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PHYSIOLOGY-Y2S2 > obesity > Flashcards

obesity Flashcards

1
Q

what is obesity?

A

excessive and abnormal increased body fat

Stored in subcutaneous tissue, adipocytes , intra-peritoneal cavity

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2
Q

what is development of obesity associated with?

A

Increased number of adipocyte and their size

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3
Q

compare previously believed and recent finding ?

A

during infancy and childhood the number of adipocytes increases

WHEREAS the size of adipocytes is the major issue im adulthood

Recent findings : new adipocytes can differentiated from other pre-adipocytes at any period of life

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4
Q

describe obesity and food intake?

A

energy balance —> energy consumption ( Metabolic function, digestion , physical activity ) is EQUAL to energy balance

Energy imbalance —-> Energy consumption is LESS than energy intake ( Eat more than consumption )

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5
Q

what controls food intake?

A

Environmental factors

Culture factors

Lifestyle : Sleep pattern , Stress

Genetic

Psychological factor

Physiological factors ( hunger and satiety )

Hunger = need to have food

Satiety = no need for food intake

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6
Q

what are the food intake basic concepts?

A

Hunger

Appetite

Satiety

Starvation

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7
Q

describe hunger?

A

Craving / seeking food ( need to eat )

Associated with other physiological factors -> Release of ghrelin , rhythmical contraction of stomach

BODY NEEDS IT

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8
Q

describe appetite ?

A

Desire for food

Associated with sensory experiences e.g sight, smell of food, and emotional factors

body doesnt need the food but the person wants to

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9
Q

describe satiety ?

A

Satisfied feeling of being full after eating

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10
Q

What is starvation ?

A

Depletion of food stores in the body tissues

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11
Q

what influeces each feeling ?

A

Environmental

Culture factors

physiological control —> brain –> HYPOTHALAMUS

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12
Q

whats the neuronal control of food intake ?

A

Lateral nuclei of hypothalamus ( LNH )

Dorsomedial nucleus

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13
Q

what is the function of lateral nuclei of hypothalamus? LNH

A

Activation of it :

Increase food intake ( HYPERPHAGIA )

Destruction of it :

Decreases food intake ,or lack of desire for food ( inanition = low fat and energy and thin )

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14
Q

what is the function dorsomedial nucleus? DMN?

A

Increases eating behavior like LNH

BUT when destroyed or has lesions—> USUALLY DEPRESS EATING BEHAVIOR

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15
Q

what nuclei is responsible for Satiety ?

A

Ventromedial nuclei of hypothalamus ( VNH )

Paraventricular nucleus ( PVN )

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16
Q

what is the function of ventromedial nuclei of hypothalamus? VNH

A

Stimulation : COMPLETE SATIETY ( aphagia )

Destruction of VNH —>

Continued eating and obesity ( NO SATIETY )

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17
Q

what is the function paraventricular nucleus ? PVN ?

A

similar to Ventromedial nuclei

LESIONS OF IT = OFTEN CAUSE EXCESSIVE EATING

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18
Q

describe feeding and satiety centers of hypothalamus ?

A

Coordinate the process that control eating behavior and perception of satiety

Hypothalamus receives several types of signal:

Neuronal from GIT providing info about stomach filling

Chemical from nutreints

GIT hormones

Hormones from adipose tissue

From central cortex ( Sigh, smell, taste )

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19
Q

what is the nucleus responsible for integrating the signals coming from hormones ?

A

Arcuate nucleus

MAIN INTEGRATIVE SITE OF INPUT SIGNALS FROM HORMONES RELEASED FROM GIT and ADIPOSE TISSUE ( like cck, ghrelin and more )

adipose relase leptin for energy balance

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20
Q

what is higher center than hypothalamus?

A

hypothalamus is the main regulating

but higher center like amygdala impact it

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21
Q

how does the arcuate nucleus manage all these aspects?

A

Two main types neurons IN the ARN :

are important to coordinate appetite and energy expenditure

1- Pre-opimelanocortin ( POMC ) neurons

2- Neurons release orexigenic substances

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22
Q

what does POMC neurons release?

A

alpha melanocyte - stimulating hormone (AMSH ) —> MAINLY

Cocaine and amphetamine - related d transcript ( CART )

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23
Q

what happens when POMC neuros are activated?

A

anorexigenic :

Decreased food intake

and

INCREASED energy expenditure

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24
Q

how does POMC make it function ?

A

POMC neurons will release :

AMSH

Which in turns act as melancortin receptors (MCR )

especially in neurons of PARAVENTRIUCALR NUCLEI ( which is responsible for satiety )

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25
how many MCRs are found in PVN ?
At least 5 melanocortin receptors TYPES: MCR3 MCR4 are the most importation
26
what happens when MCR3 and 4 are activated ?
decrease food intake Increase energy expenditure Neuronal pathways projecting from PVN to nucleus of tractus solitarius NTS pvn = satiety ( damage = excessive eating ) Eventually it increases sympathetic NS which increased energy expenditure
27
what happens if we have mutation of MCR?
Mutation POMC and MCR4 receptors = obesity in children ( cuz no satiety ) Excessive activation of MCR receptors = ANOREXIA ( no eating and excessive satiety )
28
what does Neurons release orexigenic substances release ?
Neuropeptide Y ( NYP ) Agouti- related proteins (AGRP ) OREXIGENIC = stimulates feeding
29
what is the function of NPY and AGRP?
Activation of NYP-AGRP lead is opposite to POMC : Increase food intake Less ENERGY EXPENDITURE NPY = increase when energy is low so it indicates the need for energy in body and the need to decrease expenditure AGRP is not clear understood but IT INHIBT POMC ( antagonist of MCR 3 and 4 ) increase feeding by inhibiting effect of aMSH to stimulate MCR ( so increases intake )
30
what do POMC(MSH ) /CART and AGPR/NPY target?
Target for several hormones that are involved in regulation of appetite : Ghrelin Insulin Leptin CCK
31
what happens in mutation of AGPR?
leads to excessive formation of AGRP increased food intake = and obesity
32
what are anorexigenic substances?
INHIBIT FEEDING: alpha MSH ( POMC ) Leptin Insulin CCK Glucagon like peptide CART ( pomc ) PYY All these when present and increased will inhibit feeding
33
which substances are OREXIGENIC ?
orexigenic = stimulate feeding NYP AGRP ( anatagonise MSH MRC receptors ) Ghrelin when high and present they increase eating
34
describe regulation of food intake ?
Body composition : Fat free mass = energy demand to drive and eat Fat mass = leptin = inhibition Gt EPISODIC APETTITE SIGNALS : APETITE STIMULATING HORMONES = GHRELIN Appetite inhibiting hormones = CKK, PYY , GLP1
35
describe adipose tissue and food intake ?
leptin was discovered 1994 and studies in human and animals have demonstrated that : Hypothalamus communicate wtih ADIPOCYTES but now : Adipose tissue is an inert organ for storage of energy Recent view : Adipose tissue is an endocrine gland
36
how does hypothalamus sense energy storage?
LEPTIN
37
what does LEPTIN do?
Stimulates leptin receptors in the hypothalamic nuclei DECREASES FAT STORAGE DECREASE : Production of NPY and AGPR ( we dont need to eat more ) ACTIVATION of POMC neurons --> aMSH and activation of MCR ---> eat less Increases production of corticotropin releasing hormone --> LESS FOOD INTAKE Increase sympathetic activity --> THROUGH NEURONS PROJECTING FROM HYPOTHALAMUS TO VASOMOTOR CENTERS --> INCREAE BMR and energy expenditure Decrease insulin secretion ( decrease energy stores ( but insulin increase leptin cuz it increases fat storage = leptin ) Note : can cross BBB to affect arcuate nucleis
38
what is the effect of leptin on lipid and glucose metabolism ?
Glucose metabolism : Increase insulin sensitivity Reduce glucose production and help prevent high blood sugar lipid metabolism : Promote fat breakdown and reduce fat storage and enhance fat burning for energy
39
does leptin affect appetite ?
it is supposed to decrease it but it doesnt
40
what happens in mutation in leptin ?
inhibit production of leptin or cause expression of DEFECTIVE LEPTIN receptors in hypothalamus =MORBID OBESITY
41
does the deficiency of leptin cause obesity?
Mostly in obesity theres no deficiency of leptin because leptin lvl increase with increasing adiposity OBESITY IS TO DUE LEPTIN RESISTANCE Leptin receptor or post receptor signaling pathways that normally get activated by leptin may be resistant to activation SO IT NO LONGER DECREASE FOOD INTAKE LIKE NORMALLY so its a cycle : Leptin doesnt work = eating more = fat = more leptin = leptin doesnt work = repeat =HYPERLEPTINEMEIA
42
how does leptin resistance affect insulin ?
usually leptin inhibits insulin BUT now theres resistances so it doesnt inhibit insulin = more insulin fat accumulate cuz eating = insulin resistance so now we have hyperleptinemia, hyperinsulemia and hyperlipidemia THERES ALSO HYPERGLYCEMIA cuz leptin is supposed to reduce glucose production and reduce fat storage but its not working Hyperglycemia + hyperinsulinemia + insulin resistance = diabetes mellitus
43
describe long term regulation ?
Nutritional feedback mechanisms which maintain constant stores nutrients in the tissue Not too high not too low , just balanced Glucostatic theory Lipostatic theory Aminostatic theory DESIRE FOR FEEDING INCREASES AS BLOOD LVLS OF GLUCOSE ,AMINO, LIPIDS DECREASE
44
Describe short term regulation of food intake ?
Appropriate food intake in every meal sessions Steady pace to allow appropriate digestion and absorption initiate satiety after adequate food intake in every meal IMPORTANT FOR TO RPEVENT OVEREATING
45
what are theories of food intake control ?
Neurophysiological studies supported these theoreis Increase in blood glucose lvls : INCREASE rate of firing of GlUCORECEPTORS neuros of VMN and PVN nuclei ( statiety center = make you feel full ) DECREASE the firing rate of glucosensitive neuros firing in hunger center of LHN ( feeding center = reduce wanted to eat )
46
describe thermal regulation of food intake ?
Hypothalamic interaction between TEMPERATURE REGULATORY SYSTEM and food intake regulatory systems Increase in temp = decrease food intake LOW temp = ENHANCE FOOD INTAKE BY : Increased metabolic rate Increased fat for insulation Hypothalamic thermostat and lateral AND ventromedial nuclei (LHN AND VMN )
47
What turns off the desire to eat?
Overeating is not healthy habit however there several mechanisms and factors to regulate it : GIT filling HORMONAL INVOLVEMENT
48
Describe GIT filling?
Negative feedback pathways mediated by : Activation of stretch receptors in the stomach --> Activate vagal afferent and inhibit food intake by suppressing feeding center
49
describe hormonal involvement ?
they inhibit by : Suppress food intake enhance satiety CCK, PYY, GLP , INSULINE produced by gastric = suppress further feeding ( anorexic ) LEPTIN produced by fat = inhibits food intake
50
what releases ghrelin ?
Hunger hormone OXYNTIC CELLS OF THE STOMACH but released by intestine but less extent
51
whats the effect of ghrelin ?
lvls of ghrelin rise during fasting Peak before eating Decrease after eating ITS OREXIGENIC HORMONE = make u hungry
52
what releases CCK?
gut brain peptide ENTEROENDOCRINE CELLS in : Duodenum STIMULATED BY PROTEIN AND FAT
53
whats the effect of CCK?
Gall bladder contraction INHIBIT gastric emptying REGULATE gut motility DECREASE gastric acid secretions Communicate with the brain via VAGUS NERVE, CONTRIBUTE TO SATIATION AND MEAL CESSATION ( make you feel full )
54
what releases PYY?
'' hormonal adjustment '' ENTIRE GIT Especially ileum and colon Released post prandially in proportion to CALORI INGESTED ( high calories = high PYY)
55
What does the lvl of PYY indicate ?
High levels of PYY = High number of calories and high fat meal PEAK PYY blood conce is observed 1-2 hours after ingesting a meal
56
what is the effect of PYY?
inhibit eating ( anorexic ) INHIBIT FOOD INTAKE FOR 12 HOURS
57
which hormones stimulate eating and which are not ?
ALL OF THEM INHIBIT : CCK, GIP, GLP1, OXYNOTMODULIN, PYY, INSULINE, AMYLIN, LEPTIN Except : GHRELIN, NYP AND AGPR---> Stimulate
58
what glucose lowering agent from gut?
INCREITNS : GLP ( GLUCAGON LIKE PEPTIDE ) GIP ( glucose dependent insulintropic peptide ) Released from the gut and affect pancreas NET EFFECT IS FROM THE NAME = DECREASE GLUCOSE IN BLOOD
59
what stimulates the release of incretins ?
ingestion of glucose ---> Stimulate insulin secretion from pancreatic BETA CELLS in glucose dependent manner ( insulin reduces glucose ) INHIBIT GLUCAGON SECRETION FROM ALPHA CELLS ( this also reduces glucose )
60
where does GLP1 MAINLY act?
receptors on several tissues of body

PHYSIOLOGY-Y2S2 (16 decks)

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