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GI > Monosaccharides and Glycosides > Flashcards

Monosaccharides and Glycosides Flashcards

1
Q

Sugars and sugar derivatives play numerous additional roles besides simply providing chemical energy for the synthesis of ATP. This includes functional and structural roles in

A

Glycosaminoglycans, glycolipids, and proteoglycans

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2
Q

The simple sugars galactose, glucose, mannose, and fructose have the same chemical formula (C6H12O6). Hence, these four sugars are

A

Isomers

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3
Q

Among isomers, a geometric difference at any single carbon other than the carbonyl carbon results in

A

Epimers

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4
Q

By virtue of intramolecular reactivities, sugars can exist in either straight chain or ring conformations. The predominant structure of aldoses such as glucose and galactose is a

A

Six membered hemi-acetal ring

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5
Q

This six-membered hemi-acetal ring is also referred to as a

A

Pyranose ring

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6
Q

Adopt either a five membered hemiketal ring structure (4 carbons, 1 oxygen), also called a furanose ring or a six-­membered ring

-ex: Fructose

A

Ketoses

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7
Q

Form a six membered (5 carbons, 1 oxygen) hemiacetal ring, also referred to as a pyranose ring

-ex: Glucose and Galactose

A

Aldoses

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8
Q

In all these cases, ring formation will result in two alternative configurations at the

A

Anomeric carbon (Carbon #1 of aldoses and #2 of Ketoses)

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9
Q

Structural variants about the anomeric carbon are called

A

Anomers

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10
Q

Anomers, (expressed as a and B) equilibrate with each other via the

A

Open chain intermediate

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11
Q

Mirror image structural variants are called

-ex: D- and L-Glucose

A

Enantiomers

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12
Q

A trisaccharide of galactose, glucose, and fructose

A

Raffinose

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13
Q

A Disaccharide of glucose

A

Trehalose

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14
Q

Extensively polymerized sugars are also prevalent in our diets, including

A

Amylose, amylopectin, and glycogen

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15
Q

While simple sugars are absorbed directly, disaccharides and polysaccharides must first be

A

Hydrolyzed to simple sugar constituents

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16
Q

Digestion of start begins with

A

Salivary a-amylase

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17
Q

Continues this process once the acidic contents of the stomach have been neutralized

A

Pancreatic a-amylase

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18
Q

The bulk of CHO digestion (hydrolysis) occurs at the mucosal lining of the jejunum, with the secretion of additional digestive enzymes, such as

A

Glucoamylase/maltase (a-1,4), Sucrase/isomaltase (a-1,6), and lactase

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19
Q

The products of these normally quite efficient hydrolyzing enzymes are the three simple sugars

A

Glucose, fructose, and galactose

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20
Q

ABSORPTION of these three sugars, in the intestinal epithelium, is the responsibility of which three transporters?

A

SGLT1, GLUT5, and GLUT2

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21
Q

The principal lumenal transporters

A

SGLT1 and GLUT5

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22
Q

The principle transporter into the capillaries

A

GLUT2

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23
Q

They arise by a number of means, with their root cause being the incomplete digestion

A

Di- and oligosaccharides

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24
Q

The passage of significant quantities of osmotically active complex sugars into the large intestine results in

A

Bloating, dehydration, and gas (i.e. CO2 and H2 production)

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25
Q

Failure to fully digest CHO can stem from genetic deficiency for one of the above hydrolases, temporary loss of hydrolase activity through other intestinal pathology, and

A

“Adult” onset of enzyme deficiency

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26
Q

Perhaps the most common of these age-­dependent onset phenomena

A

Lactase deficiency

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27
Q

Up to half of all adults, and up to 90% of blacks and Asians are deficient for

A

Lactase

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28
Q

Diagnosis of these enzyme deficiencies is done by

A

Oral tolerance tests

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29
Q

How do cells essentially “capture” incoming sugars?

A

Phosphorylation

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30
Q

Isn’t transported by SGLT1, GLUT2, or GLUT5, and the presence of the phosphate makes passive transit of the membrane an extremely low probability event

A

Glucose-6-phosphate

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31
Q

Glucose and galactose have the same chemical formula and are both aldoses. How does the cell convert one into the other?

A

Epimerization

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32
Q

Because glucose and fructose differ only in the location of the carbonyl carbon, how can the cell convert one to the other?

A

Isomerization

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33
Q

An additional transformation that sugars undergo is their conversion to

A

Nucleotide linked forms (ex: UDP glucose)

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34
Q

The integration of fructose into mainstream CHO metabolism requires only two steps, occurring principally in the

A

Liver, intestines, and kidneys

35
Q

Whereas intestinal fructose absorption is relatively slow, the first step in fructose metabolism is a very

A

Fast step

36
Q

Both recruit dietary fructose as a substrate, to produce fructose 6-­phosphate and fructose 1-­phosphate (F-1-­P), respectively

A

Hexokinase and Fructokinase

37
Q

Hexokinase is comparatively quite inefficient at this, hence the significant majority of fructose is converted to fructose 1-­phosphate by

A

Fructokinase

38
Q

Only makes substantial contribution to fructose metabolism at very high substrate concentrations

A

Hexokinase

39
Q

Cleaves Fructose1-­P to D-glyceraldehyde and dihydroxyacetonephosphate (DHAP)

A

Aldolase B

40
Q

Can enter pathways for glycolysis or gluconeogenesis

A

DHAP

41
Q

Can enter glycolysis or be transformed into glycerol, the backbone for lipids

A

D-glyceraldehyde

42
Q

Pathologies associated with dietary fructose take which two basic forms?

A
  1. ) Excessive intake

2. ) Hereditary deficiency for specific enzymes

43
Q

In both cases, fructose toxicity is related to the formation of large amounts of

A

F-1-P

44
Q

In both cases, fructose toxicity is related to the formation of large amounts of fructose 1-­phosphate, with very slow turnover into

A

D-glyceraldehyde and DHAP

45
Q

Because of the comparatively slow rate of catalysis by aldolase B (compared to that for fructokinase), under conditions of high dietary fructose intake there can be a significant build up of

A

F-1-P

46
Q

A buildup of F-1-P causes a sequestration of the cell’s supply of

A

Pi

47
Q

This, in turn, causes a decrease in available ATP levels, with concomitant increases in

A

ADP and AMP

48
Q

Deamination of ADP and AMP results in

A

Hyperuricemia

49
Q

Eventual action of aldolase B on this built up Fructose 1-­P supply results in elevated levels of

A

Pyruvate and lactate

50
Q

Also builds up by virtue of its competition with uric acid for filtration by the kidney

A

Lactate

51
Q

Also increases under these high fructose conditions

A

Fatty acid and TAG synthesis

52
Q

Because of these several adverse effects of high fructose in the diet, early theories that fructose is a ‘safe’ sugar for diabetics to use in place of glucose have largely been

A

Abandoned

53
Q

Apart from the adverse effects of elevated uric and lactic acids, and elevated levels of fatty acids and triacylglycerols, the liver also metabolizes fructose-­derived trioses via gluconeogenesis, thereby

A

Raising blood glucose anyway

54
Q

Inborn errors in fructose metabolism fall into which two groups?

A

Essential fructosuria and hereditary fructose intolerance

55
Q

Results from the absence of fructokinase.

-This is a rare and asymptomatic deficiency

A

Essential Fructosuria

56
Q

Can be quite serious and has biochemical consequences very similar to that described above for excessive fructose intake in a normal individual

A

Hereditary Fructose Intolerance (HFI)

57
Q

High levels of Fructose1-­P build up (up to 10 mM) even in the absence of high fructose (or sucrose) intake with

A

HFI

58
Q

Clinical manifestations of HFI include

A

Hypoglycemia, nausea, and vomiting after mild fructose exposure

59
Q

Infants with HFI struggle with a failure to thrive and develop, including longer term concerns for

A

Liver damage and dysfunction

60
Q

What is the aim of treatment for HFI?

A

Elimination of fructose from the diet

61
Q

Prevents inhibition of glucokinase by fructose 6-­phosphate

A

F-1-P

62
Q

The principal monosaccharide in seminal fluid

A

Fructose

63
Q

Fructose is synthesized in the seminal vesicles (along with other tissues, in both sexes) by the so-­called

A

Polyol pathway

64
Q

This two step conversion of glucose to fructose (polyol pathway) is driven forward by high concentrations of

A

NADPH and NAD

65
Q

The intermediate compound of the polyol pathway

A

Sorbitol

66
Q

Has a high Km for glucose

-the first enzyme in the polyol pathway

A

Aldose reductase

67
Q

Sorbitol accumulates in the lens and in other tissues in which aldose reductase is found in

A

Diabetics

68
Q

Increased intracellular sorbitol concentrations cause

A

Tissue damage

69
Q

The integration of galactose into mainstream liver CHO metabolism offers a few branch points, but also includes only a few

A

Enzymatic Steps

70
Q

Catalyzes the formation of galactose 1-­phosphate (gal1-

P)

A

Galactokinase

71
Q

Gal1-­P is then converted into

A

UDP Galactose

72
Q

Gal1-­P is then converted into UDP-­galactose by an exchange reaction with UDP-­glucose, catalyzed by

A

Galactose 1-­phosphate uridyl transferase

73
Q

The final step is the epimerization of UDP-

galactose to

A

UDP-glucose

74
Q

The final step is the epimerization of UDP-galactose to UDP-­glucose, carried out by

A

UDP-galactose 4-epimerase

75
Q

There are alternative fates for this product UDP-­glucose. It may be converted into

A

Glycogen or G-1-P

76
Q

UDP-­glucose has yet other fates in the synthesis of

A

Lactose, glycolipids, glycoproteins, and proteoglycans

77
Q

Formation of essential components of cell walls and membranes are the more critical fates for

A

Galactose

78
Q

It is possible to completely eliminate dietary galactose and yet still supply cells with all that they require through the reversible action of

A

UDP-­galactose 4-­epimerase

79
Q

Caused by a deficiency in Gal1-­P uridyl transferase, leading to a build up of both galactose and gal1-­P

A

Galactosemia

80
Q

Classical Galactosemia is caused by a deficiency in

A

Gal-1-P Uridyl transferase

81
Q

Partly because of the evident lack of toxicity in high galactose levels, it is believed most negative effects seen in galactosemia are attributable to

A

Gal-1-P

82
Q

Another problem with galactosemia is buildup in the lens of

A

Galactitol

83
Q

Can lead to cataracts by virtue of the production of galactitol in the lens, via aldose reductase

A

Galactokinase deficiency

84
Q

Galactokinase deficiency can lead to cataracts by virtue of the production of galactitol in the lens, via

A

Aldose reductase

GI (59 decks)

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