7
Q

canditate Thrifty genes

A

over active acetyl CoA
inc sensitivity to insulin
NOT inc levels of UCP

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8
Q

Why over active acetyl CoA

A

acetyl CoA carboxylase catalyzes commitment step for FA synth

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9
Q

Why inc sensitivity to insulin

A

inc metabolic flux through glycolysis, glycogen synth, triacylglycerol synth

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10
Q

why NOT inc levels of UCP

A

this would cause you to burn nrg and lose weight

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11
Q

Pima Indians… name 2 factors that likely differ between the lifestyles of these genetically similar population

A

diet

activity

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12
Q

Leptin as a “fat-o-Stat”

A

helps maintain set point weight
leptin is made by adipocytes
so more fat/fat cells= more leptin
this causes you to want to eat less and be more ative

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13
Q

How could you avoid gaining back weight lost by excercising?

A

eat less!

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14
Q

Why is it easier to lose weight quickly than weight gained slowly over time

A

gradual change causes set point to also gradually reset

long term positive nrg imbalance leads to leptin resistance through changes in leptin receptor signaling

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15
Q

leptin and obesity treatment

A

having mutations in leptin is rare, it would work for those people
IT WOULD NOT work for people who have high levels of leptin but are leptin resistant (like insulin resistant)

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16
Q

leptin production…

A

proportional to fat stores
more fat=more leptin
less fat=less leptin

17
Q

Why does it make sense that leptin and insulin have the same effect on neuronal signaling>

A

lots of insulin=lots of glucose in blood

lots of leptin=lots of fat

18
Q

based on the function and localized secretion of ghrelin and PYY, why is it good advice to eat slowly if you are trying to lose weight?

A

timing: it takes time for food to go from stomach to colon
ghrelin=EAT MORE
PYY336= don’t eat more
but we have to get from grhelin to PYY

19
Q

Type 1 diabetes

A

DONT synth insulin
insulin sensitive
lack pancreatic beta cells

20
Q

Type 2 diabetes

A

synth insulin

insulin RESISTANT

21
Q

Brain interpretation of hormonal signals:

Eat less or more?

A

leptin signal in adipose=eat less, metabolize more
grehlin signal in stomach=eat more (rises during empty stomach)
PYY336 signal in colon: rises after meal, blocks eat more pathway
insulin signal in pancreas=eat less

22
Q

Serum glucose levels

A 
drink: blood sugar levels rise
response to insulin shot:
normal: blood glucose drops
type 1: blood glucose drops
type 2: levels don't respond to insulin shot
23
Q

possible cause of diabesity

A

we have insulin, but body can’t respond
HOW???
response is WRONG
- elevated free fatty acids in serum, they are in membrane
- fatty acids lead to kinase activity
-kinase phosphorylates IRS protein, WRONGLY (phoshorys serine, not tyrosine)
-insulin receptor can’t phosphorylate the tyrosine
LOST IRS activity!!!

24
Q

norma insulin signaling and glucose uptake

A

something binds outside
response inside
Tyr-P on IRS –> activation of PI-3k pathway–> glucose uptake!

25
Q

So… on a larger scale, what causes diabesity???

A

ENVIRONMENTAL CONDITIONS!
this is NOT a genetic mutation
treat w/ diet and excercise

26
Q

why do diabetics who are treated with TZDs see a drop in blood glucose levels but also weight gain?

A

dec in circulating fatty acids result in normal insulin signaling and glucose uptake

27
Q

bad fat

A

not b/c more cals!

High LDL lelvels make it bad

28
Q

how would the function of PPAR signaling proteins explain this observation?

A

PPAR are transcription factors
they are stimed by good fats
if a fat can stimulate PPAR, it may be better

29
Q

What do PPARs do?

A

control adipocyte diff and lipid synth in adipose tissues

30
Q

What does PPAR Gamma do

A

also regulates insulin sensitivity and lipid synth in liver cells

31
Q

PPAR gamma and TZDs

A

TZDs inc insulin sensitivity by activating PPAR gamma genes

32
Q

stimulant molecs

A

works like epi, mobalize and use lots of nrg

33
Q

orlistat

A

inhibits pancreatic lipase

decs fat absorption

34
Q

olestra

A

tastes like fat

but we don’t have the enzymes to digest it

Biochem 385 Unit 2 (13 decks)

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