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Questions and Answers
What is one of the physiological functions of glucocorticoids?
What is one of the physiological functions of glucocorticoids?
- Stimulating the storage of fatty acids in adipose tissue.
- Decreasing enzyme synthesis rates.
- Inhibiting gluconeogenesis in the liver.
- Circadian control of metabolic pathways. (correct)
In what location do glucocorticoids increase gluconeogenesis?
In what location do glucocorticoids increase gluconeogenesis?
- Adipose tissue
- Muscle tissue
- Liver (correct)
- Brain
What effect do glucocorticoids have on glycogen synthesis?
What effect do glucocorticoids have on glycogen synthesis?
- Stimulation (correct)
- Reduction
- No effect
- Inhibition
How do glucocorticoids mediate their effects?
How do glucocorticoids mediate their effects?
When are cortisol levels typically at their highest?
When are cortisol levels typically at their highest?
What is immediately stimulated by epinephrine in a stressful situation?
What is immediately stimulated by epinephrine in a stressful situation?
What enzyme is increased by glucocorticoids, increasing gluconeogenesis?
What enzyme is increased by glucocorticoids, increasing gluconeogenesis?
In a stressful situation, what is induced by cortisol in adipose tissue?
In a stressful situation, what is induced by cortisol in adipose tissue?
What is the effect of cortisol-induced protein breakdown?
What is the effect of cortisol-induced protein breakdown?
What effect do stress hormones have on insulin?
What effect do stress hormones have on insulin?
What happens to the insulin requirement of diabetic patients during infections?
What happens to the insulin requirement of diabetic patients during infections?
Which of the following stimulates proteolysis in skeletal muscle?
Which of the following stimulates proteolysis in skeletal muscle?
What does tumor necrosis factor promote?
What does tumor necrosis factor promote?
What units is weight measured in when calculating BMR using the equations provided?
What units is weight measured in when calculating BMR using the equations provided?
What causes BMR to decline during extended starvation?
What causes BMR to decline during extended starvation?
What is produced on top of the BMR after a meal?
What is produced on top of the BMR after a meal?
What is the basal metabolic rate (BMR)?
What is the basal metabolic rate (BMR)?
Which of the following requires the least energy for digestion, absorption, and storage?
Which of the following requires the least energy for digestion, absorption, and storage?
Which activity is the most variable item in the energy budget?
Which activity is the most variable item in the energy budget?
What percentage of body weight does muscle account for in males?
What percentage of body weight does muscle account for in males?
In which age group does the brain account for the largest percentage of total metabolic rate?
In which age group does the brain account for the largest percentage of total metabolic rate?
Which of the following tissues has the highest metabolic rate (kcal/kg/day)?
Which of the following tissues has the highest metabolic rate (kcal/kg/day)?
Approximately what percentage of total metabolic rate is attributed to the liver in adult males?
Approximately what percentage of total metabolic rate is attributed to the liver in adult males?
Which tissue has the largest percentage of body weight in females?
Which tissue has the largest percentage of body weight in females?
Postprandial thermogenesis is affected by what two factors?
Postprandial thermogenesis is affected by what two factors?
When carbohydrate is converted to storage fat, approximately what percentage of the energy content of the carbohydrate is required?
When carbohydrate is converted to storage fat, approximately what percentage of the energy content of the carbohydrate is required?
What is produced from fatty acids?
What is produced from fatty acids?
What can be produced from glucose?
What can be produced from glucose?
What is the central molecule involved in energy production via the TCA cycle?
What is the central molecule involved in energy production via the TCA cycle?
Which of the following can be used to produce glucose 6-phosphate?
Which of the following can be used to produce glucose 6-phosphate?
What is the primary storage form of glucose in the body?
What is the primary storage form of glucose in the body?
Which of the following is the precursor to triglycerides and phospholipids?
Which of the following is the precursor to triglycerides and phospholipids?
Under what conditions are ketone bodies typically produced?
Under what conditions are ketone bodies typically produced?
What is the end product of glycolysis that enters the TCA cycle after conversion to Acetyl-CoA?
What is the end product of glycolysis that enters the TCA cycle after conversion to Acetyl-CoA?
Which molecule is used in the synthesis of fatty acids?
Which molecule is used in the synthesis of fatty acids?
What is a product of the breakdown of triglycerides?
What is a product of the breakdown of triglycerides?
What process contributes to glucose production in the liver during fasting?
What process contributes to glucose production in the liver during fasting?
After a meal, what is the primary source of glucose used by the body?
After a meal, what is the primary source of glucose used by the body?
What is the approximate total body glucose consumption (g/h) immediately after a meal?
What is the approximate total body glucose consumption (g/h) immediately after a meal?
What is the fate of lactic acid during gluconeogenesis?
What is the fate of lactic acid during gluconeogenesis?
What is the role of ketone bodies in metabolism?
What is the role of ketone bodies in metabolism?
Which metabolic pathway bypasses the need for the TCA cycle?
Which metabolic pathway bypasses the need for the TCA cycle?
What happens to total body glucose consumption during fasting?
What happens to total body glucose consumption during fasting?
What process does the liver use to produce glucose during the initial hours of fasting?
What process does the liver use to produce glucose during the initial hours of fasting?
What becomes the primary source of blood glucose 12 to 16 hours after a meal?
What becomes the primary source of blood glucose 12 to 16 hours after a meal?
How long does it typically take for liver glycogen stores to become almost completely exhausted?
How long does it typically take for liver glycogen stores to become almost completely exhausted?
What is the major source of glucose produced during gluconeogenesis?
What is the major source of glucose produced during gluconeogenesis?
Which tissues do not respond to insulin and continue to consume glucose even during long-term fasting?
Which tissues do not respond to insulin and continue to consume glucose even during long-term fasting?
What happens to the respiratory quotient during the switch from glucose oxidation to fat oxidation?
What happens to the respiratory quotient during the switch from glucose oxidation to fat oxidation?
After an overnight fast, which metabolic process contributes least to maintaining blood glucose levels?
After an overnight fast, which metabolic process contributes least to maintaining blood glucose levels?
Which substrate is primarily utilized by the brain during prolonged starvation?
Which substrate is primarily utilized by the brain during prolonged starvation?
What is the primary fate of pyruvate in the liver during prolonged fasting?
What is the primary fate of pyruvate in the liver during prolonged fasting?
During the initial stages of fasting (after liver glycogen depletion), where are the substrates used for gluconeogenesis primarily derived from?
During the initial stages of fasting (after liver glycogen depletion), where are the substrates used for gluconeogenesis primarily derived from?
What is the role of Hormone Sensitive Lipase (HSL) during prolonged fasting?
What is the role of Hormone Sensitive Lipase (HSL) during prolonged fasting?
Why is there a shift in the primary fuel source from glucose to fatty acids during prolonged fasting?
Why is there a shift in the primary fuel source from glucose to fatty acids during prolonged fasting?
What is the fate of glycerol produced during lipolysis in adipose tissue during fasting conditions?
What is the fate of glycerol produced during lipolysis in adipose tissue during fasting conditions?
Which of the graphs depicts the metabolic pathways that occur in the liver after prolonged fasting?
Which of the graphs depicts the metabolic pathways that occur in the liver after prolonged fasting?
Which molecule is being converted into Acetyl-CoA in the liver after a period of prolonged fasting?
Which molecule is being converted into Acetyl-CoA in the liver after a period of prolonged fasting?
Which of the following molecules are able to produce Glucose 6-P in the liver after a period of prolonged fasting?
Which of the following molecules are able to produce Glucose 6-P in the liver after a period of prolonged fasting?
Flashcards
Glucocorticoids
Glucocorticoids
A hormone released in response to chronic stress; it affects the liver, enzymes of amino acid catabolism, and PEP-carboxykinase.
Gluconeogenesis (↑ Liver)
Gluconeogenesis (↑ Liver)
The synthesis of glucose from non-carbohydrate precursors, increased by glucocorticoids in the liver.
Enzymes of Amino Acid Catabolism
Enzymes of Amino Acid Catabolism
Enzymes involved in breaking down amino acids.
PEP-carboxykinase
PEP-carboxykinase
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Glycogen Synthesis (↑)
Glycogen Synthesis (↑)
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Glycogen Synthase
Glycogen Synthase
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Enzyme Synthesis Rate
Enzyme Synthesis Rate
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Cortisol & Epinephrine Cooperation
Cortisol & Epinephrine Cooperation
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Stress Hormones
Stress Hormones
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Cortisol-induced Protein Breakdown
Cortisol-induced Protein Breakdown
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Insulin Resistance
Insulin Resistance
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Cytokines Metabolic Effects
Cytokines Metabolic Effects
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Interleukin-1 (IL-1)
Interleukin-1 (IL-1)
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Tumor Necrosis Factor (TNF)
Tumor Necrosis Factor (TNF)
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Mifflin-St. Jeor equation
Mifflin-St. Jeor equation
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Postprandial Thermogenesis
Postprandial Thermogenesis
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Basal Metabolic Rate (BMR)
Basal Metabolic Rate (BMR)
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Muscular Activity
Muscular Activity
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Muscle
Muscle
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Heart
Heart
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Metabolism
Metabolism
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Adipose tissue
Adipose tissue
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Brain in Children
Brain in Children
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Brain
Brain
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Kidneys
Kidneys
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Glucose (After Meal)
Glucose (After Meal)
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Glycogen (After Meal)
Glycogen (After Meal)
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Fatty Acids (After Meal)
Fatty Acids (After Meal)
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Lipids (After Meal)
Lipids (After Meal)
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Ketone Bodies (12 Hours)
Ketone Bodies (12 Hours)
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Glycogenolysis (12 Hours)
Glycogenolysis (12 Hours)
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Fatty Acids (12 hrs)
Fatty Acids (12 hrs)
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Glucose (4 Days)
Glucose (4 Days)
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Ketone Bodies (4 Days)
Ketone Bodies (4 Days)
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Glycogen (4 Days)
Glycogen (4 Days)
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Coenzyme A (CoA)
Coenzyme A (CoA)
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Tricarboxylic Acid (TCA) Cycle
Tricarboxylic Acid (TCA) Cycle
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Very-Low-Density Lipoprotein (VLDL)
Very-Low-Density Lipoprotein (VLDL)
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Glycogenolysis (Liver)
Glycogenolysis (Liver)
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Gluconeogenesis (Liver)
Gluconeogenesis (Liver)
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Ketone Bodies
Ketone Bodies
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Energy for Gluconeogenesis
Energy for Gluconeogenesis
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Lipid-Based Energy
Lipid-Based Energy
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Liver Glycogen's Role
Liver Glycogen's Role
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Gluconeogenesis Switch
Gluconeogenesis Switch
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Gluconeogenesis Substrates
Gluconeogenesis Substrates
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Insulin-Independent Glucose Use
Insulin-Independent Glucose Use
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Respiratory Quotient (RQ) Shift
Respiratory Quotient (RQ) Shift
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Ketone Bodies production
Ketone Bodies production
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Acyl-CoA
Acyl-CoA
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Acetyl-CoA production
Acetyl-CoA production
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TCA Cycle Input
TCA Cycle Input
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Pyruvate's Gluconeogenic Route
Pyruvate's Gluconeogenic Route
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Amino Acids to Glucose
Amino Acids to Glucose
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Lactate's Role
Lactate's Role
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Glycogen synthesis.
Glycogen synthesis.
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Glycerol's Gluconeogenic Role
Glycerol's Gluconeogenic Role
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Release of Free Fatty Acids
Release of Free Fatty Acids
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Study Notes
Integration of Metabolism
- Beyond self-preservation, cells and organs cooperate for the body's common good
- They manage challenges like fasting and feasting
- Coordination achieved via hormonal and nervous system signals
- Discusses metabolic adaptation to challenges, especially overeating
Insulin Release
- Insulin, the hormone of the well-fed state, is released by pancreatic ẞ-cells in response to elevated blood glucose levels
- Human pancreas contains ~1 million islets with 50% β-cells and 35-40% α-cells (glucagon)
- Glucose is the primary energy source for β-cells and the main stimulus for insulin secretion
- Glucose enters cells on GLUT1 and GLUT3 carriers, where GLUT3 has high affinity (Km 1mM) and GLUT1 has Km of 6mM
- Inside cells, glucose is phosphorylated by glucokinase, which acts as a glucose sensor, with a Km of ~6 mM
- Increased glucose metabolism raises the ATP/ADP ratio, closing ATP-regulated potassium channels (KATP)
- Membrane depolarization opens voltage-gated calcium channels, triggering exocytosis of insulin vesicles
- It also induces longer-term adaptations like increased insulin synthesis
- Insulin secretion also stimulated by amino acids, fatty acids, ketone bodies, acetylcholine, and incretins
Nutrient Use
-
Insulin channels excess nutrients into glycogen, fat, and protein synthesis
-
After a carbohydrate-rich meal, glucose is metabolized in skeletal muscle (over half), liver (20-25%), and adipose tissue (10%)
-
Insulin stimulates glucose uptake in skeletal muscle and adipose tissue using GLUT4
-
In these tissues, insulin stimulates glucose update by the glucose carrier GLUT4
-
GLUT4 transporters are located in intracellular storage vesicle membranes in the absence of insulin
-
Insulin causes storage vesicles to move to the cell surface leading to GLUT4 deposition
-
Insulin actions occur via the insulin receptor substrate, phosphoinositide 3-kinase, and protein kinase B (Akt) pathways
-
In the liver, glucose uptake is not limited by the insulin-insensitive GLUT2 transporter
-
Glycolytic enzymes are stimulated and gluconeogenic enzymes are repressed on a time scale of hours to days
-
Gluconeogenesis effects mainly mediated via inhibition of the FoxO transcription factor
-
cAMP phosphorylations are reversed within minutes through phosphodiesterase 3B stimulation and phosphatase-1 stimulation
-
Brain and erythrocytes glucose metabolism is not insulin-dependent
-
Fatty acid in adipose tissue lipolysis is significantly reduced by insulin, ensuring dietary nutrients are metabolized in the well-fed state
-
Insulin facilitates the processing of excess carbohydrate to fat in the liver by glycolysis, the pyruvate dehydrogenase reaction, and fatty acid biosynthesis
Protein Synthesis
-
Protein synthesis is stimulated by insulin, acting as a growth factor via the Ras protein and MAP kinase cascade
-
Insulin's effects on protein synthesis are mediated by the mTOR (mammalian target of rapamycin or mechanistic target of rapamycin) complex
-
mTORC1 assembles on the surface of the lysosome membrane
-
mTOR complex 2 (mTORC2) assembles under the plasma membrane
-
Both complexes mediate cellular adaptation to nutrient availability
-
mTORC2 is involved in early insulin signaling, leading to activation of Akt2
-
mTORC1 integrates nutrient availability signals and coordinates cellular responses
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mTORC1 attachment to the lysosomal membrane depends on small G proteins Rag A/B and Rag C/D, activated by free amino acids
-
At the lysosomal membrane, mTOR can be further activated
-
Most stimuli act through the tuberous sclerosis complex (TSC)
-
Active GTP-bound Rheb activates mTORC1, and the TSC complex activates Rheb
-
Insulin and growth factors inhibit the TSC complex by inhibitory phosphorylations
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Nutrient deficiency activates the AMP-activated protein kinase, inhibiting mTORC1
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Ribosomal protein synthesis is increased non-specifically by mTORC1.
-
It mediates phosphorylation of 4EBP which is an inhibitor of eukaryotic initiation factor 4E
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mTOR also affects carbohydrate and lipid metabolism
-
Increased fatty acids are mediated by the stimulation of SREBP-1c cleavage
-
Stimulation of glycolysis can be achieved through hypoxia inducible factor-1a and the Myc protein
-
Stimulation of protein synthesis is complemented by inhibition of lysosomal biogenesis and autophagy
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mTOR’s effects further include increased protein synthesis and reduced lysosomal degradation
Glucose Level
- During startvation most of the energy is retrieved from adipose tissue-derived fatty acids
- Neurons and erythrocytes depend on a glucose supply
- Glucagon is specialized for maintaining normal blood glucose during fasting
- Glucagon leads to hepatic glucose production, glycogenolysis, and gluconeogenesis by effecting the liver
Catecholamines
- Next to fasting, physical excretion is an additional challenge toward the metabolism
- Energy in muscles need to be augmented, as energy is supplemented
- These responses are coordinated by catecholamines.
- Catecholamines can rise the cellular cAMP level through B-adrenergic receptors and the calcium level through a1-adrenergic receptors
- They can elevate blood levels and it can be used in combination with hyploglycemia
- Hypoglycemic episodes are accopanied by sympthatic activity like pallor, sweating, and tachycardia
Glucocorticoids
- The hormone cortisol stimulates gluconeogensis and glycogen synthesis
- Chronic stress stimulates cortisol secretion from the adrenal cortex.
- Glucocoricoids are synergistic eith epinephrine but with one different
- Whereas, glucose metabolism works through second messengers, glucocorticoids are mainly used for regulation.
- Therefore, the body must be prepared for epinephrine
- They make epinephrine synthesis through the lipases synthesis
- As glucose is being diverted into the glyocogen, a more accurate substarate has to be implemented
Energy
- Cortisol and epinephrine work together in stressful situations
- For degenerative descendants today are trouble makers rather than life savers Cytokines are released by white blood cells during infections and similar stress hormones
- Basal Metabolic Rate is the amount of energy that in the post absorptive state that can be calculated with prediction formulas
BMR depends on body composition. Postprandia thermogenesis is produced by metabolic intersections
- The composition on conversion occurs during higher consumption on carbohydrates
Energy Expenditure
- During Long term fasting: BMRx.8
- The calories from sedentary lifestyles can increase BMR
Energy Degradation
-
For 3 or 4 after a meal is implemented an ample source is available for for only some hours
-
Table 32.6 notes all the energy resources of the 'Textbook'
-
Compared to human free-living animals, humans have enourmous amount of nutrients
-
Stored nutrients like triglycerides, glycogen, protein have energy values inside of cells
-
Compared to fat reserves, glycogen stores are punny.
Fat as depot
- The blood glucose level can decline in the limited events
- Plasma fatty acids can be low while the fatty acids can be high
CHO’s
- The liver has Michaelis constant for glucose.
- Liver converts into glucose mainly
- Triglycerides are syntehsized during this state
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Description
Explore the physiological functions of glucocorticoids, including their role in gluconeogenesis and glycogen synthesis. Learn about how they mediate effects and the impact of stress hormones on insulin. Discover connections between cortisol, tumor necrosis factor, and metabolic rate.
