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Biochemistry > Carbohydrate metabolism > Flashcards

Carbohydrate metabolism Flashcards

1
Q

Dietary Carbohydrates? (5 categories)

A

Indigestible fiber Complex Carbohydrates Disaccharides Monosaccharides Oligosaccharides

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2
Q

Examples? Indigestible fiber Complex Carbohydrates Disaccharides Monosaccharides Oligosaccharides

A

Indigestible fiber: -cellulose Complex Carbohydrates -Starch and amylopectin -Glycogen Disaccharides -Lactose -Sucrose -Maltose Monosaccharides -Fructose (some fruit, “soda pop”) -Ribose (from DNA & RNA) -Glycerol (from triglycerides) Oligosaccharides -found attached to glycoproteins, lipoproteins, proteoglycans (from bacteria), glycosaminoglycans (found in extracellular connective tissue and joints).

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3
Q

Digesting complex carbs?

A

a-amylase from saliva in mouth cleaves a-1,4 glycosidic bonds *no carbohydrate digestion in stomach (because stomach acid inhibits amylase) -complete digestion in the small intestine, where the pancreas secretes HCO3- and a-amylase

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4
Q

endoglucosidase

A

-it means specific to cleaving one bond -like how a-amylase cleaves a-1,4 glycosidic bonds

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5
Q

Starch is digested in the mouth by amylase to what products? Glucose Glucose and fructose Glucose and galactose Glucose and ribose Maltose and limit dextrins

A

Maltose and limit dextrins note: amylase cannot digest (a- 1,6 branches)

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6
Q

what do glycosidases do?

A

-convert disaccharides and oligosaccharides to monosaccharides (glycosidases are attached to membranes of absorptive cells of the brush border)

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7
Q

Glucoamylase Sucrase-isomaltase Trehalase Lactase-glucosylceramidase

A

the 4 glycosidases she talks about -I guess they are glycoproteins

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8
Q

Glucoamylase

A

-Specific for a-1,4 glycosidic bonds -Hydrolyzes sequentially from nonreducing end to form monosaccharides

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9
Q

Trehalase - deficiency has symptoms similar to a-amanitin poisoning

A

cleaves trehalose (found in mushrooms) cleaves a-1,1 bond

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10
Q

Sucrase-isomaltase

A

Nearly all of a-1,6 bonds cleaved by isomaltase-maltase activity

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11
Q

b-glycosidase complex (Lactase)

A

hydrolyzes b-1,4 bond (b-galactosidase) rate-limiting enzyme for lactose absorption

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12
Q

some carbs can’t be digested, what do we call them?

A

Dietary Fiber -Insoluble (cellulose) -Soluble (banana) Digested by bacteria -Produce gas and short chain fatty acids -10% of caloric intake

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13
Q

Lactose intolerance is the inability to convert lactose into: Glucose Glucose and fructose Glucose and galactose Glucose and ribose Maltose and limit dextrins

A

*Glucose and galactose note (bacteria will ferment lactose if enzyme isn’t present: forms lactic acid, methane, and hydrogen gas

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14
Q

glycemic index

A

= Rate of absorption -Low glycemic foods are digested more slowly, which is better for diabetic (fewer spikes in blood glucose)

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15
Q

how is glucose absorbed?

A

its polar and won’t cross the INTESTINAL EPITHELIUM membrane so need to use: -Na+ cotransport -tissue-specific transporters (glut 4)

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16
Q

Which 2 tissues increase GLUT 4 transporters on their surface in response to insulin? Adipose and muscle Liver and adipose Liver and brain Liver and muscle Kidney and brain

A

Adipose and muscle (so GLUT 4 is insulin sensitive! when insulin is around # of these transporters increases)

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17
Q

Glycogen (structure)

A
  • a- 1,4 glycosidic bonds with a- 1,6 branches every 8-10 units
  • Only one anomeric carbon (reducing end) per molecule of glycogen
  • May be simultaneously degraded from all nonreducing ends
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18
Q

Structure of Glycogen

A
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19
Q

Glycogen (purpose)

A

Emergency fuel, Stimulated in anaerobic glycolysis

liver glycogen: Primary source of glucose for maintenance of blood glucose

muscle glycogen: reservoir for ATP gen (via aerobic glycolysis)

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20
Q

Glycogen Metabolism

A
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21
Q

role of G6P?

A
  • traps glucose in cell (its the common currency baby!)
  • enzyme: glucokinase in liver (S1), hexokinase in other cell types
  • G6P is precursor of glycolysis, PPP and pathways for synthesis of other sugars
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22
Q

role of G1P?

A

G1P is precursor of glycogen synthesis

-enzyme: phosphoglucomutase (and product of glycogen degradation)

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23
Q

notes about gylcogen synthesis

A
  • a-1,4-glycosidic bonds link glucosyl residues in long chains
  • Glucosyl units added from UDP-G to nonreducing ends by glycogen synthase
  • Branching allows for increased sites for synthesis and degradation and enhances solubility
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24
Q

After 11 residues added, 6-8 cleaved by amylo-4,6-transferase (branching enzyme) and reattached by an a-1,6 bond

A

branching details

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25
Q

Step one of glycogen breakdown?

A
  • Glycogen phosphorylase works on nonreducing ends
  • produces G1P
  • sterically hindered by branches
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26
Q

Step two of glycogen breakdown?

A

Debrancher enzyme has 2 activities

  • transferase (cuts)
  • amylo-1,6-glucosidase (one glucose molecule)
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27
Q

Degradation of Glycogen

A
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28
Q

3 glycogen storage diseases?

A

von gierkes disease

McArdles disease

Hers disease

(can’t get glucose back - specific enzymes are messed up)

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29
Q

THe affected enzyme is glucose 6 phosphatase in which disease?

(provide organ affected, symptoms and treatment)

A

-von gierkes disease (will be futile cycling)

organ affected: liver

symptoms: enlarged liver and kidney, *growth failure, severe fasting hypoglycemia
treatment: Give small infrequent meals and complex carbs (treat it through the diet) – because glucose is stuck in liver (greedy dutch are hording all the sugar)

30
Q

The affected enzyme is ‘muscle glycogen phosphorylase’ in which disease?

(provide organ affected, symptoms and treatment)

A

McArdles disease

organ affected: muscles

symptoms: exercise induced muscular pain, cramps, progressive weakness
treatment: individual will be fine as long as muscle are not stressed, so don’t overdo exercising

31
Q

The affected enzyme is ‘liver glycogen phosphorylase’ in which disease?

(provide organ affected, symptoms and treatment)

A

Hers disease (no futile cycling)

organ affected: liver

symptoms: hepatomegaly, mild hypoglycemia
treatment: n/a

good prognosis -not as bad as von-gierkes

b/c we are not doing futile cycling in hers disease (bc we can’t even break down the glycogen)

32
Q

A 2-year-old girl presents with a mildly enlarged liver, history of hypoglycemia on several occasions and growth below the third percentile for her age.

A

-von gierkes disease

33
Q

Effects of Epinephrine on Glycogen Metabolism?

A

Epinephrine enhances the effects of glucagon in liver

34
Q

Glycogen Metabolism in Skeletal Muscle?

A

No G6P phosphatase in muscle -glucose trapped as glycogen -dedicated to glycolytic pathway for energy production No effect of glucagon

35
Q
A
36
Q
A
37
Q

What is normal range of blood glucose? How do insulin and glucagon affect blood glucose?

A

80-100 Glucagon – increases blood glucose Insulin – lowers blood glucose

38
Q

insulin

A

storage of glucose as TG or glycogen in muscle and adipose tissue -synthesized as proinsulin (made 1:1 with c-peptide!) -glucose is the main stimulus (along with AA, neural input, gut hormones - CCK, GIP) -inhibited by adrenergics (EP)

39
Q

glucagon

A

-glucose mobilization via glycogenolysis and gluconeogenesis (from lactate, glycerol and AAs) -FA mobilized from adipose tissue -synthesized as proglucagon in pancreatic alpha-cells (short half life once cleave - bc steroid hormone) -inhibited by glucose and insulin -stimulated by AA (and cortisol, EP, stress)

40
Q

What really matters is receptors for glucagon or insulin, with out that these hormones cannot act!! where are the receptors?

A

glucagon: acts on liver/adipose tissue -Muscle cells don’t have a glucagon receptor -cAMP mechanism insulin receptors: acts on liver (glut2), muscle/adipose (glut4) -receptor tyrosine kinase dimerization -glucose transporter in pancreas is (glut 2)

41
Q

Glucagon release does not alter muscle metabolism because of which of the following? Muscle cells lack adenylate cyclase. Muscle cells lack protein kinase A. Muscle cells lack G proteins. Muscle cells lack GTP. Muscle cells lack the glucagon receptor.

A

Muscle cells lack the glucagon receptor.

42
Q

What is the clinical significance of C-peptide?

A

-can use it to measure insulin levels (that the body has synthesized) -Don’t know if someone took insulin as medication or their body cant make it we could tell the difference

43
Q

diabetes mellitus - complications

A

Hyperglycemia – high blood glucose Can cause hyper-osmotic coma by pulling water out of cells (particularly brain cells) Polyuria – urge to urinate frequently Polydipsia – increased thirst Weight loss (type 1)?

44
Q

Different types of diabetes mellitus (3)

A

Type 1 Autoimmune destruction of b-cells Almost undetectable [insulin] in blood (measure c peptide) Type 2 (insulin resistant) Skeletal muscle and liver “resist” action of insulin Insulin level can be normal in these patients MODY (maturity onset diabetes of the young) *decreased glucokinase activity (still make some G6P tho) requires ↑ [glucose] to cause ↑ [ATP] therefore insulin release only at ↑ [glucose]

45
Q

Treating diabetes?

A

Insulin Replacement Therapy – insulin injections, inhaled insulin, long-acting insulin Sulfonylureas – block K+ channels increase insulin secretion Exercise helps insulin act more efficiently. We don’t really know why, but diabetics who exercise are better off)

46
Q

A patient with type 1 diabetes mellitus takes an insulin injection before eating dinner but then gets distracted and does not eat. Approximately 3 hours later, the patient becomes shaky, sweaty and confused. The symptoms have occurred because of which of the following? Increased glucagon released from the pancreas Decreased glucagon release from the pancreas High blood glucose levels Low blood glucose levels Elevated ketone body levels

A

Low blood glucose levels

47
Q

Synthesized in the body from glucose via the polyol pathway

A

FRUCTOSE! In the lens of the eye, can lead to cataract formation Metabolized by conversion to intermediates of glycolysis Enters cells via GLUT 5 transporters

48
Q

Insulin vs Glucagon

A
49
Q

Fructose Metabolism

A

yields intermediates of glycolysis:

dihydroxyacetone-P

glyceraldehyde-3-P

-Aldolase B is rate-limiting enzyme of fructose metabolism

50
Q

Why is essential fructosuria a benign genetic disorder, while hereditary fructose intolerance can be fatal?

A

A build up of Fructose 1 P is dangerous - occurs when an aldolase B deficiency exists

A build up of fructose is not, it just leaves in urine -deficiency in fructose kinase

51
Q

What is the purpose of the polyol pathway? And what are the 2 steps?

A
  • synthesizing fructose in the body (from glucose)
    1. Reduction of C1 by aldose reductase
    2. Oxidation of C2 by sorbitol dehydrogenase
  • in diabetics when glucose is high, this reaction takes place in the eye, but the conversion to fructose is slow (second step is slow) and sorbitol accumulates, leading to cataracts) *same thing happens when galactose is in high concentration, conversion to fructose is slow and galactitol accumulates in the eye
52
Q

Why would our body want to make fructose?

A

Sperm use fructose while in seminal fluid

53
Q

Hereditary Fructose Intolerance (HFI) substrate that accumulates, defective enzyme, clinical symptoms.

A

substrate that accumulates: Fructose 1 P

defective enzyme: deficiency in aldolase B

clinical symptoms: Fructose-1-P inhibits the breakdown of glycogen and also gluconeogenesis (Hypoglycemia, high lactate, low ATP)

54
Q

Classical galactosemia substrate that accumulates, defective enzyme, clinical symptoms.

A

substrate that accumulates: galactose 1 P

defective enzyme: deficiency in galactose 1 P uridylyltransferase

clinical symptoms: accumulation of galactitol (cataracts)

55
Q

Fructose Metabolism

A
56
Q

PPP – oxidative Phase - name 2 most important products?

A

NADPH (only source of electrons for RBCs)

ribose-5 P (nucleotide biosynthesis) or (converted to glycolytic intermediates in the nonoxidative phase of the PPP)

57
Q

What is the most important enzyme in Pentose Phosphoate pathway?

A

G6P-dehydrogenase (its the rate limiting enzyme in this pathway!) Know that this produces 2 NADPH per glucose

58
Q

PPP – NON-oxidative Phase - name 2 most important products?

A

generates 2 mol fructose 6-P and

1 mol of glyceraldehyde 3-P (from 3 mol of ribulose 5-P)

59
Q

Overview of PPP

A
60
Q

describe effects of hemolytic anemia (massive destruction of RBC) in G6PD deficient individuals.

A

Black colored urine, Low RBC count, Elevated reticulocyte count, RBC with Heinz bodies, Low hemoglobin, Elevated serum bilirubin - *because without G6PD RBCs can’t deal with peroxide the peroxide causes Oxidative damage to lipids, proteins and DNA, which leads to massive destruction of RBC

61
Q

Gluconeogenesis is glycolysis in reverse except for these 3 steps (name these 3 steps that must be bypassed by gluconeogenesis) (bypassed, meaning they require a different reaction/enzyme)

A
  • glucose to G6P
  • F6P to F1,6BP
  • PEP to Pyruvate (the reverse reaction for gluconeogenesis is complicated)

(the enzymes for glycolysis or gluconeogenesis are kinases or phosphatases! respectively - should be obvious)

62
Q

what is Gluconeogenesis

A
  • we need glucose when its low (fast)
  • Glucose is synthesized from noncarbohydrate precursors -Takes place in liver under fasting/starving conditions -Stimulated by glucagon
63
Q

noncarbohydrate precursors (carbon sources)?

A

Carbon sources are:

  • lactate (from anaerobic glycolysis in RBCs and muscle) -amino acids (alanine) (from muscle pools)
  • glycerol (from adipose tissue - TG breakdown)
64
Q

because glycolysis and gluconeogenesis are almost the reverse of each other we need to prevent futile cycling - but how?

A

*through regulation: phosphorylation, gene transcription and allosteric interactions

  • insulin stimulates glycolysis
  • glucagon stimulates gluconeogenesis

*The most important control point is between fructose 6P and fructose 1,6-BP.

65
Q

Gluconeogenesis vs. glycolysis

A
66
Q

glycolysis yields how many ATP?

A

Glycolysis yields 2 ATP

67
Q

Gluconeogenesis costs how many ATP?

A

Gluconeogenesis costs 6 ATP

68
Q

High carbohydrate mean vs. High protein meal

A

Carbohydrates increase glucose and insulin, decrease glucagon

Proteins increase glucagon with little or no change in insulin or glucose levels

69
Q

conversion between G6P and glucose

A

glucokinase: insulin stimulated, converts glucose to G6P glucose 6
phosphatase: glucagon stimulated, converts G6P to glucose

70
Q

in glycolysis are we adding or removing phosphates?

A

glycolysis we add phosphates, enzymes are KINASES

gluconeogenesis we remove the phosphates so enzymes are PHOSPHATASES

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