Integration of Metabolism Flashcards

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1
Q

why is energy intake sporadic

A

people eat different amounts of food everyday at different intervals

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2
Q

brain metabolic features

A

continuous high ATP requirement
glucose + some ketone bodies e.g. beta-hydroxybutyrate
cant use fatty acids
ketone body metabolism not as effective

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3
Q

hypo vs hyperglycaemia on the brain

A

hypo = faintness/coma
hyper = irreversible brain damage

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4
Q

light exercise muscle metabolism (when O2 not limiting)

A

oxidative phosphorylation
fat breakdown
ketone body oxidation

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5
Q

vigorous exercise muscle metabolism (when O2 limiting)

A

glycogenolysis
lactate formation (for glycolysis to continue)

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6
Q

heart metabolic features

A

constant atp requirement
fully aerobic using TCA substrates like FFAs and KBs

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7
Q

liver metabolic features

A

high metabolic activity
interconverts nutrient types
maintains blood glucose 4.0mM - 5.5mM
stores glucose as glycogen + key role in lipoprotein metabolism

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8
Q

what is gluconeogenesis essentially

A

glucose made from pyruvate

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9
Q

what enzymes need to be bypassed + why

A

hexokinase, phosphofructokinase + pyruvate kinase

reversal of their actions normally is energetically unfavourable (delta G = -90kJ/mol)

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10
Q

what enzymes are used to bypass in gluconeogenesis

A

mitochondria: pyruvate carboxylase

cytosol: phosphoenolpyruvate carboxylase, F-1,6-biphosphatase + G6-phosphatase

energetically favourable: -38kJ/mol

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11
Q

fats as fuel sources

A

FA: A-CoA (TCA) + KB (brain)
G: DHAP => gluconeogenesis

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12
Q

controlling metabolic pathways

A

earlier = more control
occurs at irreversible steps
by product inhibition of enzymes, signalling molecules

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13
Q

michaelis constant (Km)

A

concentration of substrate when enzyme function is half the maximal rate (Vmax)

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14
Q

hexokinase 1

A

in muscle
low Km - 0.1mM
active at low concs of glucose so even when glucose is low, still making ATP via glycolysis
inhibited by glucose-6-phosphate
irreversible

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15
Q

hexokinase 4

A

in liver
high Km - 0.4mM
active only on high concs of glucose
not inhibited by G6P
glucose-6-phosphatase used to reverse

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16
Q

what happens some time after a meal

A

pancreas: increased glucagon + decreased insulin
liver: increased glycogenolysis + gluconeogenesis

fatty acid breakdown

adrenaline: glycolysis, glycogenolysis, lipolysis

17
Q

prolonged fasting

A

more glucagon released + less insulin
increased FA metabolism + gluconeogemesis using TCA intermediates
gluconeogenesis using protein
KBs made from FAs + AAs in liver to meet brains needs

18
Q

T1 vs T2 diabetes

A

1: beta cell dysfunction = no insulin made
2: body doesn’t respond to insulin

19
Q

what does diabetes cause

A

hyperglycaemia
CV complications
ketoacidosis
hypoglycaemis

20
Q

insulin

A

secreted when glucose levels rise
stimulates uptake + use of glucose + storage as glycogen and fat.

21
Q

glucagon

A

secreted when glucose levels fall
stimulates production of glucose by gluconeogenesis + breakdown of glycogen and fat

22
Q

what happens straight after a meal

A

insulin released:

liver + muscle: glucose uptake - glycolysis/glycogenesis

adipose: Tg synthesis