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Noorda FOM > Module 5 ChatGPT > Flashcards

Module 5 ChatGPT Flashcards

1
Q

Insulin

A

The major anabolic hormone in the body that promotes the storage of fuels and the use of fuels for growth

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2
Q

Glucagon

A

The major hormone responsible for fuel mobilization, particularly during fasting or energy-demanding situations

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3
Q

Epinephrine

A

A hormone released in response to stress, hypoglycemia, or exercise, increasing the availability of fuels for immediate use

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4
Q

Hormones

A

Intravascular carriers of messages between their sites of synthesis and target tissues, crucial for metabolic regulation

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5
Q

Fuel Homeostasis

A

The balance between fuel storage and fuel mobilization, regulated by hormones such as insulin and glucagon, in response to daily eating patterns

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6
Q

Glucose and Metabolic Homeostasis

A

Glucose is critical for tissues like the brain, red blood cells, and muscle, which require continuous glucose supply to meet their energy needs

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7
Q

Daily Glucose Requirement

A

An adult requires at least 190 g of glucose per day, with approximately 150 g needed for the brain and 40 g for other tissues

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8
Q

Hypoglycemia

A

A condition where blood glucose drops below 60 mg/dL, limiting glucose metabolism in the brain and potentially leading to neurological symptoms

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9
Q

Fuel efflux during exercise is

A

The continuous release of fuels from storage during exercise is essential to meet the high demand for ATP

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10
Q

Hyperosmolar Effect

A

A potential metabolic derangement where high levels of circulating glucose and amino acids cause severe neurological deficits and other complications

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11
Q

Renal Tubular Threshold

A

The maximum concentration of glucose and amino acids that can be reabsorbed by the kidneys, beyond which they are excreted in urine

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12
Q

Nonenzymatic Glycosylation

A

The process by which elevated blood glucose levels cause glucose to bind to proteins nonenzymatically, altering their function and potentially damaging tissues

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13
Q

Fatty Acids and Metabolism

A

The concentration of fatty acids in the blood determines whether skeletal muscles use fatty acids or glucose as a primary fuel source

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14
Q

Ketone Body Formation

A

Ketone bodies are synthesized in the liver’s mitochondrial matrix from acetyl-CoA, which is generated from fatty acid oxidation when acetyl-CoA levels are high

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15
Q

Acetoacetate

A

A ketone body that can enter the blood directly or be reduced to beta-hydroxybutyrate. It can also spontaneously decarboxylate into acetone, which is exhaled by the lungs

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16
Q

beta-Hydroxybutyrate

A

A ketone body formed by the reduction of acetoacetate, with a blood ratio of approximately 3:1 compared to acetoacetate, determined by the mitochondrial NADH/NAD+ ratio

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17
Q

Acetone

A

A volatile compound formed by the spontaneous decarboxylation of acetoacetate, giving the breath of individuals in ketosis a fruity smell

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18
Q

Utilization of Ketone Bodies

A

Ketone bodies (acetoacetate and beta-hydroxybutyrate) are oxidized as fuels in tissues like skeletal muscle, brain, kidneys, and intestinal mucosa, but not in the liver

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19
Q

beta-Hydroxybutyrate Dehydrogenase

A

An enzyme that interconverts beta-hydroxybutyrate and acetoacetate, producing NADH in the process, with the reaction direction influenced by the mitochondrial NADH/NAD+ ratio

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20
Q

Acetoacetate Oxidation

A

Once transported into cells, acetoacetate is converted to acetyl-CoA, which enters the TCA cycle to produce energy

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21
Q

Lack of Ketone Body Utilization in Liver

A

The liver cannot utilize ketone bodies because it lacks the enzyme beta-ketoacyl-CoA transferase, which is necessary for their oxidation

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22
Q

Tissue Utilization of Ketone Bodies

A

Ketone bodies are utilized as a fuel source by the heart, brain, and muscles, but not by red blood cells (which lack mitochondria) or the liver

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23
Q

NADH/NAD+ Ratio

A

The ratio in the mitochondrial matrix that determines the equilibrium between beta-hydroxybutyrate and acetoacetate

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24
Q

Ketosis and Breath Odor

A

The fruity odor in the breath of individuals in ketosis is due to the volatile acetone, a byproduct of acetoacetate decarboxylation

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25
Q

Fuel Metabolism

A

The process by which macronutrients (carbohydrates, fats, proteins) from the diet are digested, absorbed, and oxidized to produce energy

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26
Q

Fuel Stores

A

Excess dietary fuel is stored as triacylglycerol (fat) in adipose tissue, glycogen in muscles and liver, and protein in muscles, which are used during fasting periods

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27
Q

Respiration

A

The oxidation of fuels to generate ATP, involving pathways like glycolysis, TCA cycle, and oxidative phosphorylation

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28
Q

ATPADP Cycle

A

The continuous conversion of ATP to ADP and inorganic phosphate (Pi) during energy-consuming processes, and the regeneration of ATP from ADP

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29
Q

Macronutrients

A

Carbohydrates, proteins, and fats from the diet that serve as the primary sources of energy for the body

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30
Q

TCA Cycle

A

A series of reactions in the mitochondrial matrix that oxidizes acetyl-CoA to CO2 and produces electrons for the electron transport chain, generating ATP

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31
Q

Glycolysis

A

The metabolic pathway that converts glucose to pyruvate, generating a small amount of ATP and NADH, and providing intermediates for other pathways

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32
Q

Oxidative Phosphorylation

A

The process by which ATP is generated from ADP and Pi in the mitochondria, driven by the transfer of electrons through the electron transport chain to oxygen

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33
Q

Fat Oxidation

A

The complete oxidation of triacylglycerols to CO2 and H2O, which releases approximately 9 kcal/g, making fats a dense energy source

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34
Q

Protein Oxidation

A

The oxidation of amino acids from proteins to CO2, H2O, and NH4+, yielding approximately 4 kcal/g of energy

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35
Q

Dietary Recommendations for Fats

A

Fats should account for 20%-35% of total calories, with saturated fatty acids being <10% and emphasis on unsaturated fats from fish, nuts, and vegetables

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36
Q

Alcohol Metabolism

A

Ethanol is oxidized to CO2 and H2O, yielding about 7 kcal/g, and should be consumed in moderation, with specific guidelines for men and women

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37
Q

Protein Intake

A

Adults should consume approximately 0 8 g/kg of body weight per day of high-quality protein, with attention to essential amino acids, particularly for vegans

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38
Q

Waste Disposal

A

Xenobiotic compounds and metabolic waste products from diet and air are excreted in urine and feces, maintaining metabolic balance and preventing toxicity

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39
Q

Energy Balance

A

Maintaining a balance between energy intake and expenditure is crucial for achieving and maintaining a healthy body weight and overall fitness

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40
Q

How does glucose enter the cells

A

Glucose enters cells via two main transport systems: Sodium- and ATP-independent (GLUT transporters) and Sodium- and ATP-dependent co-transport systems

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41
Q

What is the primary function of GLUT4 transporters

A

GLUT4 transporters facilitate glucose uptake in skeletal muscle, cardiac muscle, and adipocytes, and their expression is regulated by insulin

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42
Q

What are the main substrates and products of glycolysis

A

Glycolysis uses glucose as a substrate and produces pyruvate, ATP, and NADH

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43
Q

What is the net ATP gain from glycolysis

A

The net ATP gain from glycolysis is 2 ATP molecules per glucose molecule

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44
Q

What are the key enzymes of glycolysis, and why are they important

A

Key enzymes include hexokinase, phosphofructokinase, and pyruvate kinase They regulate glycolysis, controlling the flow of glucose through the pathway

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45
Q

What are the fates of pyruvate under aerobic and anaerobic conditions

A

Aerobically, pyruvate enters the TCA cycle to produce ATP Anaerobically, it is converted into lactate in humans or ethanol in yeast

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46
Q

What is the role of pyruvate dehydrogenase (PDH)

A

PDH converts pyruvate into acetyl-CoA in the mitochondria, linking glycolysis to the TCA cycle

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47
Q

What causes lactic acidosis, and what are its consequences

A

Lactic acidosis is caused by hypoxia, vigorous exercise, or mitochondrial dysfunction, leading to an accumulation of lactic acid, decreased blood pH, and potential metabolic complications

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48
Q

How is 2,3-Bisphosphoglycerate (2,3-BPG) produced, and what is its role in erythrocytes

A

2,3-BPG is produced via the Luebering-Rapoport shunt in glycolysis and reduces hemoglobin’s affinity for oxygen, facilitating oxygen release to tissues

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49
Q

What is the relationship between erythrocyte structure, metabolism, and oxygen delivery

A

Erythrocytes, which lack organelles and are biconcave in shape, rely on glycolysis for ATP and use hemoglobin to deliver oxygen to tissues

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50
Q

What is the function of GLUT1 transporters

A

GLUT1 is responsible for high-affinity glucose transport in RBCs and the blood-brain barrier

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51
Q

What are the products of glycolysis

A

The end products of glycolysis are 2 pyruvate, 2 ATP, and 2 NADH per glucose molecule

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52
Q

How does insulin affect glucose uptake

A

Insulin increases glucose uptake by stimulating the translocation of GLUT4 to the cell membrane

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53
Q

How does pyruvate enter the mitochondria

A

Pyruvate enters the mitochondria via the pyruvate translocase protein

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54
Q

What is the function of hexokinase in glycolysis

A

Hexokinase phosphorylates glucose to form glucose-6-phosphate, trapping it inside the cell

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55
Q

What regulates phosphofructokinase-1 (PFK-1)

A

PFK-1 is allosterically activated by AMP and fructose-2,6-bisphosphate, and inhibited by ATP and citrate

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56
Q

What happens to pyruvate in the absence of oxygen

A

In the absence of oxygen, pyruvate is converted into lactate in humans or ethanol in yeast

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57
Q

What are the cofactors required by pyruvate dehydrogenase

A

Pyruvate dehydrogenase requires thiamine pyrophosphate, lipoamide, CoA, FAD, and NAD+ as cofactors

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58
Q

What is the role of lactate dehydrogenase

A

Lactate dehydrogenase converts pyruvate to lactate under anaerobic conditions

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59
Q

What are the two main shunts in erythrocyte glycolysis

A

The two main shunts are the pentose phosphate pathway (HMP shunt) and the Luebering-Rapoport shunt

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60
Q

What is the effect of 2,3-BPG on hemoglobin

A

2,3-BPG decreases hemoglobin’s affinity for oxygen, facilitating oxygen release to tissues

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61
Q

What are the consequences of pyruvate dehydrogenase deficiency

A

PDH deficiency leads to lactic acidosis, neurological deficits, and various metabolic disorders

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62
Q

How is 2,3-BPG regulated in erythrocytes

A

2,3-BPG levels increase in response to chronic hypoxia and anemia to enhance oxygen delivery

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63
Q

What role does thiamine play in metabolism

A

Thiamine is a cofactor for pyruvate dehydrogenase and is essential for glucose metabolism

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64
Q

What is the Cori cycle

A

The Cori cycle involves the conversion of lactate from muscles into glucose in the liver

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65
Q

How does arsenic poisoning affect pyruvate dehydrogenase

A

Arsenic binds to lipoamide in PDH, inhibiting its activity and causing lactic acidosis

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66
Q

What is the function of GLUT2 in the liver

A

GLUT2 facilitates the uptake and release of glucose in the liver, playing a key role in glucose homeostasis

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67
Q

What enzyme deficiency can lead to methemoglobinemia

A

Deficiency in cytochrome b5 reductase can lead to methemoglobinemia

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68
Q

How does the pentose phosphate pathway relate to erythrocytes

A

The pentose phosphate pathway provides NADPH for maintaining reduced glutathione in erythrocytes

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69
Q

What is the primary source of lactate at rest

A

The primary sources of lactate at rest are red blood cells, brain, and skin

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70
Q

What is the role of pyruvate kinase in glycolysis

A

Pyruvate kinase catalyzes the final step in glycolysis, converting phosphoenolpyruvate to pyruvate and generating ATP

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71
Q

How does hypoxia affect lactic acid production

A

Hypoxia increases lactic acid production as cells rely more on anaerobic metabolism

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72
Q

What is hereditary spherocytosis

A

Hereditary spherocytosis is a condition where mutations in spectrin lead to abnormally shaped erythrocytes

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73
Q

How does insulin affect pyruvate dehydrogenase

A

Insulin activates pyruvate dehydrogenase by promoting its dephosphorylation

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74
Q

What is the effect of chronic anemia on 2,3-BPG levels

A

Chronic anemia increases 2,3-BPG levels to enhance oxygen unloading from hemoglobin

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75
Q

What is the significance of the Luebering-Rapoport shunt

A

The Luebering-Rapoport shunt allows for the production of 2,3-BPG in erythrocytes, affecting oxygen delivery

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76
Q

What are the symptoms of lactic acidosis

A

Symptoms include headaches, abdominal pain, nausea, rapid breathing, and fatigue

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77
Q

How is glucose transported in the brain

A

Glucose is transported in the brain primarily by GLUT1 and GLUT3 transporters

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78
Q

What are the metabolic products of anaerobic glycolysis

A

The primary product is lactate, which can lead to lactic acidosis if accumulated

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79
Q

What is the role of glucokinase in the liver

A

Glucokinase phosphorylates glucose, allowing it to enter glycolysis or glycogenesis in the liver

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80
Q

What is pyruvate carboxylase and where is it located

A

Pyruvate carboxylase is a mitochondrial enzyme that converts pyruvate to oxaloacetate, linking glycolysis to gluconeogenesis

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81
Q

What are the effects of metformin on lactic acidosis

A

Metformin can inhibit mitochondrial respiration, potentially leading to lactic acidosis in rare cases

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82
Q

How is 2,3-BPG involved in adaptation to high altitude

A

2,3-BPG levels increase at high altitude, enhancing oxygen delivery to tissues despite lower oxygen availability

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83
Q

What are the effects of a pyruvate kinase deficiency

A

Pyruvate kinase deficiency leads to hemolytic anemia due to impaired ATP production in erythrocytes

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84
Q

What is the function of NADPH in erythrocytes

A

NADPH helps maintain reduced glutathione levels, protecting erythrocytes from oxidative damage

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85
Q

What happens during the oxidative phase of the pentose phosphate pathway

A

NADPH is generated, which is crucial for antioxidant defense in erythrocytes

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86
Q

What is the role of phosphoglycerate kinase in glycolysis

A

Phosphoglycerate kinase catalyzes the transfer of a phosphate group from 1,3-bisphosphoglycerate to ADP, producing ATP

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87
Q

What are the products of the TCA cycle per pyruvate molecule

A

The TCA cycle produces 3 NADH, 1 FADH2, 1 GTP (or ATP), and 2 CO2 per pyruvate

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88
Q

What is the role of lactate in gluconeogenesis

A

Lactate can be converted back to glucose in the liver via the Cori cycle

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89
Q

What enzyme catalyzes the conversion of pyruvate to acetyl-CoA

A

Pyruvate dehydrogenase catalyzes this conversion, linking glycolysis to the TCA cycle

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90
Q

What is the main cause of hereditary spherocytosis

A

Mutations in the spectrin protein lead to a loss of erythrocyte membrane integrity

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91
Q

What is the significance of fructose-2,6-bisphosphate in glycolysis

A

Fructose-2,6-bisphosphate is a potent activator of phosphofructokinase-1 (PFK-1), enhancing glycolysis

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92
Q

How does thiamine deficiency affect metabolism

A

Thiamine

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93
Q

What are the primary sources of acetyl-CoA for the TCA cycle

A

Primary sources of acetyl-CoA include pyruvate from glycolysis, fatty acid oxidation, and amino acid catabolism

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94
Q

What is the main function of the TCA cycle

A

The TCA cycle generates high-energy electron carriers (NADH, FADH2) and GTP/ATP, which are used for energy production in the ETC

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95
Q

Where are TCA cycle enzymes located

A

TCA cycle enzymes are located in the mitochondrial matrix

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96
Q

What is the significance of mitochondrial compartmentalization for TCA cycle enzymes

A

Compartmentalization ensures that enzymes and substrates are localized for efficient energy production and metabolic regulation

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97
Q

What is the role of citrate synthase in the TCA cycle

A

Citrate synthase catalyzes the first step of the TCA cycle, converting acetyl-CoA and oxaloacetate to citrate

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98
Q

Which enzyme catalyzes the conversion of isocitrate to alpha-ketoglutarate

A

Isocitrate dehydrogenase catalyzes the conversion of isocitrate to alpha-ketoglutarate, producing NADH and CO2

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99
Q

What are the products of the TCA cycle per acetyl-CoA molecule

A

Each acetyl-CoA produces 3 NADH, 1 FADH2, 1 GTP (or ATP), and 2 CO2

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100
Q

What is the role of succinate dehydrogenase in both the TCA cycle and ETC

A

Succinate dehydrogenase converts succinate to fumarate in the TCA cycle and also functions as Complex II in the ETC

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101
Q

How does NADH contribute to ATP production

A

NADH donates electrons to Complex I of the ETC, driving proton pumping and ATP synthesis via oxidative phosphorylation

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102
Q

What is the function of the electron transport chain (ETC)

A

The ETC transfers electrons from NADH and FADH2 to oxygen, generating a proton gradient used to synthesize ATP

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103
Q

What is the role of Complex IV in the ETC

A

Complex IV transfers electrons to oxygen, the final electron acceptor, forming water

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104
Q

What is the proton gradient, and how is it established

A

The proton gradient is established by the ETC pumping protons across the inner mitochondrial membrane, creating an electrochemical gradient

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Perfectly
105
Q

What is the significance of the proton motive force

A

The proton motive force drives ATP synthesis by allowing protons to flow back into the mitochondrial matrix through ATP synthase

106
Q

What is oxidative phosphorylation

A

Oxidative phosphorylation is the process by which ATP is produced using the energy from electrons transferred through the ETC

107
Q

What are the consequences of ETC uncoupling

A

ETC uncoupling dissipates the proton gradient as heat, reducing ATP production and increasing thermogenesis

108
Q

What is the effect of cyanide on the ETC

A

Cyanide inhibits Complex IV, preventing electron transfer to oxygen, halting ATP production, and leading to cellular asphyxiation

109
Q

What are common inhibitors of Complex I in the ETC

A

Common inhibitors of Complex I include rotenone and barbiturates

110
Q

What is the role of ATP synthase in oxidative phosphorylation

A

ATP synthase uses the proton gradient to convert ADP and inorganic phosphate into ATP

111
Q

What happens to oxygen consumption when the ETC is inhibited

A

Oxygen consumption decreases because electron transfer to oxygen is blocked, halting ATP production

112
Q

How does the TCA cycle interact with the ETC

A

The TCA cycle generates NADH and FADH2, which donate electrons to the ETC for ATP production

113
Q

What is the role of coenzyme Q in the ETC

A

Coenzyme Q (ubiquinone) transfers electrons from Complex I and II to Complex III in the ETC

114
Q

How does Complex III contribute to the proton gradient

A

Complex III pumps protons into the intermembrane space while transferring electrons to cytochrome c

115
Q

What is the role of cytochrome c in the ETC

A

Cytochrome c transfers electrons from Complex III to Complex IV in the ETC

116
Q

What are the main components of the electron transport chain

A

The main components are Complex I, II, III, IV, coenzyme Q, and cytochrome c

117
Q

What is the effect of dinitrophenol (DNP) on the ETC

A

DNP uncouples the ETC by allowing protons to cross the mitochondrial membrane without ATP synthesis, generating heat instead

118
Q

What are the clinical signs of a deficiency in Complex I of the ETC

A

Signs include muscle weakness, neurodegeneration, and lactic acidosis due to impaired ATP production

119
Q

What is MELAS syndrome, and which part of the ETC is affected

A

MELAS syndrome affects Complex I and leads to mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes

120
Q

What is the consequence of fumarase deficiency in the TCA cycle

A

Fumarase deficiency leads to developmental delay, hypotonia, and severe metabolic acidosis

121
Q

What is Leigh syndrome, and how is it related to the ETC

A

Leigh syndrome is a neurodegenerative disorder often caused by mutations in ETC complexes, particularly Complex I and IV

122
Q

What is the role of biotin in the TCA cycle

A

Biotin is a cofactor for pyruvate carboxylase, which converts pyruvate to oxaloacetate, a TCA cycle intermediate

123
Q

What is the impact of arsenic poisoning on the TCA cycle

A

Arsenic inhibits alpha-ketoglutarate dehydrogenase, leading to energy depletion and accumulation of toxic intermediates

124
Q

What are the effects of succinate dehydrogenase deficiency

A

Deficiency can lead to muscle weakness, neurological defects, and an increased risk of tumors due to impaired TCA cycle and ETC function

125
Q

What is the role of alpha-ketoglutarate dehydrogenase in the TCA cycle

A

Alpha-ketoglutarate dehydrogenase catalyzes the conversion of alpha-ketoglutarate to succinyl-CoA, producing NADH

126
Q

What are the consequences of pyruvate dehydrogenase deficiency

A

Deficiency leads to lactic acidosis, neurodegeneration, and poor energy production due to impaired entry of pyruvate into the TCA cycle

127
Q

What is the function of Complex II in the ETC

A

Complex II (succinate dehydrogenase) transfers electrons from FADH2 to coenzyme Q, linking the TCA cycle to the ETC

128
Q

What is the role of NADH dehydrogenase in the ETC

A

NADH dehydrogenase (Complex I) transfers electrons from NADH to coenzyme Q, initiating the ETC

129
Q

What are the products of one cycle of the TCA cycle

A

One cycle produces 3 NADH, 1 FADH2, 1 GTP (or ATP), and 2 CO2 molecules

130
Q

What is the role of oxaloacetate in the TCA cycle

A

Oxaloacetate combines with acetyl-CoA to form citrate, initiating the TCA cycle

131
Q

What is the impact of a succinyl-CoA synthetase deficiency

A

Deficiency can cause encephalomyopathy, developmental delay, and lactic acidosis

132
Q

What is the effect of rotenone on cellular respiration

A

Rotenone inhibits Complex I of the ETC, reducing ATP production and leading to oxidative stress

133
Q

What is the impact of vitamin B1 (thiamine) deficiency on the TCA cycle

A

Thiamine deficiency impairs pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, leading to lactic acidosis and energy deficits

134
Q

What is the significance of cytochrome c oxidase (Complex IV) in the ETC

A

Complex IV catalyzes the final transfer of electrons to oxygen, a critical step for ATP production

135
Q

What is the role of Complex III in the ETC

A

Complex III transfers electrons from coenzyme Q to cytochrome c, while pumping protons to contribute to the proton gradient

136
Q

What are the consequences of fumarase deficiency

A

Fumarase deficiency can cause severe neurological deficits, developmental delay, and metabolic acidosis

137
Q

What is the impact of malonate on the TCA cycle

A

Malonate inhibits succinate dehydrogenase, reducing ATP production and leading to metabolic disturbances

138
Q

What are the effects of uncoupling proteins on the ETC

A

Uncoupling proteins dissipate the proton gradient as heat, reducing ATP production and increasing thermogenesis

139
Q

What is the role of Complex I in the ETC

A

Complex I transfers electrons from NADH to coenzyme Q, initiating the proton gradient essential for ATP synthesis

140
Q

What is the normal fasting blood glucose range in a healthy person

A

The normal fasting blood glucose range is approximately 80 to 100 mg/dL

141
Q

What happens to blood glucose levels after a meal in a healthy individual

A

Blood glucose levels rise to approximately 120 to 140 mg/dL but do not exceed 140 mg/dL

142
Q

What is glycogenolysis and when is it activated

A

Glycogenolysis is the breakdown of glycogen to glucose, activated during fasting to maintain blood glucose levels

143
Q

What is the primary source of blood glucose during the first few hours of fasting

A

Liver glycogen is the primary source of blood glucose during the first few hours of fasting

144
Q

Which metabolic process becomes more important during prolonged fasting

A

Gluconeogenesis becomes more important during prolonged fasting

145
Q

What are the major substrates for gluconeogenesis

A

The major substrates for gluconeogenesis are glycerol, lactate, and amino acids

146
Q

How is gluconeogenesis regulated during stress or prolonged exercise

A

Gluconeogenesis is stimulated by the availability of substrates and the activity of key enzymes, regulated by hormones like glucagon, cortisol, and epinephrine

147
Q

What is the role of pyruvate carboxylase in gluconeogenesis

A

Pyruvate carboxylase converts pyruvate to oxaloacetate, a key step in gluconeogenesis

148
Q

What activates pyruvate carboxylase during fasting

A

Acetyl-CoA activates pyruvate carboxylase during fasting

149
Q

What happens to pyruvate dehydrogenase during fasting

A

Pyruvate dehydrogenase is inactivated during fasting, preventing pyruvate from being converted to acetyl-CoA

150
Q

What is the role of PEPCK in gluconeogenesis

A

Phosphoenolpyruvate carboxykinase (PEPCK) converts oxaloacetate to phosphoenolpyruvate, a key step in gluconeogenesis

151
Q

What is the effect of glucagon on PEPCK

A

Glucagon induces the expression of PEPCK, promoting gluconeogenesis

152
Q

What is the function of glucose 6-phosphatase in gluconeogenesis

A

Glucose 6-phosphatase converts glucose 6-phosphate to glucose, allowing glucose to be released into the blood

153
Q

Which hormone decreases the transcription of PEPCK

A

Insulin decreases the transcription of PEPCK, reducing gluconeogenesis

154
Q

What is the role of glucokinase in glucose metabolism

A

Glucokinase phosphorylates glucose, trapping it in the cell for glycolysis or glycogen synthesis

155
Q

What is the primary effect of insulin on blood glucose levels

A

Insulin lowers blood glucose levels by promoting glucose uptake and storage

156
Q

What metabolic process is activated when blood glucose levels fall below the normal range

A

Gluconeogenesis and glycogenolysis are activated to raise blood glucose levels

157
Q

What are the consequences of hyperglycemia if not regulated

A

Severe hyperglycemia can lead to dehydration of tissues, hyperosmolar coma, and organ dysfunction

158
Q

What are the consequences of hypoglycemia if not regulated

A

Severe hypoglycemia can lead to brain dysfunction, coma, hemolysis, and potentially death

159
Q

Which enzyme converts pyruvate to acetyl-CoA under normal conditions

A

Pyruvate dehydrogenase converts pyruvate to acetyl-CoA under normal conditions

160
Q

Which enzymes are bypassed in gluconeogenesis compared to glycolysis

A

Gluconeogenesis bypasses pyruvate kinase, phosphofructokinase-1, and glucokinase/hexokinase

161
Q

What are the effects of cortisol on gluconeogenesis

A

Cortisol induces the expression of gluconeogenic enzymes, promoting glucose production

162
Q

How does lactate contribute to gluconeogenesis

A

Lactate, produced by muscles and red blood cells, is converted to pyruvate and then to glucose in the liver

163
Q

What is the role of the liver in maintaining blood glucose levels

A

The liver maintains blood glucose levels by storing glycogen and performing gluconeogenesis

164
Q

What happens to gluconeogenesis during a high-protein diet

A

Gluconeogenesis is stimulated during a high-protein diet due to the increased availability of amino acids as substrates

165
Q

What are Glycogen Storage Diseases (GSDs)

A

Glycogen Storage Diseases are a group of inherited metabolic disorders caused by enzyme deficiencies that affect glycogen synthesis, breakdown, or regulation

166
Q

What is the primary function of glycogen in the body

A

Glycogen serves as a storage form of glucose, primarily in the liver and muscles, to be used as an energy source during periods of fasting or intense activity

167
Q

How is GSD classified

A

GSDs are classified based on the specific enzyme deficiency and the tissues affected, such as liver, muscle, or both

168
Q

What enzyme is deficient in GSD Type I (Von Gierke disease)

A

GSD Type I is caused by a deficiency of glucose-6-phosphatase

169
Q

What are the main clinical features of GSD Type I

A

Key features include severe hypoglycemia, hepatomegaly, lactic acidosis, and hyperuricemia

170
Q

What is the primary treatment for GSD Type I

A

Treatment involves frequent feedings of glucose or cornstarch to maintain blood glucose levels and avoid hypoglycemia

171
Q

What is the enzyme deficiency in GSD Type II (Pompe disease)

A

GSD Type II is caused by a deficiency in the enzyme acid alpha-glucosidase (GAA)

172
Q

What tissues are primarily affected in GSD Type II

A

GSD Type II primarily affects the muscles, including the heart, leading to cardiomegaly, muscle weakness, and respiratory issues

173
Q

What is the inheritance pattern of GSDs

A

Most GSDs are inherited in an autosomal recessive manner

174
Q

What are the two main subtypes of GSD Type III

A

GSD Type III is divided into Type IIIa (affecting liver and muscle) and Type IIIb (affecting only the liver)

175
Q

What is the enzyme deficiency in GSD Type IV (Andersen disease)

A

GSD Type IV is caused by a deficiency in the branching enzyme, leading to abnormal glycogen structure

176
Q

What are the clinical features of GSD Type IV

A

Clinical features include hepatomegaly, muscle weakness, and progressive liver cirrhosis

177
Q

What is the key difference between GSD Type III and GSD Type IV

A

GSD Type III involves a debranching enzyme deficiency, while GSD Type IV involves a branching enzyme deficiency

178
Q

What is the prognosis for individuals with GSD Type IV

A

The prognosis for GSD Type IV is generally poor, often leading to liver failure and early mortality

179
Q

What enzyme is deficient in GSD Type V (McArdle disease)

A

GSD Type V is caused by a deficiency in muscle phosphorylase

180
Q

What are the main symptoms of GSD Type V

A

Symptoms include muscle cramps, exercise intolerance, and myoglobinuria following strenuous activity

181
Q

What is the role of glycogen phosphorylase in muscle cells

A

Glycogen phosphorylase breaks down glycogen into glucose-1-phosphate during muscle activity

182
Q

What dietary recommendations are made for individuals with GSD Type V

A

A high-protein diet with moderate carbohydrate intake is recommended to enhance muscle glycogen availability

183
Q

What is the enzyme deficiency in GSD Type VI (Hers disease)

A

GSD Type VI is caused by a deficiency in liver glycogen phosphorylase

184
Q

What are the clinical features of GSD Type VI

A

Features include mild hypoglycemia, hepatomegaly, and growth retardation, with symptoms often improving with age

185
Q

What enzyme is deficient in GSD Type IX

A

GSD Type IX is caused by a deficiency in the phosphorylase kinase enzyme

186
Q

What is unique about the inheritance pattern of GSD Type IX

A

GSD Type IX can be inherited in an X-linked recessive pattern, unlike most other GSDs

187
Q

What are the effects of GSD on fasting tolerance

A

Individuals with GSD have reduced fasting tolerance due to impaired glycogen breakdown, leading to hypoglycemia

188
Q

How is GSD typically diagnosed

A

GSD is diagnosed through a combination of clinical features, enzyme activity assays, and genetic testing

189
Q

What are potential long-term complications of GSD

A

Long-term complications may include liver cirrhosis, cardiomyopathy, and progressive muscle weakness

190
Q

What is the importance of early diagnosis and management in GSD

A

Early diagnosis and management are crucial to prevent severe hypoglycemia, organ damage, and improve overall quality of life

191
Q

What are the symptoms of hypoglycemia in GSD

A

Symptoms include sweating, confusion, tremors, irritability, and in severe cases, seizures or unconsciousness

192
Q

How does GSD Type III affect growth and development in children

A

Children with GSD Type III may experience growth retardation and delayed puberty due to chronic hypoglycemia

193
Q

What is the role of liver biopsy in GSD diagnosis

A

Liver biopsy can help identify abnormal glycogen accumulation and assess enzyme activity

194
Q

What is the relationship between GSD and exercise intolerance

A

GSD, particularly types affecting muscle (e g , Type V), often leads to exercise intolerance due to insufficient glycogen breakdown

195
Q

What are the four types of hypoglycemia

A

The four types of hypoglycemia are insulin-induced, postprandial, fasting, and alcohol-related hypoglycemia

196
Q

How is insulin-induced hypoglycemia treated

A

Mild cases are treated with oral carbohydrates, while severe cases may require subcutaneous or intramuscular glucagon

197
Q

What causes postprandial hypoglycemia

A

Postprandial hypoglycemia is caused by an exaggerated insulin release following a meal

198
Q

What is fasting hypoglycemia and its common causes

A

Fasting hypoglycemia occurs due to reduced hepatic glycogenolysis or gluconeogenesis, often seen in liver disease or adrenal insufficiency

199
Q

What are the symptoms of alcohol-related hypoglycemia

A

Symptoms include agitation, impaired judgment, and combativeness due to decreased glucose synthesis caused by ethanol metabolism

200
Q

What are the two types of hyperglycemia

A

The two types of hyperglycemia are fasting hyperglycemia and postprandial hyperglycemia

201
Q

What role does insulin play in fuel metabolism

A

Insulin promotes glucose storage as glycogen, conversion to triglycerides, and protein synthesis while inhibiting fuel mobilization

202
Q

What is the main action of glucagon during fasting

A

Glucagon stimulates glycogenolysis and gluconeogenesis to maintain blood glucose levels during fasting

203
Q

What are the primary counterregulatory hormones to insulin

A

The primary counterregulatory hormones are glucagon, epinephrine, norepinephrine, cortisol, and growth hormone

204
Q

What happens to insulin and glucagon levels after a high-carbohydrate meal

A

Insulin levels rise while glucagon levels decrease, promoting nutrient storage and inhibiting gluconeogenesis

205
Q

What is the role of cortisol in metabolism during stress

A

Cortisol increases glucose production from amino acids, enhances lipolysis, and suppresses immune responses

206
Q

How does epinephrine affect glucose metabolism

A

Epinephrine stimulates glycogenolysis, inhibits insulin secretion, and increases glucose availability during stress

207
Q

What is the primary function of the ?1-adrenergic receptor

A

The ?1-adrenergic receptor increases heart rate and force of contraction in response to norepinephrine

208
Q

Where are ?2-adrenergic receptors found, and what is their function

A

?2-adrenergic receptors are found in the liver, skeletal muscle, and smooth muscle, where they mediate glycogenolysis and muscle relaxation

209
Q

What is the role of ?3-adrenergic receptors in adipose tissue

A

?3-adrenergic receptors stimulate fatty acid oxidation and thermogenesis in adipose tissue

210
Q

How does cortisol influence gene transcription

A

Cortisol binds to intracellular receptors, influencing gene transcription by interacting with chromatin in the cell nucleus

211
Q

What are the three basic types of hormone signal transduction

A

The three types are receptor coupling to adenylate cyclase, receptor kinase activity, and receptor coupling to PIP2 hydrolysis

212
Q

What is the role of cAMP in glucagon signaling

A

cAMP acts as a second messenger, activating PKA, which phosphorylates key enzymes in carbohydrate and fat metabolism

213
Q

What is the main function of insulin in the body

A

Insulin facilitates glucose uptake, promotes glycogen and fat storage, and stimulates protein synthesis

214
Q

What is the role of glucagon in regulating blood glucose

A

Glucagon raises blood glucose by promoting glycogen breakdown and gluconeogenesis in the liver

215
Q

How is insulin secretion regulated

A

Insulin secretion is primarily regulated by blood glucose levels, with additional modulation by amino acids and gastrointestinal hormones

216
Q

What is the relationship between insulin and glucagon during fasting

A

During fasting, insulin levels decrease while glucagon levels rise, leading to glucose release from the liver and fatty acid mobilization

217
Q

How do catecholamines like epinephrine and norepinephrine affect metabolism

A

They increase fuel mobilization, enhance cardiac output, and prepare the body for stress (fight-or-flight response)

218
Q

What is the function of the insulin receptor

A

The insulin receptor, through its tyrosine kinase activity, initiates a signaling cascade that regulates glucose uptake and metabolism

219
Q

What are the effects of insulin on protein synthesis

A

Insulin stimulates protein synthesis by promoting amino acid uptake and enhancing mRNA translation

220
Q

What is the role of glucagon in lipid metabolism

A

Glucagon stimulates lipolysis in adipose tissue, releasing fatty acids as an alternative energy source

221
Q

What is the effect of insulin on glycogen synthesis

A

Insulin promotes glycogen synthesis by activating glycogen synthase and inhibiting glycogen phosphorylase

222
Q

What are the effects of hypoglycemia on the body

A

Hypoglycemia can cause symptoms like sweating, confusion, tremors, and in severe cases, seizures and loss of consciousness

223
Q

How does cortisol impact glucose metabolism

A

Cortisol promotes gluconeogenesis and inhibits glucose uptake in tissues, contributing to elevated blood glucose levels during stress

224
Q

What are the primary metabolic effects of fasting

A

Fasting leads to increased gluconeogenesis, lipolysis, and ketogenesis to maintain energy supply

225
Q

What are the key hormones involved in the fed state

A

Insulin is the key hormone in the fed state, promoting nutrient storage and utilization

226
Q

What is the effect of glucagon on hepatic fructose 2,6-bisphosphate

A

Glucagon decreases hepatic fructose 2,6-bisphosphate, inhibiting glycolysis and activating gluconeogenesis

227
Q

What is the role of the hypothalamus in glucose regulation

A

The hypothalamus triggers the release of counterregulatory hormones like glucagon and epinephrine in response to low blood glucose

228
Q

What is the significance of GLUT transporters in insulin secretion

A

GLUT transporters facilitate glucose entry into ?-cells, triggering insulin release through metabolic signaling pathways

229
Q

How does alcohol consumption affect glucose metabolism

A

Alcohol metabolism increases NADH, diverting gluconeogenic precursors away from glucose production and potentially leading to hypoglycemia

230
Q

What is the function of glucagon-like peptide 1 (GLP-1)

A

GLP-1 enhances insulin secretion in response to food intake and slows gastric emptying, contributing to blood glucose regulation

231
Q

What is the relationship between cortisol and epinephrine during stress

A

Cortisol and epinephrine work synergistically to increase blood glucose levels and energy availability during stress

232
Q

What is insulin resistance, and how does it affect metabolism

A

Insulin resistance is the reduced response of tissues to insulin, leading to elevated blood glucose and altered lipid metabolism

233
Q

How does glucagon influence amino acid metabolism

A

Glucagon promotes the use of amino acids for gluconeogenesis, particularly during fasting or low-carbohydrate intake

234
Q

What is the impact of epinephrine on muscle metabolism

A

Epinephrine stimulates glycogenolysis in muscle tissue, providing glucose for immediate energy during physical activity

235
Q

What role does insulin play in lipid metabolism

A

Insulin inhibits lipolysis in adipose tissue and promotes the storage of triglycerides

236
Q

What is the primary function of glucose in metabolism

A

Glucose serves as a primary energy source, providing ATP through glycolysis, the TCA cycle, and oxidative phosphorylation

237
Q

What enzyme converts glucose to glucose 6-phosphate in the liver

A

Glucokinase converts glucose to glucose 6-phosphate in the liver, especially active in the fed state

238
Q

What is the role of glycogen in the body

A

Glycogen acts as a storage form of glucose in the liver and muscles, providing a rapid source of energy during fasting or exercise

239
Q

How is glycogen synthase regulated

A

Glycogen synthase is activated by dephosphorylation when insulin levels are high and glucagon levels are low

240
Q

What is the key regulatory enzyme in glycolysis

A

Phosphofructokinase-1 (PFK-1) is the key regulatory enzyme in glycolysis, activated by fructose 2,6-bisphosphate and AMP

241
Q

What happens to pyruvate in the presence of oxygen

A

Pyruvate is converted to acetyl-CoA by pyruvate dehydrogenase, entering the TCA cycle for further energy production

242
Q

What is the role of acetyl-CoA in fatty acid synthesis

A

Acetyl-CoA provides the two-carbon units for fatty acid synthesis in the cytosol, following its conversion from pyruvate in the mitochondria

243
Q

How does insulin affect acetyl-CoA carboxylase

A

Insulin activates acetyl-CoA carboxylase by dephosphorylation, promoting fatty acid synthesis

244
Q

What is the significance of malonyl-CoA in lipid metabolism

A

Malonyl-CoA inhibits carnitine palmitoyltransferase I (CPTI), preventing fatty acid oxidation in the mitochondria during the fed state

245
Q

How is glucose 6-phosphate used in lipogenesis

A

Glucose 6-phosphate enters glycolysis, where it is eventually converted to acetyl-CoA, a precursor for fatty acid synthesis

246
Q

What happens to citrate in the cytosol during lipogenesis

A

Citrate is cleaved by citrate lyase into acetyl-CoA and oxaloacetate, providing substrates for fatty acid and cholesterol synthesis

247
Q

How does fasting affect liver glycogen levels

A

During fasting, liver glycogen is degraded to maintain blood glucose levels, driven by the activation of glycogen phosphorylase

248
Q

What triggers gluconeogenesis during prolonged fasting

A

Gluconeogenesis is triggered by increased availability of precursors and the induction of enzymes like PEPCK and glucose 6-phosphatase

249
Q

What role does AMP play in regulating metabolism

A

AMP activates AMP-activated protein kinase (AMPK), which promotes glucose uptake and fatty acid oxidation, particularly during low energy states

250
Q

What happens to fatty acids during fasting

A

Fatty acids are released from adipose tissue and oxidized in the liver, producing acetyl-CoA for ketone body synthesis

251
Q

What is the role of pyruvate dehydrogenase (PDH) in energy metabolism

A

PDH converts pyruvate to acetyl-CoA, linking glycolysis to the TCA cycle for ATP production

252
Q

What is the function of ketone bodies during fasting

A

Ketone bodies serve as an alternative energy source, particularly for the brain, during prolonged fasting when glucose is scarce

253
Q

What is the effect of insulin on GLUT4 transporters in muscle cells

A

Insulin increases the number of GLUT4 transporters on the muscle cell membrane, enhancing glucose uptake

254
Q

How is glycolysis inhibited during fasting

A

Glycolysis is inhibited by low levels of fructose 2,6-bisphosphate, which decreases PFK-1 activity, favoring gluconeogenesis

255
Q

What enzyme is responsible for the final step of gluconeogenesis

A

Glucose 6-phosphatase catalyzes the conversion of glucose 6-phosphate to glucose, enabling its release into the bloodstream

256
Q

What happens to pyruvate carboxylase activity during fasting

A

Pyruvate carboxylase activity increases during fasting, promoting gluconeogenesis by converting pyruvate to oxaloacetate

257
Q

What is the relationship between citrate levels and fatty acid synthesis

A

High citrate levels in the cytosol promote fatty acid synthesis by providing acetyl-CoA and activating acetyl-CoA carboxylase

258
Q

How does fasting influence ketone body production

A

Fasting increases ketone body production as fatty acids are oxidized in the liver, with acetyl-CoA being converted to ketone bodies

259
Q

What is the effect of NADH on isocitrate dehydrogenase

A

High levels of NADH inhibit isocitrate dehydrogenase, leading to citrate accumulation and promoting fatty acid synthesis in the cytosol

260
Q

How does glucagon influence liver metabolism during fasting

A

Glucagon activates glycogenolysis and gluconeogenesis in the liver, raising blood glucose levels

Noorda FOM (18 decks)

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