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Biochem Self Study > Amino acid catabolism Pt. 2 & Diabetes > Flashcards

Amino acid catabolism Pt. 2 & Diabetes Flashcards

1
Q

The urea cycle makes ammonia into urea so…

A

excess nitrogen can be excreted

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2
Q

Urea cycle Step 0

A

Ammonia and CO2 are made into Carbamoyl phosphate

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3
Q

Ammonia and CO2 are made into…..

A

Arginine, then into urea

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4
Q

Urea Cycle Step 1

A

Carbamoyl + Ornithine -> Citrulline

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5
Q

Urea cycle step 2

A

Citrulline + Aspartate -> Argininosuccinate

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6
Q

Urea cycle step 3

A

Argininosuccinate -> Arginine

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7
Q

Urea cycle step 4

A

Arginine -> Ornithine + Urea

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8
Q

Glutamine, Glutamate and Alanine “____” amino groups into the urea cycle

A

Feed

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9
Q

Carbamoyl phosphate synthase I

A

the first nitrogen enters from ammonia.
The terminal phosphate groups of two molecules of ATP are used to form one molecule of carbamoyl phosphate
(two activation steps)

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10
Q

Urea cycle takes place in…

A

in mitochondria and cytosol of liver

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11
Q

One amino group enters the urea cycle as ________, formed in the matrix

A

carbamoyl phosphate

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12
Q

The other amino group enters as _____, formed in the matrix by ________ of ________ by glutamate

A

aspartate, transsmination, oxaloacetate

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13
Q

Energetic cost of urea synthesis

A

4 ATP bonds but get 2.5 ATP back so about 1.5 ATP/urea

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14
Q

Nitrogen metabolism

A
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15
Q

Proline synthesis

A

Glutamate -> -> -> Proline
- 1 ATP, 2 NADPH used

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16
Q

Aspartate synthesis

A

Oxaloacetate + Glutamate -> Aspartate + alpha-Ketoglutarate

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17
Q

Asparagine synthesis

A

(not a transamination reaction)
Aspartate + ATP -> beta-aspartyladenylate –(b)–> Asparagine

b: Glutamine -> Glutamate

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18
Q

Alanine synthesis

A

Alanine –(a,b)–> Pyruvate -> Glucose or Acetyl CoA

a = Alanine: alpha-ketoglutarate aminotransferase

b = Alpha-ketoglutarate -> Glutamate

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19
Q

Serine synthesis

A

3-phosphoglycerate + NAD+ –> –> –> Serine

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20
Q

Glycine Synthesis

A

Serine –(a,b)–> Glycine

a = serine hydroxymethyltransferase

b = tetrahydrofolate -> Methylene-tetrahydrofolate

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21
Q

Tetrahydrofolate

A

carries a variety of single carbon units

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22
Q

Cysteine synthesis

A

Serine + Homocysteine –> Cysteine + a-ketobutyrate

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23
Q

Tyrosine synthesis

A

Phenylalanine –> Tyrosine

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24
Q

Nitrogen excretory product

A

mammals - urea
birds - uric acid
fish - ammonia

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25
Q

Transaminases

A

amino groups transferred to Glu and Asp

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26
Q

Glutamate dehydrogenase

A

amino group of Glu released as ammonium ion

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27
Q

Urea cycle

A

Ammonium ion, carbon dioxide, and the terminal group of Arg utilized to make urea

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28
Q

Warburg Effect

A

main product of aerobic glycolysis in cancer cells is lactic acid

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29
Q

Importance of Nucleotides: ATP

A

energy storage

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30
Q

Importance of Nucleotides: UTP

A

carbohydrate metabolism

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31
Q

Importance of Nucleotides: CTP

A

phospholipid metabolism

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32
Q

Importance of Nucleotides: GTP

A

protein synthesis

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33
Q

Importance of Nucleotides: NAD, NADP, FAD

A

coenzymes

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34
Q

Importance of Nucleotides: AMP, ADP, ATP, etc.

A

allosteric regulators

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35
Q

Importance of Nucleotides: cAMP, cGMP

A

second messengers

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36
Q

Importance of Nucleotides: dATP, dGTP, dCTP, dTTP

A

DNA synthesis

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37
Q

Importance of Nucleotides: ATP, GTP, CTP, UTP

A

RNA synthesis

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38
Q

Five nitrogen bases

A

Adenine, Guanine, Cytosine, Thymine, Uracil

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39
Q

Nucleotide synthesis

A
  • Ribonucleotides synthesized first
  • Deoxyribonucleotides formed from ribonucleotides by ribonucleotide reductase using NADPH

-dUMP is methylated to make dTMP

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40
Q

Methotrexate

A

slows cell growth

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41
Q

Two types of Diabetes

A

Diabetes Mellitus, Diabetes Insipidus

42
Q

Diabetes Mellitus

A

body does not produce enough insulin or does not properly respond to insulin, which results in high glucose levels

43
Q

Diabetes insipidus

A

(rare) characterized by excessive thirst and excretion of large amount of dilute urine. Results from malfunction of the vasopressin/antidiuretic hormone system

44
Q

Both types of diabetes are characterized by….

A

required urination
Mellitus - sweet urine
Insipidus - unsweetened urine

45
Q

Oral glucose tolerance test

A

determines the rate of glucose removal from blood

OGTT levels between 140-200 mg/dL indicate impared tolerance

> 200 confirms diabetes

46
Q

Uncontrolled diabetes results in ______

A

very high blood glucose concentrations

47
Q

Two types of Diabetes Mellitus

A

Type I and Type II

48
Q

Type I Diabetes

A

develops when the body produces little or no insulin

no known way to prevent or cure

49
Q

Type II Diabetes

A

Develops when the body becomes resistant to insulin

50
Q

Type I Diabetes develops when….

A

the body’s immune system destroys pancreatic beta cells

51
Q

Type I diabetes accounts for…

A

5% to 10% of diagnosed cases

52
Q

Demographic of Type I diabetes

A

usually strikes children and young adults

53
Q

Type I diabetes is treated with

A

injected insulin by syringe or pump

54
Q

Type II diabetes accounts for

A

90% of all cases of diabetes

55
Q

Type II diabetes begins as

A

insulin resistance

as the need for insulin rises, the pancreas gradually loses ability to produce it

56
Q

Type II Diabetes Demographic

A

associated with older age, obesity, family history of diabetes, history of physical inactivity, and race

57
Q

Reduce change of developing Type II diabetes and improve outcome

A

Exercise and losing weight

58
Q

Type II Diabetes Treatment

A

treated with injected insulin or other drugs

59
Q

history of diabetes

A

In 1921 in Ontario, Canada. Frederick Banting and Charles Best, kept a severely diabetic dog alive for 70 days by injecting it with dog pancreas

60
Q

Insulin stimulates

A

Lipogenesis

  • insulin stimulates glucose uptake, glycolysis, fatty acid synthesis but inhibits lipolysis
  • Net result is lipid accumulation
61
Q

The fasting state

A

or diabetic state, epinephrine and glucagon are elevated

62
Q

Lack of insulin secretion or response to insulin leads to

A

GLUT4 (in adipose and muscle) sequestered in the vesicles in the cytosol

Glucose absorption is significantly reduced

Glycolysis pathway is inhibited

63
Q

Gluconeogenesis in the liver occurs (diabetes)

A

even though there is enough glucose available, contributing to high blood glucose level in diabetic patients

64
Q

Lipoprotein lipase (diabetes)

A

is inhibited, leading to high concentrations of VLDL and Chylomicrons in blood and hypertriacyglycerolemia

65
Q

Type I Diabetes (cont.)

A

No insulin secretion

Triacyglycerides in adipose cells are broken down into fatty acids and supplied to other tissues for energy (Lipolysis)

Excessive production of ketone bodies in liver from fatty acid beta oxidation leads to ketoacidosis

66
Q

Type II Diabetes (cont.)

A

Patients make insulin but are “insulin resistant” (receptors on liver or muscle cells become insensitive)

Beta-cells don’t make enough insulin to either inhibit gluconeogenesis in the liver or to stimulate glucose uptake by muscle

Lipolysis in adipose cells stil inhibited by insulin. therefore, insulin-resistant diabetic patients rarely have ketoacidosis

67
Q

Sulfonylurea drugs like Amaryl and Glucotrol

A

treat type II diabetes

68
Q

Targets of sulfonyl drugs

A

ATP-gated K+ channels

increase insulin release from pancreatic beta celss

69
Q

Roles of Hormones in Fed State

A

Hormones: Insulin

Role: Stimulates glucose uptake by tissues in response to high blood glucose.

Effect: Promotes glucose export to the brain, adipose, and muscle tissues.
Metabolism: Excess glucose oxidized to acetyl-CoA for fatty acid synthesis and exported as triacylglycerols in VLDLs.

70
Q

Lipogenic Liver in Fed State

A

State: Well-fed state

Metabolism: Glucose, fatty acids, and amino acids enter the liver.
Insulin Response: Released to regulate blood glucose and stimulate glucose uptake.

Liver Actions: Glucose oxidized to acetyl-CoA for lipid synthesis, excess amino acids converted to pyruvate and acetyl-CoA.

71
Q

Dietary Fat Transport in Fed State

A

Transport: Dietary fats move as chylomicrons via the lymphatic system.
Destination: From the intestine to muscle and adipose tissues.

72
Q

Roles of Hormones in Fasting State

A

Hormones: Glucagon

Prevention: Prevents blood sugar from dropping too low.

Liver Response: Induces breakdown of liver glycogen to release glucose into the bloodstream.

73
Q

Glucogenic Liver in Fasting State

A

State: Fasting state

Metabolism: Liver becomes the principal source of glucose for the brain.
Substrates: Amino acids from protein degradation, glycerol from TAG breakdown used for gluconeogenesis.

Fuel Usage: Fatty acids used as the principal fuel, excess acetyl-CoA converted to ketone bodies for export.

74
Q

Hyperglycemia and Alpha-cell Function

A

Contribution: Inappropriately increased alpha-cell function contributes to hyperglycemia.

Causes: Loss of tonic restraint by high local insulin concentrations on alpha-cells.

Possible Mechanisms: Beta-cell failure, alpha-cell insulin resistance, and involvement of incretin hormones.

75
Q

Mechanism of Insulin-Stimulated Glucose Uptake

A
  1. Insulin release in response to high blood glucose.
  2. Insulin binds to receptors on cells, triggering a signal pathway.
  3. Signal transduction leads to GluT4 translocation to the cell membrane.
  4. GluT4 facilitates glucose transport into the cell.

Result: Blood glucose levels decrease, and cells use glucose for energy.

76
Q

Importance of Insulin-Stimulated Glucose Uptake

A

Significance: Crucial for maintaining blood glucose homeostasis.

Function: Provides cells with needed glucose for energy production.

77
Q

Mechanism of Insulin Secretion from Beta Cells

A
  1. Beta cells release insulin to reduce blood glucose.
  2. GLUT2 transports glucose into beta cells.
  3. Glucose is metabolized, leading to ATP production.
  4. ATP-sensitive potassium channels close, causing cell depolarization.
  5. Voltage-gated calcium channels open, triggering insulin granule exocytosis.
  6. Other Nutrients and Hormones: Free fatty acids, amino acids, melatonin, estrogen, leptin, growth hormone, and glucagon-like peptide-1 regulate insulin secretion.
  7. Beta cells act as a metabolic hub connecting nutrient metabolism and the endocrine system.
78
Q

Quick Response to Blood Glucose Changes

A

Purpose: Allows the body to respond swiftly to blood glucose level changes.
Result: Maintains homeostasis in the body.

79
Q

Acute Diabetes Conditions

A

Conditions:
Hypoglycemia: Low blood sugar, occurs rapidly with insulin overdose.

Diabetic Ketoacidosis: Causes dehydration, labored breathing, coma, and death; results from insufficient insulin leading to excessive ketone body production.

80
Q

Hypoglycemia

A

Cause: Too much insulin injected.

Risk: Can lead to coma and death.

Onset: Occurs very fast, within minutes to hours.

81
Q

Diabetic Ketoacidosis

A

Cause: Insufficient insulin leading to excessive ketone body production.

Symptoms: Dehydration, labored breathing, coma, and death.

Onset: Develops more slowly, over many hours to days.

82
Q

Chronic Diabetes Conditions

A

Conditions:
Chronic Renal Disease: Affecting 10-20% of diabetics, leading cause of end-stage renal disease.

Nerve Disease (Peripheral Neuropathy): Affects 60-70% of diabetics, causing impaired sensation or pain in hands or feet.

Amputations: Most common reason for non-traumatic amputations, typically toes and feet.

Cardiovascular Disease and Stroke: 2-4 times higher in diabetics, exacerbated by smoking.

High Blood Pressure (Hypertension): Most diabetics have elevated blood pressure.
Blindness (Diabetic Retinopathy): Most common reason for blindness in working age.

83
Q

Measurement of Blood Glucose

A

Methods:
Glucometer: Device for determining blood glucose concentrations at the moment, changes rapidly.

Hemoglobin A1c: Glycated form of hemoglobin indicating blood glucose concentrations over weeks or months, changes slowly.

84
Q

Chronic Renal Disease

A

Prevalence: Affects 10-20% of diabetics.
Consequence: Leading cause of end-stage renal disease.

85
Q

Nerve Disease (Peripheral Neuropathy)

A

Prevalence: Affects 60-70% of diabetics.
Symptoms: Impaired sensation or pain in hands or feet.

86
Q

Amputations

A

Prevalence: Most common reason for non-traumatic amputations.
Affected Areas: Usually toes, feet, etc.

87
Q

Cardiovascular Disease and Stroke

A

Risk: 2-4 times higher in diabetics.
Exacerbating Factor: Smoking worsens the risk.

88
Q

High Blood Pressure (Hypertension)

A

Prevalence: Most diabetics have high blood pressure.

89
Q

Blindness (Diabetic Retinopathy)

A

Prevalence: Most common reason for blindness in working age.

90
Q

Hemoglobin A1c Test

A

Development: Introduced in 1979.

Significance: Standard measurement for blood sugar control in the Diabetes Control and Complications Clinical Trial (1983-1993).

Outcome: People who controlled blood glucose had fewer complications.

91
Q

Importance of Hemoglobin A1c Test

A

Pre-1979: Little emphasis on maintaining strict control over blood glucose levels.

Post-1979: Hemoglobin A1c became a key indicator of blood glucose control.

92
Q

Hemoglobin Glycation

A

Process: Elevated blood glucose leads to glycation of proteins.

Measurement: Level is proportional to blood glucose concentrations.

Estimation: Used to estimate blood glucose concentrations over weeks, specifically through hemoglobin A1c levels.

93
Q

Glycated Hemoglobin Levels

A

Life of RBC: Reflects glucose concentration over the life of a red blood cell (120 days).
Importance: Last 2 weeks are crucial.

Separation: Glycated hemoglobin is separated from normal hemoglobin based on size and charge.

Expression: Expressed as a percentage of total hemoglobin.

94
Q

Normal and Extreme A1c (%) Levels

A

Normal Range: 5%
Extreme Range: 13%
Target: Aim to keep below 7%.

95
Q

Risk Reduction (A1c Levels)

A

Correlation: For every 1% reduction in glycosylated A1c.

Outcome: Corresponds to a 10% decrease in the risk of vascular complications.

96
Q

Why High Glucose is Bad

A

Reason: Inappropriate glycation of proteins.

Consequence: Glycated proteins have altered activities, solubilities, and degradation properties.

97
Q

HbA1c Formation during Hyperglycemia

A

Process: Glucose reacts non-enzymatically with the NH2 group on the amino terminus of hemoglobin.

Result: Forms HbA1c, accounting for more than 12% of total hemoglobin in a diabetic patient.

98
Q

Effects of Glycation on Proteins

A

Changes: Glycated proteins exhibit altered activities, solubilities, and degradation properties.

Example: Blurred vision due to diabetic cataracts caused by increased glycation of lens proteins, making the eye lens cloudy.

99
Q

Diabetic Cataracts

A

Cause: Increased glycation of lens proteins.

Effect: Cloudiness in the lens of the eye, leading to blurred vision.

100
Q

Increased Risk for Cardiovascular Disease

A

Risk Factor: Glycated proteins and lipoproteins.

Recognition: Recognized by macrophages.

Consequence: Can lead to accelerated atherosclerosis.
Outcome: Increased risk for cardiovascular disease.

Biochem Self Study (7 decks)

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