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Cell Metabolism and Metabolic Control > Carbohydrates > Flashcards

Carbohydrates Flashcards

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1
Q

How do control mechanisms differ between organisms?

A

Basic features are similar; complexity of these varies to match the environment

e. g. bacteria continually adapt due to a short lifetime, humans less so
e. g. carbon cycle, cells working in a paracrine, autocrine or exocrine manner to best cope with environmental demands

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2
Q

What is flux?

A

Direction of carbon skeletons - determines their fate, e.g. pentose phosphate, ATP production etc

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3
Q

Where are all enzymes for glucose handling?

A

Within the cell - these regulate fate of glucose and control net direction of movement

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4
Q

Futile cycle?

A

The energy required to make G6P with no return; this is coordinated to produce useful precursors for energy production further down to recoup these losses

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5
Q

Function of glycolysis and gluconeogenesis

A

ATP from glycolysis (substrate level phosphorylation) and CAC (mitochondria and some cells, ox phos)
Storage glycogen - muscle and liver
FA and TAG synthesis
Glycolytic cells i.e. those that lack mcs like RBCs, kidney, or that cannot transport FAs e.g. neurones
Other sugar production

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6
Q

What metabolites in glycolysis cross over with other pathways?

A

G6P
Pyruvate
Acetyl CoA

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7
Q

Glucose transporters

A

GLUT1-12, specific for tissues/sugar type
GLUT4 = major, in muscle
GLUT2 = liver
Each is regulated differently, but main response is the insulin, especially GLUT4

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8
Q

Structure of GLUTs?

A

12 transmembrane proteins forming central core to let glucose through
Tissue specific expression through promoter-regulated control; myocyte enhancer factor MEF-2 binds thyroid hormone receptor, dimerises, and binds to promotor of GLUT4
(time-specific control)

Developmental control - GLUT1 switches to GLUT4 from foetal to neonatal (newborn) muscle

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9
Q

Regulation of GLUTs?

A

Exist in pools in the cells, moved to and from the membrane in vesicles. e.g. GLUT4 in specific vesicles moved to membrane in response to insulin
Endosomal GLUT1/4 vesicles moved to membrane by muscle contraction (calcium signalling) or anoxia (low O2)

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10
Q

Varberg effect?

A

Anoxia means electron transport chain can’t be used = glycolysis must be used for energy. The switch to this is the Varburg effect

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11
Q

Overall glucose uptake increase due to:

A

Regulation after food; insulin directs excess to adipose tissue for storage as TAGs
Energy production regulation; exercise/anosmia to fuel movement or replenish glycogen stores

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12
Q

GLUT2

A

Liver-specific, no regulation of movement to/from plasma membrane
Dependent on glucose conc in blood stream, and is fully reversible

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13
Q

OVERALL REG OF UPTAKE

A

GLUT tissue-specificity
Compartmentalisation of GLUT within cell
ER partitioning (??)
Subcellular transport e.g. into mitochondria
Concentration gradients in absence of transporters

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14
Q

Glucose - G6P?

A

Hexokinases phosphorylate to form G6P, G6P-phosphase reverses
G6P is an allosteric inhibitor of HxK, via feedback inhibition

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15
Q

Control of phos/dephosphorylation?

A

Enzyme presence/absence
Tissue-specific isoenzymes
State - G6Pase increases activty in starved states, hexokinase massively drops

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16
Q

Hexokinase isoenzymes?

A

I (A), II (B), III (C)

IV (D) = glucokinase, liver, high affinity

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17
Q

Glucokinase?

A

Saturates at 10-15mM of glucose, greater than physiological glucose concentration so can sense excess/lack
Present in liver, where blood from intestines first arrives
Also in pancreatic B cell, where insulin is released

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18
Q

Regulation of glucokinase?

A

Glucokinase gene: complex promoter binds many elements for net effect
Transcription: insulin up via SREBP-1c, CREB down via glucagon – PKA
GK protein - compartmentation with GRP
Degradation - stimulated by glucagon

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19
Q

Glucokinase regulatory protein

A

Glycolysis = in cytosol
GK localises to cytosol in fed states
When not needed, medium-term control occurs through nuclear sequestration by GRP, binding GK
F6P, further down pathway from G6P, activates GRP to sequester GK in feedback inhibition
Insulin and F1P inhibit GRP

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20
Q

Regulation of G6Phosphatase

A

4 subunits, translocases T1-3 and a catalytic G6Pase unit
T1 = entry of G6P
T3=exit of glucose
T2-exit of P
Complexes hold catalytic unit in an active conformation

G6Pase unit - FKHR and Foxo1a needed for transcription
Foxo1a dephos via insulin signalling = inactivates transcription = glycolysis

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21
Q

F6P - F16BP

A 
Forward = phosphofructokinase PFK, all cells
F16BPase = glucogenic tissues e.g. liver, muscle
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22
Q

Phosphofructokinase control

A

Allosteric control = ATP and citrate inhibit
AMP/Pi and F26BP stimulate

Isoenzymes:
PFK-1 = F6P-F16BP
PFK-2 = F6P-F26BP OR reversal

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23
Q

Role of F26BP?

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A

Stimulates PFK-1

Inibits F16BPase

24
Q

PFK-2?

Study These Flashcards
A

Forms F26BP
Bifunctional - single chain with N terminal PFK-2 activity
C terminal F26BPase activity to reverse

Phosphorylation of either end can fold/unfold and expose that activity to bias activity

This can also have isoforms within itself - alternative splicing varies in cells/cell types to change activity ratio

25
PFK-2 isoforms and regulation?
L-type - PKA phosphorylates, activated by glucagon, inhibiting PFK-2 activity to favour F26BPase H and i type - AMP-activated PK phosphorylates, by hypoxia and exercise, to favour PFK-2 activity Long-term, i-type induced transcriptionally by hypoxia L-type decreased in starvation and diabetes
26
Phosphoenolpyruvate (PEP) -- pyruvate cycle
PEPCK: oxaloacetate --- PEP PK (pyruvate kinase): PEP --- pyruvate PC (pyruvate carboxylase): Pyr --- Oxaloacetate Pyruvate dehydrogenase: Pyr --- Acetyl CoA
27
Pyruvate kinase
Cytosolic, encoded by two genes, two transcripts from each for isoenzymes: PKL; R protein, in RBCs L protein, in liver, kidney PKM; M1 protein, in muscle, heart, brain M2 protein, minorly in most tissues, major in tumours, foetal form too
28
Regulation of R and L isoenzymes?
Feedforward activation by F16BP Feedback inhibition by ATP Inhibited also by AAs, PKA via glucagon, to favour amino acid conversion to glucose in starvation SREBP-1c linked to L form long-term control via genes
29
Acetyl CoA (acoa) fates?
Sterols Ketones FAs, triglycerides, phospholipids: oxidised in CAC for ATP
30
Oxaloacetate fates?
Glucose Transamination for AAs CAC intermediate replenishing
31
Pyruvate dehydrogenase (PDH) regulation
Forms acCoA Regulatory or catalytic Phosphorylation by PDH kinase = inactive Dephos by PDH phosphatase = active
32
PDH kinase and phosphatase regulation
KINASE By metabolites: activated by acCoA and NADH, products of PDH i.e. feedback inhibition acCoA also from FA oxidation = cross talk Inhibited by ADP PHOSPHATASE Insulin signalling activates Also coordinates with FA use in starvation
33
Glucose-FA cycle
Preferential use of FAs for ATP FAs = acCoA = CAC = ATP Citrate from CAC = inhibits PFK to stop F6P transfer acCoA inhibits PDH, preventing pyruvate -- acCoA (direct to other use)
34
Pyruvate carboxylase (PC)
Required for glucose synthesis in the liver (pyruvate -- oxaloacetate precursors) Mitochondrial localisation and activity - single gene with isoforms produced by tissue-specific alternative promoters Allosterically activated by acCoA
35
Pyruvate carboxylase isoenzymes?
Proximal promoter use: liver, adipose tissue for inducible transcription Increased by glucagon and glucocorticoids Decreased by insulin Distal promoter: kidney, constitutive transcription
36
Phosphoenolpyruvate carboxykinase (PEPCK)
Cytosolic (inducible) and mitochondrial isoforms from two separate genes Transcriptional regulators: Foxo1, Creb, SREBP, HND etc SREBP-1c inhibits in fed state CREB, nuclear receptor upregulate in starvation
37
PEPCK isoforms and regulation
Cytosolic: conversion of AA to glucose, inducible Mitochondrial: lactate recycling (Cori cycle), consitutive
38
Pentose phosphate pathway
Usually less than 10%, 5-50% of glucose catabolism In cells undergoing: active cell division e.g. tumours active FA synthesis e.g. adipocytes Circular pathway; G6P -- 6 phosphogluconate -- ribulose 5 phosphate
39
Function and regulation of pentose phosphate pathway
Produces: NADPH - for biosynthetic pathways e.g. FA Ribose sugars - nucleotides e.g. in dividing cells Catalysed by two dehydrogenases, G6PDH/6PGDH, regulated by gene transcription of each
40
Other sugars?
Fructose -- F1P by fructokinase in the liver, enters glycolysis Lactose -- galactokinase, for glucose and galactose
41
Glycogen synthesis
Built on a fixing protein, localisation of which controls place and amount Addition of UDP-glucose to glycogenin sequentially = glycogen, using UTP and a number of synthases/branching enzymes
42
Glycogen breakdown
Addition of phosphate to C1 = G1P, isomerised by phosphoglucomutase to G6P Sequential clipping of sugar residue bonds with inorganic phosphate by glycogen phosphorylase and debranching enzymes
43
Complexes in glycogen turnover (7)
``` Glycogenin and other backbone proteins Enzymes for synthesis Enzymes for breakdown Regulatory protein kinases Regulatory protein phosphatases e.g. PP-1G Cytoskeleton interactions Glycogen storage diseases ```
44
Glycogen regulation
Storage sites/amounts differ Most cells = small amounts, short term fuel reserve Muscle - 200g, longer, in absence of G6P or oxygen Liver - 70g, in starvation for tissues with absolute requirement e.g. brain
45
Glycogen synthase regulation
Allosteric regulation in response to external conditions GSa = active, b = inactive Protein kinases e.g. PKA (starvation), AMPK (hypoxia), GSK3 (insulin-responsive,blocks PKA and AMPK), Ca-dependent (muscle in anaerobia), inactive to b Protein phosphatase 1G activates, stimulated by G6P allosterically and through signalling pathways of insulin
46
Glycogen phosphorylase
GPb = inactive, a = active PP-1G inactivates, helped by G6P and insulin inactivate Glycogen phosphorylase kinase phosphorylates b to activate it to GPa, AMP allosterically activates (OPPOSITE TO SYNTHASE)
47
Glycogen phosphorylase kinase regulation
GPKa and b again GPKa - protein kinases activate by phosphorylating, stimulated by cAMP, Ca2+, AMP =glycogen breakdown GPKb - protein phosphatase 1G, stimulated by G6P and insulin SAME AS SYNTHASE
48
Glycogen compartmentation of regulation
Only one pair of enzymes activated at a time Phosphorylase activity decreases rapidly with insulin GS activation delayed until GP inactive This is latency coordination - may be due to movement of phosphatases in the compartment
49
CAC regulation
Many metabolic starting points i.e. glucose, FAs, ketones, AAs Inputs have varying efficiencies e.g. some AAs better, favour FA Controlled by citrate synthase, ATP and a-ketoglutarate dehydrogenase Control also spares acCoA and AAs
50
Carbohydrates to other metabolites?
Pentose phosphate pathway = nucleic acids F16BP--PEP and acCoA from pyruvate = lipids Oxaloacetate from pyruvate = AAs = proteins
51
Isoenzymes in pathway?
``` GLUT Hexokinases PFK GP glycogen phosphatase GS glycogen synthase PK pyruvate kinase PC pyruvate carboxylase PEPCK ```
52
Where does insulin/glucagon regulate?
``` GLUT Hexokinases GP and GS G6P -- pentose sugars (dehydrogenases G6PDH/6PGDH) PFK PK, PC, PDH, PEPCK ```
53
Where does transcription regulate?
Hexokinases G6P -- pentose sugars (dehydrogenases G6PDH/6PGDH) PFK PK, PC, PEPCK
54
Where does SREBP-1c regulate?
Hexokinases G6P -- pentose sugars (dehydrogenases G6PDH/6PGDH) PDH, PEPCK
55
Where does phosphorylation by PKA regulate?
Hexokinases GP, GS PFK PK, PC, PEPCK
56
Where does allosteric regulation occur?
GP, GS PFK, F16BPase PK, PDH
57
Where does compartmentation control regulate?
GLUT Hexokinase, G6Pase GS, GP

Cell Metabolism and Metabolic Control (8 decks)

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