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GI > Carbohydrate Metbaolism > Flashcards

Carbohydrate Metbaolism Flashcards

1
Q

What are the different polymers and their bonds?

A

starch: amylose- alpha 1,4 and amylopectin - alpha 1,6; glycogen and glycoconjugates

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2
Q

What are the different disaccharides and their bonds?

A

lactose- beta1,4 reducing sugars, sucrose- alpha 1,2 non-reducing sugar and trehalose

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3
Q

What are the five categories of fiber?

A

cellulose, hemicellulose, lignins, pectins, and mucilages and gums

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4
Q

What do bacteria in the gut (normal flora) digest fiber into?

A

convert it to lactate, short chain fatty acids (acetic acid, propionic acid, and butyric acid), these can be used by the body and account for up to 10% of the calories

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5
Q

What use can indigestible fibers have in medicine?

A

soften stool, help bowel movement, used to treat diverticulitis

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6
Q

What is diverticular disease?

A

characterized by the development of sacs or pouches in the colon due to weakening of muscles and submucosal structures

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7
Q

What is the glycemic index?

A

measure of a given food on raising blood glucose levels; defined by blood glucose concentrations over a two-hour period after ingestion of a food as compared relative to that of equivalent amount of indigested bread or glucose

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8
Q

when are high GI foods good?

A

for physical activity that require quick energy

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9
Q

when are low GI foods good?

A

for physical activity that require sustained energy

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10
Q

What do glycosidases do?

A

hydrolysis of glycosidic bonds found in carbohydrate polymers and oligosaccharides; have specificity for sugar moiety and anomeric (alpha or beta) configuration

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11
Q

What enzyme is in the saliva that digests carbohydrates?

A

salivary alpha amylase

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12
Q

What enzyme is in the small intestine that digests carbohydrates?

A

alpha amylase, into duodenum from the pancreas; tri and oligosaccharides maltose and isomaltose, in the intestinal wall: glycoamylase, trehalase, sucrase, lactase, maltase, and isomaltase

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13
Q

What enzyme in the stomach digests carbs?

A

alpha dextrins

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14
Q

Where is sucrase-isomaltase complex highest? What does it do?

A

highest in the jejunum; digests sucrose into glucose and fructose and isomaltose to generate glucose, also exhibits maltase activity which digests maltose to generate glucose; 80% of maltase activity in intestine

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15
Q

Where is beta-glycosidase complex (lactase-glucosylceramidase) highest? What does it do?

A

highest in jejunum, hydrolyzes lactose to generate galactose and glucose; first one lost and last one recovered after injury

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16
Q

What does trehalase do?

A

hydrolyzes trehalose to generate 2 glucose units

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17
Q

What does glucoamylase do? Where is it the highest?

A

hydrolyzes non-reducing terminal alpha 1,4 glucoside in starch, glycogen, alpha dextrins, and maltose; highest in ileum

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18
Q

What do sodium dependent glucose transporters do and where are they located?

A

mucosal side of epithelial cells of intestines and kidney and transport glucose and galactose against concentration gradient; driven by high [sodium] at luminal side and facilitated Na/K ATPase mediated efflux of Na at serosal side

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19
Q

Where are facilitated glucose transporters located? How do they function?

A

distributed in a tissue/cell specific fashion, intestinal epithelium they are at mucosal and serosal sides; transport glucose, galactose and fructose following the concentration gradient; 5 different glucose transporters (GLUT 1-5), exhibit different sugar specificty

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20
Q

Where are GLUT 1 transporters?

A

erythrocyte, blood brain barrier, blood retinal barrier, blood placental barrier, blood testis barrier; expressed in cell types with barrier functions; high affinity glucose transport system

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21
Q

Where are GLUT 2 transporters?

A

liver, kidney, pancreatic beta cell, serosal surface of intestinal mucosa cells; high capacity, low affinity transporter; may be used as the glucose sensor in the pancreas

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22
Q

Where are GLUT 3 transporters?

A

brain (neurons); major transporter in the central nervous system, high affinity system

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23
Q

Where are GLUT 4 transporters?

A

adipose tissue, skeletal and heart muscle; insulin sensitive transporter, in presence of insulin the number of transporters increases on the cell surface; high affinity system

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24
Q

Where are GLUT 5 transporters?

A

intestinal epithelium, spermatozoa; actually a fructose transporter

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25
Q

Why is it important that the liver have a GLUT 2 transporter?

A

the high capacity low affinity for glucose ensures the liver only receives glucose at a high blood glucose level; like after a high carbohydrate meal

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26
Q

What is lactose intolerance?

A

deficiency of lactase in small bowel, race-related; either late onset or secondary to mucosal injury fro conditions: kwashiorkor, colitis, gastroenteritis, tropical and nontropical sprue, and excessive alcohol consumption; when not digested lactose is converted to lactic acid, methane and hydrogen gas by bacteria and diarrhea due to osmotic effect of undigested sugar

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27
Q

What is trehalase deficiency?

A

trehalose containing foods cannot be digested; which can cause diarrhea

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28
Q

Where is glycogen stored in the body?

A

glycogen constituents up to 4% of the fresh liver and 0.7% of the muscle

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29
Q

What are the general structural features of glycogen?

A

it is a glycoprotein with alpha 1,4 and alpha 1,6 bonds; the reducing end is attached to the protein glycogenin

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30
Q

How is glucose added to glycogen in the cell?

A

glucose absorbed, hexokinase or glucokinase in the liver phosphorylates glucose to glucose 6-phosphate which becomes glucose 1-phosphate by phosphoglucomutase, UDP-glucose pyrophosphorylase takes glucose-1P to UDP-G which either goes to other paths or glycogen synthase turns it into glycogen

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31
Q

How is glycogen brokendown?

A

glycogen phosphorylase to remove external glucose down to 4 units/chain; debrancher enzyme to transfer 3 glucose to end of glycogen leaving glucose-1P which becomes glucose-6P by phosphoglucomutase; then in only the liver glucose-6 phosphatase turns it into glucose to be released

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32
Q

How is new glycogen formed from the start?

A

initiated by glycogenin, serves as a primer and exhibits glycogen synthase activity to form hexa-glucose-glycogenin; followed by repeated actions of glycogen synthase and 4:6-transferase to complete glycogen synthesis

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33
Q

What is glycogenolysis? What is the state of enzymes during this?

A

hydrolyze glycogen, glycogen phosphorylase and phosphorylase kinase are maintained at phosphorylated state; protein kinase is activated; at the same time protein phosphatase is kept at a low level

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34
Q

What is glycogenesis? What is the state of enzymes during this?

A

synthesize glycogen; glycogen synthase is maintained at dephosphorylated state, protein kinase is inactivated; protein phosphatase is kept at a high level

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35
Q

How is protein phosphatase effected by hormonal regulation?

A

insulin enhances PP activity by stimulating phosphorylation of one soecific site in glycogen (G)-binding subunit; which prevents glucagon-induced phosphorylation of another site in the G-subunit, this step in inactivation of PP

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36
Q

During fasting what are the hormone or signaling levels in the blood or tissue? Response from the liver tissue?

A

Blood: glucagon up, insulin down, Tissue: cAMP up; glycogen degradation up, glycogen synthesis down

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37
Q

During fasting what are the hormone or signaling levels? Response from the muscle tissue?

A

insulin down; glycogen synthesis down; glucose transport down

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38
Q

After carbohydrate meal what are the hormone, signaling, or glucose levels in the blood or tissue? Response from the liver tissue?

A

glucagon down, insulin up, glucose up in the blood; tissue cAMP down, glucose up; glycogen degradation down, glycogen synthesis up

39
Q

After carbohydrate meal what are the hormone, signaling or glucose levels in the blood? Response from the muscle tissue?

A

blood: insulin up; glycogen synthesis up, glucose transport up

40
Q

After exercise what are the hormone, signaling or glucose levels in the blood and tissue? Response from the liver tissue?

A

blood: epinephrine up; tissue: cAMP up and Ca-calmodulin up; glycogen degradation up, glycogen degradation up; glycogen synthesis down

41
Q

After exercise what are the hormone, signaling or glucose levels in the blood and tissue? Response from the muscle tissue?

A

blood: epinephrine up; tissue: AMP up, Ca-calmodulin up; glycogen synthesis down, glycogen degradation up, or glycolysis up

42
Q

In glycogen storage disease where glycogen synthase enzyme is affected what organ is involved and what is the clinical manifestation?

A

liver; hypoglycemia, failure to thrive, early death

43
Q

In glycogen storage disease where glucose 6-phosphatase enzyme is affected what organ is involved and what is the clinical manifestation?

A

live; enlarged liver and kidney, growth failure, fasting hypoglycemia, acidosis, lipemia, thrombocyte dysfunction, hypoglycemia is the most dysfunction

44
Q

In glycogen storage disease where lysosomal alpha-glucosidase enzyme is affected what organ is involved and what is the clinical manifestation?

A

all organs with lysosomes; infantile- early onset progressive muscle hypotonia, cardiac failure, death before 2; Juvenile- later onset myopathy with variable cardiac involvement; adult- limb girdle muscular dystrophy; glycogen deposits accumulate in lysosomes

45
Q

In glycogen storage disease where amylo-1,6-glucosidase enzyme is affected what organ is involved and what is the clinical manifestation?

A

liver, skeletal muscle, heart; fasting hypoglycemia, hepatomegaly in infancy in some myopathic features. Glycogen deposits have shorter outer branches

46
Q

In glycogen storage disease where amylo-4,6-transferase enzyme is affected what organ is involved and what is the clinical manifestation?

A

liver; only linear chain, hepatosplenomegaly; symptoms may arise from a hepatic reaction to the presence of a foreign body, usually fatal

47
Q

In glycogen storage disease where muscle glycogen phosphorylase enzyme is affected what organ is involved and what is the clinical manifestation?

A

skeletal muscle; exercise induced muscular pain, cramps, and progressive weakness, sometimes with myoglobinuria

48
Q

In glycogen storage disease where liver glycogen phosphorylase enzyme is affected what organ is involved and what is the clinical manifestation?

A

liver; hepatomegaly, mild hypoglycemia, good prognosis

49
Q

In glycogen storage disease where phosphofructokinase-I enzyme is affected what organ is involved and what is the clinical manifestation?

A

muscle and RBC; exercise induced muscular pain, cramps, and progressive weakness, sometimes with myoglobinuria, enzymatic hemolysis

50
Q

In glycogen storage disease where phosphorylase kinase enzyme is affected what organ is involved and what is the clinical manifestation?

A

liver; hepatomegaly, mild hypoglycemia, good prognosis

51
Q

In glycogen storage disease where cAMP dependent protein kinase A enzyme is affected what organ is involved and what is the clinical manifestation?

A

liver; hepatomegaly

52
Q

What tissues use glucose as the major fuel source?

A

the brain and the RBC

53
Q

Why is glucose the sole fuel source for RBCs?

A

only generate energy through glycolysis because they lack mitochondria

54
Q

Why is it important for the body to have a mechanism to control blood glucose levels?

A

the RBCs only use it and can’t survive without it, but the rest of the body can’t survive without the oxygen the RBCs carry

55
Q

What is the normal cycle of blood glucose after a meal?

A

rise to 80-100, within 30-60 min rises to 120-140, by about 2 hours after meal glucose level returns to fasting level

56
Q

What happens if blood glucose levels continue to rise what happens?

A

could result in tissue dehydration, if severe dehydration could occur in the brain,

57
Q

what happens if blood glucose continues to fall in fasting?

A

light headedness and dizziness could result, followed by drowsiness, eventually coma or death

58
Q

What happens in the first few hours of fasting?

A

liver glycogen provides the source of blood glucose by glycogenolysis; gluconeogenesis provides additional source of blood glucose

59
Q

What effect does a high carbohydrate meal have on blood glucose hormones?

A

stimulates the release of insulin from beta cells and inhibits the release of glucagon from alpha cells

60
Q

What effect does a high protein meal have on blood glucose hormones?

A

stimulates the release of both insulin and glucagon but do not effect blood glucose levels

61
Q

What effect does mixed meals have on blood glucose hormones?

A

release of insulin but not glucagon is stimulated

62
Q

What do growth hormones or glucocorticoids (cortisol)?

A

help maintain blood glucose levels by inhibiting glucose uptake in muscle uptake in muscle and adipose tissues (anti-insulin activities) and stimulating gluconeogenesis

63
Q

What is the fate of glucose in the liver after a meal?

A

part is used immediately for energy and most is converted to glycogen (stored in the liver) and triglyceride (transported and stored in adipose tissue)

64
Q

High blood glucose levels result in increased glycogen synthesis by what?

A

increasing glucose transport into the liver via facilitated glucose transporter (GLUT 2), elevated intracellular levels increase glucokinase activity resulting in elevated Glc-6P and glycogen synthesis; increasing secretion of insulin, induces glucokinase gene expression and enhances glycogen synthesis by activating protein phosphatase to dephosphorate kinase and glycogen synthase (stimulation) and glycogen phosphorylase (inhibition); inhibiting glucagon secretion resulting in inhibition of glycogen degradation

65
Q

Which glucose transporters and where are affected by insulin?

A

GLUT 4 recruitment to the cellular surface in muscle and adipose but not liver, brain, or RBC

66
Q

What effect does insulin have in peripheral tissues?

A

stimulates glycogen synthesis in resting muscle cells and in liver; it greatly stimulates transport of glucose into muscle cells but only slightly stimulates it into the liver cells

67
Q

How is glycogenolysis stimulated?

A

glucagon causes activation of liver andenylate cyclase, resulting in increased cAMP which activates protein kinase A to inhibit glycogen synthase, activate glycogen phosphorylase and inhibit protein phosphatase-1 at specific site in G subunit

68
Q

What causes the stimulation of gluconeogenesis?

A

4 hours after a meal, the liver is supplying glucose generated by glycogenolysis and gluconeogenesis to the blood; 3 key enzymes for gluconeogenesis- phosphoenolpyruvate carboxykinase, fructose-1,6-biphosphate and glucose-6-phosphate are induced and activated; 3 glycolysis enzymes- glucose kinase, phosphofructokinase-1 and pyruvate kinase are suppressed

69
Q

What causes the stimulation of lipolysis?

A

hormonal changes during fasting stimulate breakdown of adipose triglycerides, resulting in production of glycerol and fatty acids; glycerol serves as carbon source for gluconeogenesis in the liver while fatty acids undergo beta-oxidation of fatty acids in liver help drive gluconeogenesis

70
Q

What happens to blood glucose in a prolonged fasting state?

A

dramatic elevation of blood ketone body levels after 3-5days fasting; they provide major energy source for the body while glucose provides only 1/3 of energy under normal conditions; rate of gluconeogenesis in liver is decreased and proteins from muscle and other tissues are spared

71
Q

In what order do fuel sources get used in a muscle from its storage?

A

creatine phosphate provides first source for ATP (only lasts milliseconds), glycogen in muscle that contains fast twitch glycolytic fibers; Ca released from SR binds to calmodulin to activate phosphorylase kinase leading to activation of glycogen phosphorylase, if intense epinephrine also stimulates glycogenolysis

72
Q

How are fuels used from the blood?

A

blood glucose produced by glycogenolysis and gluconeogenesis in liver with supplemented with ketone bodies are pulled from the blood by muscles after they use creatine phosphate and stored muscle glycogen and finally ketone bodies supplemented with blood glucose

73
Q

How is fructose absorbed? What percent of the diet is fructose?

A

GLUT-5 facilitated transport; 20% of diet

74
Q

What are the first steps of fructose metabolism?

A

it is phosphorylated, broken down to a triose and a triose phosphate via fructose kinase and aldolase B (in liver, small intestine, and proximal epithelium of renal tubule),

75
Q

What happens to triose and triose phosphate in fructose metabolism?

A

converted to glucose via gluconeogenesis, to pyruvate via glycolysis,pyruvate is converted to acetyl-CoA which can either generate ATP or used to synthesize fatty acids and cholesterol, or to glycerol by triose phosphate isomerase and glycerol dehydrogenase, glycerol and fatty acids generated are the precursors of triglycerides; conversion of fructose to triglycerides and cholesterol accumulated in the liver causes a NAFLD

76
Q

In what parts of the body is fructose synthesized via Polyol path? From what?

A

seminal fluid, lens, retina, blood vessels, and peripheral nerves; synthesized from glucose

77
Q

What is fructosuria? cause? symptoms?

A

fructose kinase deficiency leads to secretion of fructose into the urine, producing elevated reducing sugars but no detectable glucose; asymptomatic because muscle and adipose hexokinase can provide alternative path for metabolizing fructose

78
Q

What two things cause fructose intolerance?

A

aldolase B deficiency and fructose 1,6 bisphosphate deficiency

79
Q

What are the features of aldolase B deficiency?

A

results in accumulation of fructose 1-P inside liver cells which ties up intracellular phosphate pool, resulting in reduction of ATP production; inhibits glycogen phosphorylase, aldolase and phosphohexose isomerase but stimulates glucokinase; high fructose foods causes nausea, vomiting followed by signs of hypoglycemia, lead to liver damage and cirrhosis

80
Q

What are the features of fructose 1,6 bisphosphatase deficiency?

A

can cause fructose intolerance also; gluconeogenesis is blocked so unable to sustain long periods of fasting or exercise

81
Q

What is the source of galactose metabolism and how is it moved to the site of the metabolism?

A

major source is lactose broken down by lactase and actively transported into the intestinal epithelial cells and out of these cells into the blood by glucose transporter and then transported to other parts including the liver, lens etc; converted to glucose

82
Q

What are the steps of galactose metabolism?

A

galactose to galatose1P by galactokinase; galactose1P and UDP glucose to UDP galactose and glucose 1P by galactokinase1P uridylytransferase; UDP-galactose to UDP glucose by UDP-glucose epimerase

83
Q

What is galactosemia?

A

severe genetic disease of impaired galactose metabolism; consumption of milk induces vomiting and diarrhea, failure to remove galactose from the diet of infant results in failure to thrive, mental retardation, liver damage, and cataracts

84
Q

What causes the formation of cataracts in galactosemia?

A

accumulation of galactitol, a product of aldose reductase in the lens

85
Q

What is the cause and the characteristics of classic galactosemia?

A

deficiency of galactose 1-phosphate uridylyltransferase results in accumulation of galactose 1-P in the tissue and appearance of galactose in the blood and urine, can suffer from liver damage and cataract

86
Q

What is the cause and the characteristics of non-classic galactosemia?

A

deficiency of galactose kinase results in accumulation of galactose; suffer from cataract but not liver damage

87
Q

How is galactosemia diagnosed?

A

elevated reducing power (due to galactose) in the urine but a negative glucose oxidase test; galactose 1-P-uridylyl transferase activity can be determined in RBC

88
Q

What are the similarities of the mannose and fucose pathways?

A

interconnected; both are converted to activated sugars, GDP-mannose and GDP-fucose, for synthesis of glycoconjugates

89
Q

What is the fate of dietary mannose?

A

converted by hexokinase to mannose-6-P (also derived from glucose and fructose)

90
Q

What is the fate of dietary fucose?

A

converted to GDP-fucose, also derived from mannose by way of GDP-mannose

91
Q

What is CDG?

A

congenital disorders of glycosylation developed from defect in mannose metabolism, type I is a defect in lipid-linked oligosaccharide synth, type II includes all others

92
Q

What is leukocyte adhesion deficiency II (LADII)?

A

comes from defect in transport of GDP-Fuc from cytoplasm to the lumen of the Golgi, activated sugar unavailable for synthesis of blood group substances, including ABO (H), Lewis, and sialyl Lewis x blood types; Bombay blood type is detected and leukocyte trafficking to lymphoid tissues and sites of tissue injury is compromised; suffer from frequent infections

93
Q

How is CDG and LAD-II treated?

A

CDG-Ib have been treated with oral mannose (can cause liver disease) and LAD-II patients treated with fucose have shown efficacy

94
Q

What is the Hexosamine metabolic pathway?

A

N-acetylglucosamine (GlcNAc) can come from glucose and dietary glucosamine serve as source of GlcNAc, GalNAc and NeuAc found in glycoconjugates; UDP-GlcNAc is formed first, in turn is converted to UDP-GalNAc and CMP-NeuAc; these nucleotide sugars are activated sugar donors for synthesis of all glycoconjugates

GI (9 decks)

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