Appetite Flashcards

0
Q

Define appetite.

A

The natural instinctive desire for food.

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1
Q

What is easier if you are physically fit in relation to energy intake?

A

Regulating body weight

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2
Q

Appetite is the interaction between:

A

Biology (including psychology) and the environment

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3
Q

Define hunger

A

A craving for food. Caused by emptiness and resulting in hyper motility of the stomach.

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4
Q

How does hunger trigger eating behaviour?

A

Via numerous neuro-hormonal mechanisms

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5
Q

Define satiation

A

Characterised by sensation of a full stomach. Leads to a person stopping eating during a meal so determines the size of a meal

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6
Q

Define satiety

A

Sensation of fullness, period of hunger inhibition from one meal to another. Determines meal pattern and frequency.

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7
Q

What can affect the accuracy of body weight measurements?

A

Oedema - water retention

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8
Q

What does VAS stand for?

A

Visual analogue score

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9
Q

How long is a VAS line?

A

100mm equals 10cm

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10
Q

What is the main limitation with VAS scores?

A

Only repeatable within one person cannot compare 2 people

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11
Q

Name the two sensory signals that can affect energy intake.

A

Psychosocial - food preferences from childhood. Perceived weight etc
Organoleptic - don’t tend to over eat unpleasant food

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12
Q

Where do the signals come from in short term and long term?

A

Short term - post meal signal, hormones

Long term - signal from body fat store

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13
Q

Name the meal related afferent signals.

A

Gherlin
PYY
GLP-1

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14
Q

Name the long term afferent signals.

A

PP
Insulin
Lepton

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15
Q

Where does Ghrelin come from?

A

Stomach

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16
Q

Where does PYY and GLP-1 come from

A

Intestine

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17
Q

Where does PP and insulin come from

A

Pancreas

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18
Q

Where does leptin come from

A

White adipose tissue

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19
Q

If you are hungry you have increased levels of ?

20
Q

What is the only hormone that makes you eat?

21
Q

The interheart study states MI risk increases with increased cholesterol, increased non HDL cholesterol, apo B conc and a decrease in HDL and Apo A. Apo B/Apo A1 ratio was a better risk marker of MI than the ratio of cholesterol/HDL. Apo B better marker than cholesterol and LDL. And Apo A1 better than HDL chol

A

McQueen et al 2008

22
Q

McQueen 2008

A

Interheart study MI risk Apo a1 and Apo B

23
Q

Best way to improve blood lipid profile is to replace Trans fats with unsat fats from unhydrogenated oils. Also to replace sat fats with cis unsat fats decrease cad risk. Not high carb diet

A

Mensink 2003

24
Mensink 2003
Replace Trans with unsat. Replace sats with cis unsat
25
Liu 2000
Increase fruit and veg
26
Increased fruit and veg decreases risk of MI and protective against CVD.
Liu 2000
27
Kromhout 2011
Low sat fat, low as poss Trans. Make sure fulfil n3 and n6s
28
Low sat. Low as poss Trans. N3 and n6. 5% sat fat replaced by n6 equals 10% decrease in chd. People who eat fish once a week decrease CVD by 15%
Kromhout 2011
29
Astrup 2010
Chd risk decreased when sat fats replaced with pufas. In western diet 1% of energy from sat replaced with pufas lowers LDL could reduce chd by 2-3%
30
Sources of n3
Flaxseed and oily fish (alpha linolenic)
31
Source of cholesterol
Eggs and prawns
32
Apo A
Co factor for lcat found on cms and HDL
33
Apo b48
On cm remnants returns to liver
34
Apo 100
Bind to LDL receptors. Vldls, idls, Ldl
35
Apo c
LPL binding
36
Apo e
Reputable by liver
37
Lcat stands for
Lecithin cholesterol acyl transferase
38
Hepatic lipase
On the liver cells, hepatocytes, tags from idl to form LDL
39
Cetp does?
Moves cholesterol esters to LDL and vldl
40
3 uses of cholesterol
Cell membranes, bile acids, steroid hormones
41
HDL Apo ?
A1
42
Non LDL Apo?
Apo B
43
Origin of Apo b 48
Intestine
44
Origin of Apo b 100
Liver
45
Apo c2 activates?
LPL, cleaves tags
46
What happens to excess LDL particles.
Invade arterial wall and become oxidised and create foam cells
47
Exogenous pathways equals
Chylomicrons packaged in enterocytes in small intestine, through lypthatic system