Chapter 12: Bioenergetics And Regulation Of Metabolism Flashcards

1
Q

ATP energy

A

About -30 kJ/mol

Energy turnover in all cell types

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2
Q

CAMP

A

-50.4 kJ/mol

Second messenger

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3
Q

Creatine phosphate

A

-43.3 kJ/mol

Direct phosphorylation in muscle

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4
Q

Glucose-6-phosphate

A

-30.5 kJ/mol

Intermediate of glycolysis and gluconeogenesis

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5
Q

AMP

A

-9.2 kJ/mol

ATP synthesis

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6
Q

ATP cleavage

A

Transfer of a high-energy phosphate group from ATP to another molecule

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7
Q

Phosphoryl group transfers

A

The overall free energy of the reaction will be determined by taking the sum of the free energies of the individual reactions

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8
Q

Flavoproteins

A

Contain a modified vitamin B2, or riboflavin; either flavin adenosine mononucleotide (FMN) or flavin mononucleotide (FAD); most notable for their presence in the mitochondria and chloroplasts as electron carriers; involved in the modification of other B vitamins to active forms; function as cofactors for enzymes in the oxidation of fatty acids, the decarboxylation of pyruvate and the reduction of glutathione

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9
Q

Postprandial (absorptive) state

A

Absorptive or well-fed state, occurs shortly after eating; marked by greater anabolism and fuel storage than catabolism; generally lasts three to five hours after eating a meal

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10
Q

What are the three major target tissues for insulin?

A

Liver, muscle, and adipose tissue
Liver: glycogenesis, lipogenesis (fatty acids and triacylglycerols) - most energy needs are met by the oxidation of excess amino acids
Muscle: glycogenesis, protein synthesis, glucose uptake, amino acid uptake
Adipose: TAG synthesis, glucose and TAG uptake
Insulin increases lipoprotein lipase activity which clears VLDL and chylomicrons from the blood; insulin decreases TAG breakdown in adipose tissue and the formation of ketone bodies by the liver

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11
Q

What tissues does insulin not work on?

A

Nervous tissue and red blood cells
Nervous tissue: derives energy from oxidizing glucose to CO2 and water in postprandial and postabsorptive states
RBC: anaerobic use of glucose

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12
Q

Postabsorptive (fasting) state

A

Glucagon, cortisol, epinephrine, norepinephrine, and growth hormone oppose the actions of insulin AKA counterregulatory hormones because of their effects on skeletal muscle, adipose tissue, and the liver
Liver: glycogenolysis, gluconeogenesis (12 hours to reach max velocity)
Skeletal muscle: release of amino acids provide carbon skeleton and energy for gluconeogenesis (caused by decrease in insulin)
Adipose tissue: release of fatty acids provide the carbon skeleton and energy for gluconeogenesis (caused by decrease in insulin)

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13
Q

Which tissue is least able to change its fuel source in periods of prolonged starvation?

A

Cells that depend on anaerobic mechanisms for energy (ex. RBC)

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14
Q

In which tissues is glucose uptake not affected by insulin?

A

Nervous tissue, kidney tubules, intestinal mucosa, RBCs, and β-cells of the pancreas

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15
Q

What is the most important controller of insulin?

A

Plasma glucose; above a threshold of 100 mg/dL or about 5.6 mM of glucose, insulin secretion is directly proportional to plasma glucose; glucose must enter the β-cells and be metabolized to ATP; ATP increase stimulates exocytosis of insulin via several ion and VG-channels; also affected by glucagon and somatostatin

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16
Q

Glucagon

A

Increased liver glycogenolysis - activation of glycogen phosphatase and inhibition of glycogen synthase
Increased liver gluconeogenesis - promotes conversion of pyruvate to PEP via pyruvate carboxylase and PEPCK, increases conversion of F-1,6-BP to F-6-P by fructose-1,6-bisphosphatase
Increased liver ketogenesis and decreased lipogenesis
Increased lipolysis in the liver via activation of hormone-sensitive lipase in the liver (note glucagon is not considered a major fat-mobilizing hormone)

17
Q

What controls glucagon release?

A

Hypoglycemia (promoter) and hyperglycemia (inhibitor); (basic) amino acids (lysine, arginine and histidine) promote glucagon secretion; secreted in response to ingestion of a meal rich in proteins

18
Q

Cortisol

A

Promotes the mobilization of energy stores through the degradation and increased delivery of amino acids and increased lipolysis; elevates blood glucose levels, increasing glucose availability for nervous through inhibition of glucose uptake in muscle, lymphoid and fat tissue while increasing hepatic output of glucose via gluconeogenesis (from amino acids) and permissive function that enhances the activity of glucagon, epinephrine, and other catecholamines

19
Q

Side effects of long-term use of glucocorticoids?

A

Hyperglycemia which stimulates insulin; promotes fat storage rather than lipolysis

20
Q

Catecholamines

A

Secreted by the adrenal medulla and include epinephrine and norepinephrine; increase the activity of the liver and muscle glycogen phosphorylase, promoting glycogenolysis and increasing glucose output from the liver (not muscle - no glucose-6-phosphatase; increased lipolysis in adipose tissue via HSL; acts directly on heart to increase the basal metabolic rate through the SNS

21
Q

Thyroid hormones

A

T4 -thyroxine - increase in metabolic rate occurs after a latency of several hours but lasts for several days; converted to T3 by deiodinases
T3 - triiodothyronine - increase in metabolic rate occurs rapidly but is short-lasting

22
Q

What are the effects of thyroid hormones?

A

Lipid and carbohydrate metabolism; accelerate cholesterol clearance from the plasma and increase the rate of glucose absorption from the small intestine; epinephrine requires thyroid hormones to have significant metabolic effects

23
Q

Liver metabolism

A

Well-fed: glucose and amino acids
Fasting: fatty acids
1) Maintains a constant level of blood glucose under a wide range of conditions
2) Synthesizes ketones when excess fatty acids are being oxidized

24
Q

Well-fed state liver metabolism

A

The liver extracts excess glucose and uses it to replenish its glycogen stores; remaining glucose is used to synthesize fatty acids via acetyl-CoA; insulin increase after a meal stimulates both glycogen synthesis and fatty acid synthesis in the liver; fatty acids are converted to TAGs and released into the blood as VLDL; liver dervies most of its energy from the oxidation of excess amino acids

25
Q

Liver metabolism during fasting

A

Liver releases glucose into the blood; increase in glucagon during fasting promotes both glycogen degradation and gluconeogenesis; lactate from anaerobic metabolis,, glycerol from TAGs and amino acids provide carbon skeletons for glucose synthesis

26
Q

Adipose tissue metabolism

A

Well-fed: glucose
Fasting: fatty acids
Insulin triggers FA release from VLDL and chylomicrons; lipoprotein lipase (enzyme found in the capillary beds of adipose tissue) is induced by insulin; fatty acids released from lipoproteins are taken up by adipose tissue and re-esterified to TAGs for storage; glycerol phosphate comes from glucose; insulin suppresses the release of fatty acids from adipose tissue; during the fasting state, decreased levels of insulin and increased epinephrine activity rate from HSL

27
Q

Resting skeletal muscle

A

Glucose and fatty acids; major consumer of fuel; insulin promotes glucose uptake in skeletal muscle, which replenishes glycogen stores and amino acids used for protein synthesis; both excess glucose and amino acids can be oxidized for energy; in the fasting state, resting muscle uses fatty acids derived from FFA in the bloodstream as well as ketone bodies

28
Q

Active muscle metabolism

A

Creatine phosphate - a very short-lived source energy (2-7 seconds) which transfers a phosphate group to ADP to form ATP; skeletal muscle has stores of both glycogen and some triacylglycerols; blood glucose and FFA can also be used; short bursts of high intensity exercise are also supported by anaerobic glycolysis drawing on stored muscle glycogen; during moderately high-intensity continuous exercise, oxidation of glucose and fatty acids are both important, but after 1 to 3 hours, muscle glycogen stores are depleted and the intensity of exercise slows to a rate that can be supported by oxidation of fatty acids

29
Q

Cardiac muscle metabolism

A

Well-fed: fatty acids
Fasting: fatty acids, ketones
Mimics skeletal muscle after prolonged exercise
In a failing heart, glucose oxidation increases and β-oxidation falls

30
Q

Brain metabolism

A

Well-fed: glucose
Fasting: glucose (ketones for prolonged fasting - up to 2/3 of the brain’s energy supply)
Consumes ~25% of the total glucose despite comprising only ~2% of the total body weight
Tightly regulated blood glucose levels to maintain a sufficient glucose supply for the brain; normal function depends on a continuous glucose supply from the bloodstream; in hypoglycemic conditions (<70mg/dL), hypothalamic centers in the brain sense a fall in blood glucose level, and the release of glucagon and epinephrine is triggered; fatty acids cannot cross the BBB; relies on blood glucose from gluconeogenesis and glycogenolysis between meals

31
Q

Respiratory quotient (RQ)

A

RQ = CO2 produced/O2 consumed

32
Q

Basal metabolic rate (BMR)

A

Measured by calorimeters; based on heat exchange with the environment

33
Q

ghrelin

A

Secreted by the stomach in response to signals of an impending meal; sight, sound, taste, and especially smell all act as signals for its release; ghrelin increases appetite and stimulates secretion of orexin

34
Q

Orexin

A

Further increases appetite; involved in alertness and the sleep-wake cycle as well; triggered by ghrelin release and hypoglycemia

35
Q

Leptin

A

Hormone secreted by fat cells that decreases appetite by suppressing orexin production

36
Q

Respiratory quotient with carbohydrates? With lipids?

A

1; 0.7

37
Q

Threshold for uncompensated weight gain?

A

Lower than for weight loss —> easier to gain weight than lose it