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Noorda FOM > Module 6 ChatGPT > Flashcards

Module 6 ChatGPT Flashcards

1
Q

Hormone-Sensitive Lipase (HSL)

A

An enzyme phosphorylated by PKA to become more active, playing a key role in converting diglycerides to monoacylglycerol plus free fatty acids during lipolysis

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2
Q

Adipose Triglyceride Lipase (ATGL)

A

The rate-limiting enzyme of triglyceride degradation, catalyzing the conversion of triglycerides to diglycerides and free fatty acids

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3
Q

Comparative Gene Identification-58 (CGI-58)

A

A protein that regulates ATGL by binding to it when released from perilipin 1 (PLIN1) upon PKA activation

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4
Q

Perilipin 1 (PLIN1)

A

A protein that binds to triacylglycerol droplets, regulating their degradation
Phosphorylation by PKA releases CGI-58, activating ATGL

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5
Q

Glyceroneogenesis

A

The process by which adipocytes resynthesize triglycerides from glycerol 3-P (derived from amino acids or lactate) and free fatty acids, reducing fatty acid export

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6
Q

Fatty acids during fasting are

A

Released into the blood during lipolysis, travel complexed with albumin, and are oxidized to CO2 and water in muscle cells for energy

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7
Q

Ketone Bodies

A

Produced by the liver from acetyl-CoA during prolonged fasting and released into the blood for use as an energy source

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8
Q

Gluconeogenesis from Glycerol

A

Glycerol derived from lipolysis in adipose cells is used by the liver as a carbon source during fasting to produce glucose

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9
Q

cAMP in Adipose Cell

A

A secondary messenger that increases in response to the decrease of insulin and increase of glucagon during fasting, stimulating lipolysis

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10
Q

PKA (Protein Kinase A)

A

An enzyme activated by increased cAMP levels that phosphorylates hormone-sensitive lipase (HSL), enhancing its activity in lipolysis

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11
Q

Monoacylglycerol Lipase

A

The enzyme that converts monoacylglycerol to free glycerol and a free fatty acid during lipolysis

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12
Q

Triglyceride Synthesis in Adipocytes

A

Occurs simultaneously with glyceroneogenesis to regulate the amount of fatty acids released into circulation by resynthesizing triglycerides from glycerol 3-P and free fatty acids

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13
Q

Fatty Acid Transport

A

Fatty acids released during lipolysis travel in the blood complexed with albumin and enter muscle and other tissues for oxidation to produce energy

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14
Q

beta-Oxidation

A

The metabolic process by which fatty acids are broken down in the mitochondria of cells to generate acetyl-CoA, which can be used to produce energy or ketone bodies during fasting

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15
Q

Liver Function During Fasting

A

The liver uses glycerol derived from adipose tissue lipolysis for gluconeogenesis, converting it into glucose to maintain blood sugar levels

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16
Q

Perilipins

A

A family of proteins that regulate the breakdown of stored fats in adipocytes by binding to lipid droplets and controlling access to lipases

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17
Q

Phosphatidic Acid

A

An intermediate in the synthesis of triacylglycerols and the precursor of glycerolipids found in cell membranes and blood lipoproteins

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18
Q

Glycerol 3-Phosphate (Glycerol 3-P)

A

The molecule providing the glycerol backbone for triacylglycerol synthesis, produced in the liver by glycerol kinase or from DHAP

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19
Q

Dihydroxyacetone Phosphate (DHAP)

A

A glycolysis intermediate converted to glycerol 3-P in the liver and adipose tissue, serving as a source of glycerol for triacylglycerol synthesis

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20
Q

Triglyceride Synthesis in Liver and Adipose Tissue

A

Involves the reaction of glycerol 3-P with fatty acyl-CoA to form phosphatidic acid, followed by dephosphorylation to DAG, and then formation of triacylglycerol

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21
Q

VLDL (Very Low-Density Lipoprotein)

A

Lipoprotein particle formed in the liver from triacylglycerol, cholesterol, phospholipids, and proteins, primarily apoB-100, which is necessary for lipid transport

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22
Q

Microsomal Triglyceride Transfer Protein (MTP)

A

A protein required for the assembly of both VLDL in the liver and chylomicrons in the intestine, crucial for lipid transport

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23
Q

Apolipoprotein B-100 (ApoB-100)

A

The major protein component of VLDL, encoded by the same gene as apoB-48, with a longer sequence that enables lipid transport in the blood

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24
Q

Apolipoprotein B-48 (ApoB-48)

A

A truncated version of apoB-100, resulting from RNA editing in intestinal cells, involved in the formation of chylomicrons for dietary lipid transport

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25
Q

Abetalipoproteinemia

A

A genetic disorder caused by the lack of MTP activity, leading to the inability to assemble chylomicrons and VLDL particles, affecting lipid absorption and transport

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26
Q

Lipoprotein Lipase (LPL)

A

An enzyme synthesized by adipose tissue, secreted into capillaries, and responsible for digesting triacylglycerols from chylomicrons and VLDL, releasing fatty acids

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27
Q

Insulin’s Role in Adipose Tissue

A

Stimulates LPL synthesis, glucose metabolism, glycolysis, and conversion of glucose to fatty acids, leading to increased triacylglycerol storage in adipose cells

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28
Q

Phosphofructokinase-1 (PFK-1)

A

A glycolytic enzyme activated by insulin through increased fructose 2,6-bisphosphate levels, promoting the conversion of glucose to pyruvate

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29
Q

Pyruvate Dehydrogenase (PDH)

A

An enzyme dephosphorylated and activated by insulin, allowing pyruvate from glycolysis to enter the TCA cycle for further oxidation in adipose cells

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30
Q

VLDL (Very-Low-Density Lipoprotein)

A

A type of lipoprotein made by the liver that transports endogenous triglycerides, cholesterol, and apolipoproteins in the bloodstream

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31
Q

VLDL Assembly

A

Occurs in the liver from triglycerides, cholesterol, and apolipoproteins, then processed in the Golgi complex before being secreted into the blood

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32
Q

VLDL Conversion

A

In the bloodstream, VLDL is converted into intermediate-density lipoprotein (IDL) and low-density lipoprotein (LDL)

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33
Q

VLDL vs Chylomicrons

A

VLDL particles are more dense than chylomicrons because they contain a lower percentage of triglycerides and more protein

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34
Q

Apolipoprotein CII

A

An apolipoprotein acquired by VLDL from HDL in the bloodstream, which activates lipoprotein lipase (LPL) to cleave triglycerides in VLDL

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35
Q

Lipoprotein Lipase (LPL)

A

An enzyme attached to capillary endothelial cells that cleaves triglycerides in VLDL and chylomicrons, producing fatty acids and glycerol

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36
Q

LPL Isozyme in Muscle

A

Has a low Km, allowing muscle to use fatty acids from VLDL and chylomicrons as a fuel source even at low blood concentrations of these lipoproteins

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37
Q

LPL Isozyme in Adipose Tissue

A

Has a high Km, making it most active after meals when blood levels of chylomicrons and VLDL are elevated, facilitating fat storage

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38
Q

IDL (Intermediate-Density Lipoprotein)

A

A lipoprotein particle generated after VLDL has been processed by LPL; can further lose triglycerides to become LDL

39
Q

LDL (Low-Density Lipoprotein)

A

A lipoprotein formed from IDL that is rich in cholesterol and transports it to cells in the body

40
Q

Chylomicrons

A

Lipoproteins synthesized in the small intestine that transport exogenous (dietary) lipids, containing more triglycerides and less protein than VLDL

41
Q

VLDL and HDL Interaction

A

VLDL particles acquire apolipoproteins CII and E from HDL to become mature VLDL particles in the bloodstream

42
Q

Apolipoprotein B48 vs B100

A

Chylomicrons contain apolipoprotein B48, while VLDL contains apolipoprotein B100, reflecting their different origins and roles in lipid transport

43
Q

Nascent VLDL Particles

A

Newly synthesized VLDL particles that are not fully mature; they acquire additional apolipoproteins (CII and E) from HDL to become fully functional

44
Q

Role of VLDL in Lipid Transport

A

VLDL primarily transports endogenous lipids (lipids synthesized by the body) from the liver to peripheral tissues

45
Q

Triglyceride Content in VLDL

A

VLDL particles contain a lower amount of triglycerides compared to chylomicrons, making them denser and richer in protein content

46
Q

Golgi Complex and VLDL

A

The Golgi complex processes VLDL before it is secreted into the bloodstream, ensuring proper assembly and functionality of the lipoprotein particles

47
Q

Fatty Acid Storage in Adipose Tissue

A

Fatty acids derived from VLDL are stored in adipose tissue as triglycerides after being released by LPL and taken up by adipose cells

48
Q

Endogenous vs Exogenous Lipid Transport

A

VLDL is responsible for transporting endogenous lipids synthesized by the liver, while chylomicrons transport exogenous lipids absorbed from the diet

49
Q

Apolipoprotein E

A

A component of VLDL obtained from HDL, important for the recognition and uptake of VLDL remnants (such as IDL) by the liver

50
Q

Chylomicron Remnants

A

The remnants left after chylomicrons have delivered dietary triglycerides to tissues; these are taken up by the liver for further processing

51
Q

Apolipoprotein B100

A

The main protein of VLDL, required for its synthesis and stability, and also involved in the interaction with LDL receptors in peripheral tissues

52
Q

VLDL Secretion by Liver

A

The liver secretes VLDL into the bloodstream after assembly, where it plays a critical role in distributing lipids throughout the body

53
Q

HDL (High-Density Lipoprotein)

A

A lipoprotein that transfers apolipoproteins to VLDL and chylomicrons, helping them to mature and function properly in lipid transport

54
Q

Cholesterol in VLDL

A

VLDL particles also carry cholesterol along with triglycerides, contributing to the distribution of cholesterol to tissues and eventually forming LDL

55
Q

What are the two categories of amino acids

A

Amino acids are categorized into essential and non-essential Essential amino acids must be obtained from the diet, while non-essential amino acids can be synthesized by the body

56
Q

What is the role of transaminases in amino acid metabolism

A

Transaminases transfer the amino group from an amino acid to a keto acid, facilitating the production of new amino acids and the metabolism of nitrogen

57
Q

What is the significance of pyridoxine (vitamin B6) in transamination reactions

A

Pyridoxine acts as a cofactor for transaminases, enabling the transfer of amino groups during transamination reactions

58
Q

What happens to ammonia in the liver

A

Ammonia is converted into urea in the liver through the urea cycle, which is then excreted in the urine to prevent toxicity

59
Q

What is the Cori cycle

A

The Cori cycle involves the conversion of lactate produced in muscles back to glucose in the liver, which can then be reused for energy

60
Q

What is the role of glutamate in amino acid metabolism

A

Glutamate can undergo oxidative deamination, releasing ammonia and converting to alpha-ketoglutarate, a key intermediate in the TCA cycle

61
Q

What are glucogenic amino acids

A

Glucogenic amino acids are those that can be converted into glucose through gluconeogenesis

62
Q

What are ketogenic amino acids

A

Ketogenic amino acids are those that can be converted into ketone bodies, which serve as an alternative energy source

63
Q

What is hyperammonemia, and what are its effects

A

Hyperammonemia is an elevated level of ammonia in the blood, leading to neurological symptoms such as cerebral edema, asterixis, and coma

64
Q

What is the most common urea cycle disorder

A

The most common urea cycle disorder is ornithine transcarbamylase (OTC) deficiency, which leads to hyperammonemia and elevated orotic acid levels

65
Q

What are the key symptoms of phenylketonuria (PKU)

A

Symptoms of PKU include intellectual disability, light skin and hair, a musty odor, and eczema It is caused by a deficiency in phenylalanine hydroxylase

66
Q

What is the treatment for phenylketonuria

A

Treatment includes a low-phenylalanine diet and supplementation with tyrosine In cases of malignant PKU, tetrahydrobiopterin supplements may be required

67
Q

What enzyme deficiency leads to maple syrup urine disease

A

Maple syrup urine disease is caused by a deficiency in the branched-chain alpha-keto acid dehydrogenase complex (BCKD)

68
Q

What are the symptoms of maple syrup urine disease

A

Symptoms include sweet-smelling urine, irritability, poor feeding, vomiting, lethargy, and in severe cases, cerebral edema and seizures

69
Q

What is alkaptonuria, and what are its key symptoms

A

Alkaptonuria is caused by a deficiency in homogentisate oxidase, leading to dark urine, ochronosis (bluish-black pigmentation), and joint pain

70
Q

What causes homocystinuria, and what are its symptoms

A

Homocystinuria is often caused by a deficiency in cystathionine beta-synthase, leading to marfanoid habitus, ectopia lentis, and increased risk of thrombosis

71
Q

What is the difference between homocystinuria and Marfan syndrome

A

Homocystinuria causes downward lens dislocation and is associated with atherosclerosis, while Marfan syndrome causes upward lens dislocation and affects the aorta

72
Q

What is the primary diagnostic test for cystinuria

A

The sodium cyanide nitroprusside test detects cystine in the urine, helping to diagnose cystinuria, which causes cystine kidney stones

73
Q

What is the treatment for cystinuria

A

Treatment includes alkalinization of urine with potassium citrate or acetazolamide and, if necessary, chelation therapy with penicillamine

74
Q

What is propionic acidemia, and what causes it

A

Propionic acidemia is caused by a deficiency in propionyl-CoA carboxylase, leading to the accumulation of propionic acid and metabolic acidosis

75
Q

What is methylmalonic acidemia, and how is it diagnosed

A

Methylmalonic acidemia is caused by a deficiency in methylmalonyl-CoA mutase or vitamin B12 It is diagnosed by elevated methylmalonic acid levels

76
Q

What are the symptoms of organic acidemia

A

Symptoms include vomiting, poor feeding, hypotonia, seizures, hepatomegaly, and metabolic acidosis

77
Q

What is the role of lactulose in treating hyperammonemia

A

Lactulose acidifies the gut, converting ammonia to ammonium, which is then excreted, lowering blood ammonia levels

78
Q

What are the metabolic consequences of a urea cycle defect

A

Urea cycle defects lead to hyperammonemia, which can cause neurological damage, seizures, and coma if untreated

79
Q

What is the role of benzoate in the management of hyperammonemia

A

Benzoate binds with glycine to form hippurate, which is excreted in urine, helping to reduce ammonia levels in hyperammonemia

80
Q

What is the clinical significance of a musty” odor in urine

A

A musty odor in urine is a characteristic sign of phenylketonuria (PKU), caused by the accumulation of phenylketones

81
Q

What is the treatment approach for maple syrup urine disease

A

Treatment involves dietary restriction of branched-chain amino acids (valine, leucine, isoleucine) and thiamine supplementation

82
Q

What causes ornithine transcarbamylase deficiency

A

Ornithine transcarbamylase deficiency is an X-linked recessive disorder caused by mutations in the OTC gene, leading to hyperammonemia

83
Q

What are the primary features of alkaptonuria

A

Features include dark urine, ochronosis, and arthralgias, resulting from a buildup of homogentisic acid due to a deficiency in homogentisate oxidase

84
Q

What is the role of the urea cycle in the body

A

The urea cycle converts toxic ammonia into urea, which is then excreted in the urine, preventing ammonia accumulation and toxicity

85
Q

What is asterixis, and what condition is it associated with

A

Asterixis is a flapping tremor of the hands when the wrists are extended, commonly associated with hyperammonemia and hepatic encephalopathy

86
Q

What dietary management is recommended for individuals with propionic acidemia

A

A low-protein diet is recommended, avoiding substances that metabolize into propionyl-CoA, such as isoleucine, valine, methionine, and threonine

87
Q

What is the impact of homocystinuria on the cardiovascular system

A

Homocystinuria increases the risk of atherosclerosis and thrombosis, potentially leading to stroke, myocardial infarction, or thromboembolism

88
Q

What are the key symptoms of methylmalonic acidemia

A

Symptoms include vomiting, lethargy, hypotonia, metabolic acidosis, and developmental delay, typically presenting in infancy

89
Q

What enzyme is deficient in phenylketonuria (PKU)

A

Phenylketonuria is caused by a deficiency in phenylalanine hydroxylase, preventing the conversion of phenylalanine to tyrosine

90
Q

What is the function of cystathionine beta-synthase

A

Cystathionine beta-synthase catalyzes the conversion of homocysteine to cystathionine, a key step in methionine metabolism

91
Q

What is the cause of orotic aciduria, and how does it differ from OTC deficiency

A

Orotic aciduria is caused by a deficiency in uridine monophosphate synthase (UMPS) and is distinguished from OTC deficiency by the absence of hyperammonemia

92
Q

What are the treatment options for homocystinuria

A

Treatment includes dietary modification, increasing intake of B6, B12, folate, and cysteine, depending on the specific enzyme deficiency

93
Q

What is the importance of thiamine in amino acid metabolism

A

Thiamine (vitamin B1) is a cofactor for the branched-chain alpha-keto acid dehydrogenase complex, essential for the metabolism of branched-chain amino acids

94
Q

What condition is characterized by a sweet-smelling” urine

A

Maple syrup urine disease is characterized by sweet-smelling urine due to the accumulation of branched-chain amino acids and their keto acids

Noorda FOM (18 decks)

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