obesity Flashcards

1
Q

what is android and gynoid fat distribution

A

describes the pattern of fat distribution in males and females
males - android around the abdomen creating an apple shapes body

females - gynoid fat gathers around the hips creating a pear shapes body

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2
Q

describe ways we can measure obesity (and praps their limitation)

A
  1. BMI - kg divided by m2 . 18-25 is good BMI, 40-50 is morbildy obese.
    DOESN’t consider muscle mass as its just body mass in general, not specifically fat mass
  2. Waist: hip ratio below 0.95 in males and below 0.8 in female is good, above 1 and 0.85 is high risk of obesity. BUT doesnt consider the distribution of fat mass as it may be mesenteric, within the peritoneal cavity
  3. Body scans - DEXA or MRI can show the fat distribtution cleaelry, may vary in individuals with the same waist:hip!!
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3
Q

what would a postivie eneegy balance result in?

A

postive enery balance means your energy initake is more than your energy output so you wil experiecne weight gain as there is ENERGY STORAGE

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4
Q
which of these are anorexogenic signals
NPY
POMC
GABA
AgRP
A

anoregenic is a satiety signal, it will mean you are full and inhibit appetite

POMC/CART is the anorexogenic signal. these neurons project from the arcuate nucleus to the PVN

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5
Q

leptin - actions in satiety?

A

leptin = lose weight
Released from fat cell,its an adipokine

it can stimulate POMC/CART neurons to suppress appetite and can inhibit the NPY/AgRP neurons too

ghrelin is the opposite and can stimulate NPY/AgRP neurons as its released from stomach in response to undernutrition

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6
Q

what is PYY

A

it is another hormone released by the gut but in resposne to overnutrition/will supress appetite
it does this by by exciting anorexgenic neurons in arcuate nucleus

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7
Q

how is lipids in diet take up by cells? (exogenous pathway)

Which lipoprotein

A

this is the exogenous pathway of cholestrol uptake

food/chyme mixes with bile salts to emulsify them and react with pancreatic lipase
FFA+ glycerol taken up by enterocytes of the gut
re-esterified to TAG and cholesterol into the lipoprotein CHYLOMICRON which has ApopB48 recognized by liver cells

travels in circulation, degraded by LPLipase to hydrolyse TAG to FFA andglycerol and taken up by tissue to be used as energy or stored

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8
Q

what are PPARgamma and C/EPB alpha

A

markers of adipogenesis// increase in number of fat cells within adipose tissue

Genes of terminal adipocyte differentiation

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9
Q

what does lipgenesis involve

A

lipogenesis is the creation of new lipid. catalyzed by fatty acid synthase
substrate needs to be uptaken into adipocyte cell in order to do this (upregulate GLUT4, CD36, lipoproteinlipase expression)

lipolysis is the breakdown of lipids which can be done by hormone sensitive lipase

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10
Q

what aspect of the arcuate nucleus enables it to integrate endocrine signals from the body?

A

the blood brain barrier is particularity fenestrated at the arcuate nucleus allowing it to be uniquely exposed to hormones and nutrients
these signals are integrated by the arcuate nucleus allowing it to regulate feeding and satiety signals

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11
Q

what are the components of our energy expenditure?

A

the resting metabolic rate - thermic effect of food (digest,absorb,metabolise) and metabolism
non resting metabolic rate - spontaneous activity or exercise

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12
Q

what deteemines the BMR? what is BM rate affected by>?

A

contribution of adipose tissure, skeletal muscle, organs and other tissue
but in terms of body mass they are disproportionately affect BMR as the organs make up less than 5% body mass yet contribute to nearly 60% BMR

affected by age, weight, gender, height

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13
Q

where can Brown adipose tissue be found? what does it do? why is is called brown?

A
between shoulderblades, interscapula
peri-renal and peri-cardinal
BROWN as its full of mitochondria
>> this is activated in thermogenesis // nonshivering thermogenesis to regulate body temperature
> very profound in newborns
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14
Q

why is thermogenesis more important in small rodents

A

they have a larger SA:V so will lose heat more easily compared to larger organisms so there is a greater need to thermoregulate and possesss brown or beige adipose tissue

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15
Q

how does diet induced thermogenesis occur?

A

as we eat, satiety signals are relayed to the hypothalamus
this then prompts the SNS to be activated and release the neurotransmitter noradrenaline which acts on B3 adrenergic receptor present on BAT
this promotes lipolysis of BAT allowing the mitch to use this energy to create heat!

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16
Q

how does thermogenesis (either diet induced or nonshivering) affect the WAT depots?

A

can decrease the depots!

as lipolysis is occurring in BAT then lipid in circulation will dro`p. So mass of WAT will drop too to replace this!

17
Q

what is a marker of nonshovering htemogeneis?

A

UCP-1 protein which enables mitochondria to producde ATP via oxidative phosphorylation

18
Q

how is lipids synthesised by liver take up by cells? (endogenous pathway)

A

Hepatocytes can create VLDL, HDL and LDL to transport TAG and cholesterol in circulation
lipoprotein lipase release contents to tissues so glycerol and FFA can be used for energy or stored as fat

APopE receptors can take up the remnants of VLDL and chylomicron remnants via the remnant receptors and recycle them for the liver to use/ create more lipoproteins

19
Q

decribe the enzymes involved in lipgeneisis and lipolysis

A

so lipoproteins release the FFA and glycerol. The tissues can use fatty acid synthase to re-esterify them and store as fat in adipose tissue = genesis

so for cells to use fat as energy, hormone sensitive lipase can respond to adrenaline to hydrolyse lipids to FFA and glycerol which can the be used in FA metabolism to generate ATP but also ketone bodies if there is excess = lipolysis

20
Q

why does physical activity burn more energy than it needs to

A

so energy is being used to generate heat from muscle contraction

but ALSO WAT is being converted to beige adipose tissue too (irisin) // browning of WAT
> mediated by hormone irisin which expression is induced during exercise

21
Q

describe the action of irisin

A

encoded by FNDC5 gene which its expression was shown to be induced during exercise

one of the cleaved products of FNCD5 is irisin which can increase UCP1 (thermogenesis marker) in WAT tissue demonstrating that irisin can activate the browning of WAT in response to exercise

22
Q

can you name an example of how genetics can implicate obesity?

A

prader willi syndrome, individuals are hyperphagic as they are unresponsive to satiety signals
this is a genetic impriting disorder on chromosome 15q11 and there is a loss of paternal gene expression IGF2

> can be epigenetic factors like DMR methylation which repress gene expression or due to gene deletions

23
Q

is genetics a mahjor contributor to obestiy prevelence?

A

i mean no, for example a MC4r deletion will prevent integration of satiety signals in the melonocortin pathway resulting in severe obestiy but it only accounts for 1% of all obestiy cases

more likely that it predisposes you to obesity and increase your susceptibility of it

24
Q

what are the sings of metabolic syndrome (consequence of obesity)

A

insulin resistnace - lead to hyperglycaemia, diabetes, kidney pathys

dyslipidaemia - imbalance between cholestrol, LDL and HDL - lead to AS

hypertension - lead to CVD, odema

vasular dysregulation - lead to AS,, CVD

25
Q

what are the signs of Cardiovasuclar complications (consequcne of obesity)

A

hypertension
cerebral vasular, CVD/CAD, PVD – AS
obstructive sleep apnoae - soft tissue enlarges on tongue

26
Q

what are the sings of reproductive issues (consequence of obesity)

Why is that though?

A

PCOS, precocious puberty, androgenisation (male characteristic in females like hirtuism)

impotence (ED) and infertility in males

27
Q

what an adipokine?

A

cytokine releasded by adipose tissue to regulate energy metabolism
> leptin, adiponectin, resistin