Nst 160 Midterm 2

Front 1

liver and glucose homeostasis

Back 1

key organ - main site of gluconeogensis ------

receives glucose from intestine via the portal vein

Front 2

fates of glucose

Back 2

can either go to pyruvate via glycolysis or to glycogen in the liver or muscle

Front 3

glycogen breakdown

Back 3

via glycogenolysis and it turns into energy and pyruvate

Front 4

gluconeogenesis

Back 4

supported by aa and by TAG but not by FA

Front 5

brain's response to low glucose

Back 5

--pititary gland - releases cortisol -----------

adrenal medulla - releases epi --> makes glucose ------

sympathetic system - releases norepi and ACh --> increases fat and muscle increase production and uptake . muscle stimulates breakdown of aa

Front 6

gluconeogenesis

Back 6

in liver - coordinated by muscle(lactate and aa) and adipose ( tag --> fa and glycerol)

Front 7

hierarchy of response to low glucose

Back 7

1) insulin decreases

2) glucagon increases

3) epinephrine increases - critical when glucagon is gone but not as effecient

4) cortisol adn growth hormones - adapations to prolonged fasting and insulin resistin

Front 8

insulin biosynthesis

Back 8

in beta cells in central part of islet cells

arterial blood can enter so it can sense directly how much glucose is in the blood---- uptake facilitated by GLUT 2 --------

insulin is a pepetide hormone and its amino terminal gets cleaved along with some other parts in the golgi adn then there are two peptide chains joined by a disulfide bond -------------

c peptides are also released when insulin is made - this is how you can test how much de novo insulin is in the system ----------------

they also secrete islet amyloid polypeptides that can make up amyloid fibrils that aggregate

Front 9

mechanism of insulin secretion

Back 9

glucose enters via glut 2 and this goes to pyruvate (into TCA cycle) --> increase ATP --> closes K+ channels --> depolarization --> opens Ca2+ channels --> fusion of vescicles that lead to insulin secretion

Front 10

uncoupling protiens

Back 10

idk what is but if you increase them you decrease insulin secretion

Front 11

sirt and insulin secretion

Back 11

sirt inhibits PCP1 which causes a faster closing of the K+ channels which leads to more secretion

Front 12

c peptide

Back 12

released with insulin, good for testing how much insulin is in the blood because insulin is degraded fast but this isnt

Front 13

other factors that affect insulin secretion

Back 13

AC, PLC, activate cAMP or insitol pathway

Front 14

glucose trasnporters

Back 14

SGLT 1/2 - in intestine and kidney - active transporter

GLUT 1 - in brain

GLUT 4 - insulin sesnsitive, translocated in muscle and fat when high glucose

GLT 2 - no affinity but high capacity - in beta cells and liver

Front 15

canonical insulin signalling

Back 15

akt/pkb and mek ---> insulin receptor and IGFR regulate metabolism

- activation of insulin receptor can chane transcription for many processses

Front 16

lipid metabolism

Back 16

insulin promotes TG storage and mobilization by increase LPL and FA uptake, inhibit HSL and increasing lipogensis

Front 17

obesity

Back 17

a measure through BMI - caused by energy imbalance but can be influences by genetics and monogenetic mutations - potentially other thigns as well like sleeping, smoking, prenatal effects, pollution

Front 18

BMi

Back 18

body weight (kg) / body height squared (m)

Front 19

what are the different forms of diabeted insipidus and what is the common traits

Back 19

1) central 2) nephrogenic 3) dipsogenic 4) gestational - all diabetes insipidus has polyuria (excessive pee) and polydipsia (excessive thirst)

Front 20

cenetral diabetes insipidus

Back 20

most common form - defeciency or resistance to vasopression/adh. the brain can sense the amount of water via hormones in the hypothalamus. something can go wrong in the hormones or in the kidney

Front 21

vasopressin

Back 21

regulates aquaporins in the kidney which regulates water trasnport. increases when there is high sodium in blood volume. increased vasopressin retains water and constricts the blood vessels and it is made in the hypothalamus

Front 22

nephrogenic diabetes insipidus

Back 22

lack of vasopressin response in kidneys

Front 23

dipsogenic

Back 23

defective thirst regulatino

Front 24

gestational

Back 24

increased levels of vasopressinase during pregnancy

Front 25

diabetes mellitus in general

Back 25

based on hyperglycemia, problems with lipid metabolism, and excreting too much glucose in the urine. both have genetic and environmental factors

Front 26

type 1 DM

Back 26

lack of insulin with death of beta cells. diabetic ketosis leads to an earlier detection of the disease. (hyper production of ketone bodies). this is an autoimmune response - mostly genetic (HLA region) but could also be caused by an environmental factors. t cells destroy infected beta cells adn then eventually all of them. the remaining beta cells can compensate but only for so long. enviro factors include breast feeding, microbiome, vitamin d

Front 27

type 2 DM

Back 27

insulin resistance, muscle, fat, liver problems. most prevalent form. also has a genetic factor but not a single one - hard to pinpoint. everytime you secrete insulin you secrete the amyloid fibrils ! not good cause you're secreting more insulin. glucolipotoxicity

Front 28

diagnosis of DM

Back 28

normal insulin --> increased insulin and increased glucose --> no insulin and increased glucose . to test, you look at hemoglobin A1C in fasted state or you can do an oral glucose challenge

Front 29

type 2 DM physiological effects

Back 29

muscle: type 4 no longer works - liver: increased hepatic output - adipose: increased lipolysis --> increased FFA

Front 30

MODY

Back 30

diabetes in the young - monogenetic mutation. obesity not as frequent. diagnosis is much earlier

Front 31

gestational diabetes

Back 31

only while pregnant. not quite sure why this happens but it is also sort of because of the increase in hormones like progesterone

Front 32

insulin signalling

Back 32

1) insulin binds to receptor --> autophos and conformational change

2) irs 1binds to ptb domain which phos irs1

3) pi 3 binds to irrs1-p and phos other pi's

4) pi's bind to PKB and recruits it to membrane where it is phos and activates

5) activated pkb is released from membrane and promotes glut 4 uptake and glycogen synthesis (by PKB phos GSK3 which inactives GSK bucause GSK inhibit glycogen synthase)

Front 33

lipodystrophy

Back 33

complete lack of adipose tissue leads to severe insulin resistance and reqiures fat transplantation or leptin injections

Front 34

good fat

Back 34

non visceral fat (subcutaneous). good fat activates insulin sensitivity and increases leptin and adiponectin. decreases tag synthesis and increase beta ox and increases insulin

Front 35

bad fat

Back 35

visceeral fat. decreases insulin sensivity and activates proinflam like tnf alpha. visceral fat releases lots of fa

Front 36

adiponectin levels when obese

Back 36

decrease while leptin increases

Front 37

free fa effects

Back 37

in the liver: increases IR and increase gluconeogensis, inapropriate glucose release

in the pancreas: increase insulin release acutely but chronically it causes beta cell death

in muscle: insulin resistnace nad decreased glucose uptake

Front 38

insulin resistance and inflammation

Back 38

activated macrophages in skeletal muscle and liver release adipokines. macrophages explode in stressed cells --> release TNF alpha

kuffner cells sense lipi accumulateion and lead to JNK and IKK beta

proinflammatory cytokines --> NFkB

Front 39

er stress from obesity

Back 39

activate unfolded protein response. caused by too many TAG and FA breaking the membranes. leads to insulin resistance

Front 40

unfolded protein response

Back 40

1too much cholestrol and tag creates er stress which activates IRE1 which activates XBP1 causing enhancement of phospholpiid biosyntehsis which increase membrane biosynthesis. also activates jnk and ikk

Front 41

function of xbp1

Back 41

reduces the free cholesterol to phospholipid ration - mitigating er stress

Front 42

PKR and er stress

Back 42

PKR phos eif2 - antagonizes SREBP activation to decrease cholestrol synthesis

Front 43

er stress and irs1

Back 43

increased adipose promotes er stress. ire1 : jnk phos irs 1 which downregulates insulin signalling

Front 44

jnk

Back 44

phos irs 1 and 2 and inhibits signals through ap 1

Front 45

ikk

Back 45

inhibits thru transcriptional events mediated by NFkB

Front 46

metabolic overload in the liver

Back 46

fa cannot be shuttled into mitochondria because of impaired oxidation due to increased malyonyl coa. too many fa tried to be mitagated by making tag but this causes er stress. also increased DAG which activates stress kinases --> IR

Front 47

metabolic overload in muscle

Back 47

accumulation of lc-coa's, dag, tag --> IR. glucose uptake goes down. lazy mitochondria cannot handle the increase in fa --> reactive oxidatives. triggers stress kinases like PKC --> phos irs1 --> IR

Front 48

diabetic ketoacidosis

Back 48

occurs in type 1 DM.

low pH and hyperglycemia. ketone bodies are produced by the liver and a part of the normal fastng response. symptoms: deep sighing(a response of bicarbonate going to co2 as a buffer) and fruity breath due to protein denaturation. severe dehydration and poydipsia. results from absolute insulin def and hormones excess. treatment: hydrate with iv full and insulin

Front 49

hyperglycemic hypersomolar state

Back 49

in type 2 diabetes.

similar to ketoacidosis.

symptoms: dehydration, hyperosmolarity

Front 50

acute diabetic complications

Back 50

ketoacidosis and hyperglycemic hypersomolar state

Front 51

chronic diabetic complications

Back 51

nueropathy (eye disease) microvascular, macrovascular, and nonvascualar

Front 52

hyperglycemia

Back 52

extracellular --> nonenzymatic glycosolation of proteins --> AGES and HEMO A1C

intracellular --> disturbances of the polyol pathway

Front 53

AGES what are

Back 53

end product of extracellular hyperglycemia / nonenzymatic glycosation. 1) reversible schiff base 2) irreversable crosslinked amadori products .

Front 54

AGES effects

Back 54

vessel wall stiffness, trapping protiens in the crosslinks including antibodies, resistance to degration, increased foam cells --> athersclorosis . increase vascular permeability and ECM production and cell proliferation

Front 55

polyol pathway:; why happen

Back 55

alternative handling pathway for glucose. creates sorbitol and fructose

Front 56

polyol pathway: machanism

Back 56

1) reduce by aldose reductase --> sorbitol 2) fructose and nadh

Front 57

results of the polyol pathway

Back 57

cannot get rid of sorbitol, increased cell osmolarity (cells burst), increased AGES, PCK activation, abnormal enzyme behavior due to insertion of glucose into the hexosamine pathways

Front 58

macrovascular complications

Back 58

arise from damages blood cells --> aterosclorosis

Front 59

types of microvascular complications

Back 59

retinopathy, neuropathy, nephropathy

Front 60

nephropathy

Back 60

causes cellular damages including thickening of the basement membremae, chronic renal failture. accelerated by hypertension. nephrons die and you leak out good things. leads to nephronic syndrome --> wasting ad protein loss --> infections, anemia, malnutrition, rickets, altered blood lipids. treatment: diet with moderate protein and low sodium

Front 61

neuropathy

Back 61

nuerons die and vascular occlusions. injuries go untreated. does not happen in brain. can lead to bacterial infections and GENGREENE and amputations

Front 62

retinopahty

Back 62

thickening of the baseent membrean and loss of pericytes which express Aldose reductase and control blood flow. this leads to hemorrages. maculopathy on macula reduce sight. capillary clsorue and angiogenseiss

Front 63

diabetic complications in pregnancy

Back 63

miscarriages, large babies, and babies with hypoglycemia

Front 64

what organ controls how much glucose tissues take up?

Back 64

liver

Front 65

what organ controls how much glucose tissues take up?

Back 65

liver

Front 66

glycogen

Back 66

can give muscles bursts of energy. has high water content. cannot be packed close. has 1,4 alpha bonds with 1,6 aloha branches. the braches act as fast response to low energy.

Front 67

what organ controls how much glucose tissues take up?

Back 67

liver

Front 68

glycogen

Back 68

can give muscles bursts of energy. has high water content. cannot be packed close. has 1,4 alpha bonds with 1,6 aloha branches. the braches act as fast response to low energy.

Front 69

how do u make glcogen

Back 69

glcogenin is the center residue. glucose 6 phos goes into UTP and g1p which adds together to make a UDP glucose. this autocatalyzes the first 5 residues but then glycogen synthase takes over. branching enzyme transfers 7/11 of glycogens into a branch.

Front 70

what organ controls how much glucose tissues take up?

Back 70

liver

Front 71

glycogen

Back 71

can give muscles bursts of energy. has high water content. cannot be packed close. has 1,4 alpha bonds with 1,6 aloha branches. the braches act as fast response to low energy.

Front 72

how do u make glcogen

Back 72

glcogenin is the center residue. glucose 6 phos goes into UTP and g1p which adds together to make a UDP glucose. this autocatalyzes the first 5 residues but then glycogen synthase takes over. branching enzyme transfers 7/11 of glycogens into a branch.

Front 73

what is an allosteric activator of glycogen synthase

Back 73

glucose 6 phos

Front 74

what organ controls how much glucose tissues take up?

Back 74

liver

Front 75

glycogen

Back 75

can give muscles bursts of energy. has high water content. cannot be packed close. has 1,4 alpha bonds with 1,6 aloha branches. the braches act as fast response to low energy.

Front 76

how do u make glcogen

Back 76

glcogenin is the center residue. glucose 6 phos goes into UTP and g1p which adds together to make a UDP glucose. this autocatalyzes the first 5 residues but then glycogen synthase takes over. branching enzyme transfers 7/11 of glycogens into a branch.

Front 77

what is an allosteric activator of glycogen synthase

Back 77

glucose 6 phos

Front 78

how is glycogen broken down into glucose?

Back 78

debrancher enzyme --> glycogen phosphorylase and vita B6 makes g6p --> muscle or liver to blood (via g6phosphatase)

Front 79

what organ controls how much glucose tissues take up?

Back 79

liver

Front 80

glycogen

Back 80

can give muscles bursts of energy. has high water content. cannot be packed close. has 1,4 alpha bonds with 1,6 aloha branches. the braches act as fast response to low energy.

Front 81

how do u make glcogen

Back 81

glcogenin is the center residue. glucose 6 phos goes into UTP and g1p which adds together to make a UDP glucose. this autocatalyzes the first 5 residues but then glycogen synthase takes over. branching enzyme transfers 7/11 of glycogens into a branch.

Front 82

what is an allosteric activator of glycogen synthase

Back 82

glucose 6 phos

Front 83

how is glycogen broken down into glucose?

Back 83

debrancher enzyme --> glycogen phosphorylase and vita B6 makes g6p --> muscle or liver to blood (via g6phosphatase)

Front 84

what is an inhibitor of glycoen synthase?

Back 84

ampk

Front 85

how does insulin and glucagon affect glycogen/g1p cycling?

Back 85

Back (Definition)

Front 86

what are the phosporases or phosphatases for glycogen synthase and glycogen phosphatase?

Back 86

pka and protein phosphatase

Front 87

what must glucose do before it can go into the blood stream? and why?

Back 87

be cycled through glycogen. because you never want to have no glycogen

Front 88

what do orecigenic signals do? and what is an example?

Back 88

increase appetite. agrp

Front 89

what must glucose do before it can go into the blood stream? and why?

Back 89

be cycled through glycogen. because you never want to have no glycogen

Front 90

what do orecigenic signals do? and what is an example?

Back 90

increase appetite. agrp

Front 91

what does an anorecigenic signal do? what is an example?

Back 91

stops feeding. pomc.

Front 92

what must glucose do before it can go into the blood stream? and why?

Back 92

be cycled through glycogen. because you never want to have no glycogen

Front 93

what do orecigenic signals do? and what is an example?

Back 93

increase appetite. agrp

Front 94

what does an anorecigenic signal do? what is an example?

Back 94

stops feeding. pomc.

Front 95

what does metformin do?

Back 95

stimulated ampk

Front 96

fox o1 and gluconeogenesis

Back 96

akt phos's fox o1 and it leaves the nucleus and it inhibits GNG

during mild fasting or long term (sirt 1) de phos fox o1, fox o1 goes unto the nucleus and increases GNG through pepCK

glucose is released into the blood and it activates sestrin which activates ampk which stimulates fa ox

Front 97

gluconeogenesis and CREB/CRTC2

Back 97

when glucagon is high, it p's creb which is in dimer with crtc2 --> increases GNG/

when there is insulin, akt is active and p's SIK which p's CRTC2 which inhibits it

Front 98

von gierke's disease

Back 98

glycogen storage disease: growth failure, lacticidosis, hypoglycemia, g6pase

Front 99

pompe's disease

Back 99

glycogen storage disease: muscle weakeness, heart failure, glucosidase

Front 100

cori's/forbes

Back 100

glycogen storage disease: hypoglycemia, myopathy, growth retardation, debrancher

Front 101

andersen

Back 101

glycogen storage disease: cirrohsis, death by 5, branching

Front 102

mcardle's

Back 102

glycogen storage disease: exercise cramps, renal failure, muscle glycogen phosphorylase

Front 103

hers'

Back 103

glycogen storage disease: hypoglycemia, liver glycogen phosphorylase

Front 104

tarui's

Back 104

glycgen synthase disease: exercise cramps, weakness, growth retardation, phosphofructokinase

Front 105

brown adipose tissue characteristics

Back 105

multiocular, generate heat, endocrine function, limited, inverse correlation with outdoor temp, depensd on nutritional status, becomes less functional with ageb

Front 106

brown adipose functins

Back 106

inversely related with adipoisty and bmi. expresses UCP1. increases TAG clearance, generates heat via UCP1 via fa ox

Front 107

mechanism of UCP1

Back 107

mitochondrial respiration, as yu make NAD+, o2--> h20 via ETC then ATP via ATP synthase. cells with BAT make HEAT insteaed of ATP

Front 108

is warm or cold better for BAT?

Back 108

cold

Front 109

UCP1 null mouse effects

Back 109

mouse lost weight because it is used to the fa methods of BAT but it is just doing it in ineffecient methods?

Front 110

regulatin of UCP1

Back 110

1) sensed by sympathetic NS -->norepi --> beta adrenergic --> cAMP + PKA --> CRPP --> stimulates GNG and lipolysis.

2) thyroxine is taken up by BAT --> activates ppars

Front 111

type 1 nuclear receptors

Back 111

steriod receptors. in cytoplasm, binds, dimerizes and enters nucleus binds to DNA (HRE) --> activates transcription

Front 112

what nuclear receptor is for steriods?

Back 112

type 1

Front 113

type 2 nuclear receptors

Back 113

for the other stuff like thyroid and -XRs. these are being sensed in larger quantities. already bound to DNA as heterodimers with HREs and RXRs. if there is no ligand, there is a corepressor atached. if there is a ligand, a co activator replaces it

Front 114

type 3 receptors

Back 114

binds to direct repeats

Front 115

type 4 receptors

Back 115

only bind a single DNA binding domain. binds to a single half site HRE

Front 116

where are glucocorticoids produced and what kind of nuclear receptor do they bind?

Back 116

adrenal gland on top of the kidney. type 1 (bcsteriod)

Front 117

effects of cortisol

Back 117

increased during fasting. stimulates fa metab, stimulates GNG and glucose release in the liver, inhibits uptake of glucose by muscle, increase breakdwn of muscle protien

Front 118

cushing's syndrome

Back 118

verprduction of cortisol. central obesity and insulin resistance. abnormal body shape and euphoria

Front 119

vitamin d pathway and where

Back 119

vita d -- 25 hydroxylase --> 25 OH D. happens in kidney. type 2 receptor.

Front 120

function of vitamin d

Back 120

calcium hmeostasis. release calcium from bone and reabsorb it in the kidney. prmotes calcium absorption in the intestine

Front 121

retinioc acid recptor

Back 121

type 2 recptor
functions: growth, vision, reproduction, developemnt
binds throguh RXR or RAR

Front 122

estrogen receptor

Back 122

type 1

effects glucse uptake by muscle, prevents visceral fat, increases central sensitivit of leptin, increases leptin receptors in adipose: prevents development of obesity and insulin resistnece

Front 123

thryoid hormone

Back 123

type 2. iodinated aa derivitives. synthesis and secretin stimulated by TSH . can decrease weight (increasing heart rate and body temperature), lwoer cholestrol. loss of TSH can cause cardiac problems, muscle wasting, bone fatigue, etc
the hypothalamus controls how much hormone you make and it is sensed by the pituitary

Front 124

dietary fa regulation of gene trx

Back 124

by binding like with ppars or by indirectly changing like srebp

Front 125

ppars

Back 125

for fa and deritivies. three forms: alpha, gamma, delta. type 2. no fa --> n transcription.

Front 126

ppar alpah

Back 126

activated by unsta fa and fibrates. increases mito and peroxisomal breakdown of FA. increases lipid oxidation, ketogenesis and glucose sparing (to help fight starvation). increases HDL. found in liver, heart, kidneys, BAT

Front 127

ppar gamma

Back 127

activated by fa, prostoglandinds and txds (inflam). stimulates differentiation of adipocytes and fa uptake and storage. changes adipokine expression. (increases adiponectin but decreases leptin) increase adipose size and more adipose in the right places.

Front 128

ppar delta/beta

Back 128

activated by long chain fa. increases muscle's fa ox and switch from type 2 to type 1 muscle fibers. in adipose, skin, brain, everywhere.

Front 129

endocrine control of feeding is regulated where?

Back 129

arcuate nucleaus in the brainstem/hypothalamus

Front 130

agrp/npy

Back 130

orexigenic - make u hungry ! they increase food uptake by changing behavior

Front 131

npy

Back 131

binds to a gcpr. stimmulated by fasting. you will not immediately starve without it because of backup mechanisms

Front 132

agrp

Back 132

in skin color and fur (agouti) binds to melocortin receptrs and coexpressed by npy. long term --> obesity.

Front 133

orexins

Back 133

two peptides linked to feeding, sleep and activity. delays onset of satiety. if you have a low level you stop eating earlier.

Front 134

disruption of orexins

Back 134

narcolepsy

Front 135

reward system in response to feeding

Back 135

rewarding nature of food. stimulates feedings. incolces opiods, endocann, dpaminergic and serotonin.

Front 136

rimbonabant

Back 136

antagonizes reward system - antiobesity drug

Front 137

pomc/cartt

Back 137

anoerectic signals telling you are full and should not eat.

Front 138

cart

Back 138

wide spread in the CNS. food intake, bdy weight, reward ,endocrine functions. in arc expression decreased with fasting. also reduces refeeding response. blocks npy singal. mutatins leads to obesity

Front 139

pomc

Back 139

expressed in tissues. in arc, msh alpha goes to the melocortin receptors/pathways (MC4)

Front 140

MC4/melocortin receptor

Back 140

how does it work with both of them?
msh alpha (pomc) stabilizes active form

agonizing --> increases cAMP.

agrp disrupts the active form and there is no activation.

Front 141

effects of losing mc4

Back 141

obestity

Front 142

perihperal signals coming from the gi tract in response to feeding

Back 142

gherlin and GLPg

Front 143

gherlin

Back 143

gherlin receptors are on agrp/npy. released by empty stomach. also increased by lasck of sleep. it is released right before you would normally eat and supressed at night. regulated by circadian rhyhm

Front 144

GLP

Back 144

glucagon like peptide. from intesetine - released after intestine senses different nutrients. prepares body for carb rich meal. stimulates insulni release and inhibits appetite and food intake.

Front 145

signals frm pancreas in resposne to feeding

Back 145

insulin, pp, somatostatin

Front 146

somatostatin

Back 146

is released by beta cells in response to high glucose and alanin . inhibits gi secretions

Front 147

pp

Back 147

released by islets after eating. reduces food intake and slows absrorption

Front 148

adipokines in response to feeding

Back 148

for long term regulation. leptin, ampk

Front 149

leptin

Back 149

exclusively produced by adipose and sensed by hypothalamus. more leptin suppresses fedeings and down regulates npy and mcs, orexins, and sgrp. upregulates the other ones.

Front 150

what activaets leptin

Back 150

mtor

Front 151

ampk in response to feeding

Back 151

fuel sensor. integrates all the signals.

Front 152

characteristics of alzheimemrs

Back 152

amyloid fibesr and nueronal tangles (microtubulues - phos tau --> destabilize and accumulates inside nueron )

Front 153

molecular mechanisms of AD

Back 153

1) systemic defeciency --> impairs learning

prcess

2) in brain, insulin cpmpeptes with AB for insulin degrading enzymes --> amyloid plaques build up

3) IR --> hyperphos tau --> nueronal tangels
4) accumulation of AGES --> oxidiative stress, mitochondrial dysfunction, nueronal death --> inflammation pathways

Front 154

amyloid plaques

Back 154

can build up in the brain during AD. cause a positive feedback loop that enhances phos of tau and nueronal tangels.

Front 155

apo e2

Back 155

duoble cys. can make CVD workse because you cannot clear the VLDL particles --> inflam --> heart disease

Front 156

apo e4

Back 156

is assciated with AD. because the brain moves lipids around and astrocytes are improtant for this. astrocytes need nutrients and apo e4 are not giving it to the,/ .

Front 157

which apo e makes AD wrse?

Back 157

e4

Front 158

how to treat AD

Back 158

exercise? lowering choelstrol, ppar agonists, insulin and glp receptor agonists can reverse hte beta amlyoid fibers and insulin resistance. intranasal insulin --> straigh tot the dome.

Front 159

first line of defense against diabetes

Back 159

exercise and good diet.

Front 160

lifestyle management for diabetes

Back 160

dietary habits, physcial activity, behavior modification

Front 161

mediterranean diet

Back 161

high fiber low fat

Front 162

physical activity

Back 162

moderate - best if yu do with diet

Front 163

insulin replacement therapy

Back 163

fast activing - right before meal. slow release - befre bed. gd for type 1 diabetes. con: if you inject too much you can becoe hypoglycemic. and u must inject a lot so a lot of people do not keep up with it.

Front 164

sulphonylureas

Back 164

diabetes treatment - for type 2 - for stimulating endogenous insulin production. inhibits k+ channels causing depolarization of ca++ channels leading to insulin release. side effects: could cause weight gain + hypoglycemia. it could also exhaust beta cells

Front 165

stimulate glp1 signals

Back 165

diabetes treamtent. glp is produced by the small intestine. makes you feel full and increase the amt of insulin released. a synthetic version is degraded quickly . delays gastric emptying

Front 166

dipeptydl peptidase 4 inhibitors

Back 166

stablilize endogenusly released glp1 so it is not degraded as quickly . you wouldn't have to inject as much insulin.

Front 167

metformin

Back 167

stimulates ampk . increase glucse uptake enchances fa ox and decreased glucse being relae. insulin sensitizer.

Front 168

fibrates

Back 168

ppar alpha agonists. diabetes treatment. liver can break down more fa by making more mitochondria. increase beneficial HDL and decrease TAG

Front 169

glutazones

Back 169

type 2 receptor - ppar gamma agonist. increases size of adipocytes --> increase good fat. caused heart attacks. used for diabetes treatment.

Front 170

ppar delta agonists

Back 170

diabetes treatment. highly expressed in muscle. increase HDL decrease TAG and chlestrol

Front 171

statins

Back 171

ultimately lowers LDL. huge drug

Front 172

inhibit reabsorption o f glucse in the kidney

Back 172

diabetes treamtment. glucose is reabsorbed thru SGLT2. can cause bladder infections.

Front 173

fen-phen

Back 173

diabtets treatment. increases seratonin levels whichahs anorertic effects. causes heart problems.

Front 174

alpha glucosidase

Back 174

inhibits digestion of glucose and not proteins

Front 175

orlistat

Back 175

binds to the active site of pancreatic lipase. prevents genertaion of FA --> gives to colon. nasty po.

Front 176

ezetimibe

Back 176

blocks dietary cholestrol by blocking trasnprter

Front 177

sibutramine

Back 177

causes satitety by increasing serotnin thru inhibition of reuptake

Front 178

DNMT1

Back 178

makes sure that a methyl group stays on one of the DNA strands durign replicatin.

Front 179

methylation in epigenetics

Back 179

germ cells have some methylated patches. there is a global wave of demethylaation and then ne that is sex specific

this process is driven by development and differentiation

Front 180

exceptions in demethylation (epigenetics)

Back 180

patterns for sex specificity are not erased

Front 181

what effect does methylation have on genes

Back 181

supresses them

Front 182

what is required for methyaltion

Back 182

folate / folic acid - acts as a methyl donor

Front 183

agouti mice deomstrate what principle?

Back 183

epigenetics - range of colors means that there is differences in methlyation and transposns

Front 184

what must glucose do before it can go into the blood stream? and why?

Back 184

be cycled through glycogen. because you never want to have no glycogen

Front 185

what do orecigenic signals do? and what is an example?

Back 185

increase appetite. agrp

Front 186

what does an anorecigenic signal do? what is an example?

Back 186

stops feeding. pomc.

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what does metformin do?

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stimulated ampk

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fox o?

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not quite sure what it does but it is involved in feeding.

liver: it regulates glucose and lipid metab --> prevents fa syn

beta cells: regulates proliferation, differentiation and stress resistance

arn - not sure!