Module 1 Section 5 (Endocrine Control of Fuel Metabolism) Flashcards

1
Q

Describe fuel metabolism in the liver, fat, cells, muscle, and brain during fasted and fed conditions.

A

Metabolism is the sum of all chem reactions that occur in all organism which includes the synthesis, degradation, transport of substances into and b/w cells and the transformation of proteins, carbs and fats.
- These reactions = intermediary or fuel metabolism

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2
Q

Contrast the cellular response to insulin in liver cells, fat cells, and muscle cells.

A

.

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3
Q

Describe how the release of insulin and glucagon are regulated, and once released, how they regulate fuel metabolism.

A

Decr in blood glucose —(+)—> a-cells ——> incr glucagon ——> incr blood glucose to normal

OR

Decr in blood glucose —(-)—> B-cells ——> decr insulin ——> incr blood glucose to normal

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4
Q

Explain why it’s important for some tissues to be insulin-independent for glucose uptake.

A

If the tissues had only an insulin-dependent transporter they would be starved of glucose during the fasted state, with lethal consequences. The insulin-independent transporter allows continued transport down the glucose concentration gradient, even as the blood glucose concentration falls.

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5
Q

What is the difference b/w anabolic and catabolic reactions?

A

Anabolic reactions (anabolism): synthesis of larger organic macromolecules from smaller organic molecular subunits used for repair, growth and the storage of excess ingested nutrients.

Catabolic reactions (catabolism): the breakdown of larger organic macromolecules either through the process of hydrolysis into smaller molecules, or oxidation of smaller molecules (glucose) to yield ATP

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6
Q

How is excess glucose, FAs and AAs stored?

A

Excess glucose

  • Stored in the liver and skeletal muscle as glycogen
  • Once glycogen stores are full, any extra glucose -> free FAs and glycerol for the synthesis of triglycerides (occurs in adipose tissue)

Excess FA
- Stored as triglycerides

Excess AA
- Excess not needed for protein synthesis are not stored and are instead used for structural proteins or converted to glucose and FA for eventual storage as triglycerides

~ Excess nutrients are usually stored as triglycerides in adipose tissue. When needed energy —(catabolism)—> FFA and glycerol

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7
Q

The body has 2 functional metabolic states. What are they?

A

Absorptive state

  • During this, anabolism dominates as ingested food -> digested and absorbed -> circulation
  • Ingested simple carbs -> converted in the liver to glucose -> released to be available as fuel or stored as glycogen
  • Ingested fats and proteins = immediately used or stored

Postabsorptive state

  • During this, several hrs after ingesting food, cartabolism dominates
  • Glycogen stores in liver and skeletal muscle become primary energy source
  • If this state persists, glycogen alone can’t meet the body’s needs, so lipolysis occurs to break down triglycerides
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8
Q

What are some other energy sources?

A

Glycerol

  • Comes from backbone of triglycerides when they’re broken down
  • Can be converted to glucose by the liver

Lactic acid

  • Can be formed by glycolysis
  • Can also be converted to glucoose by the liver

Ketone bodies

  • Group of compounds produced in the liver in times of glucose shortages
  • When liver uses FFAs as energy, they are oxidized to acetyl CoA, which doesnt produce any additional energy through the citric acid cycle
  • Acetyl CoA -> converted to ketone bodies -> released into blood
  • In times of starvation, the brain can use ketone bodies, instead of glucose as an energy source
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9
Q

What is the pancreas?

A

It’s an organ that has both exocrine (glands that secrete their products through ducts opening onto an epithelium instead of directly into the bloodstream) and endocrine functions (plays a role in determining the body’s metabolic state).

  • Exocrine important for digestion
  • Exocrine function of the pancreas are localized to the Islets of Langerhaans which are clusters of cells found throughout the pancreas.
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10
Q

What are the major types of cells in the islets of Longerhoans

A
  • a-cells -> produce and secrete glucagon
  • B-cells: produce and secret insulin
  • Delta cell: produce and secrete somatostatin
  • Pancreatic polypeptide (PP) cell: plays a role in reducing appetite
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11
Q

What is the purpose of somatostatin? Where is it stored, produced and released?

A

In response to circulating glucose and AAs following a meal, the δ cells release somatostatin.

The effect is to slow down the digestive system to inhibit digestion and absorption of nutrients. It works in a negative-feedback way to prevent too many nutrients from being absorbed.

It’s stored in the pancreas. It’s produced in the cells lining the digestive tract, where it acts as a paracrine hormone (hormone that has effect only in the vicinity of the gland secreting it) to inhibit digestion. It’s released by the hypothalamus where it inhibits the secretion of GH and TSH

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12
Q

What is insulin? What does it do?

A

It’s a small peptide hormone produced by B-cells of the pancreatic islets. It’s the dom hormone in the absorptive state and plays a major role in anabolism.

It regulates blood sugar (effects carbs), and it also has an effect on fats and proteins.

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13
Q

What are the factors that influence blood glucose conc? **

A

Factors that incr blood glucose
- Glucose absorption from the digestive tract
- Hepatic glucose production:
• Through glycogenolysis of stored glycogen
• Through gluconeogenesis

Factors that decr blood glucose
- Transport of glucose into cells:
• For utilization for energy production
• For storage as glycogen through glyconeogenesis
• For storage as triglycerides
- Urinary excretion of glucose (occurs only abnormally, when blood glucose level becomes so high it exceeds the reabsorptive capacity of kidney tubules during urine formation).

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14
Q

Discuss the effect insulin has on carbohydrates? (4)

A

1) Increase the uptake of glucose into most cells
- Insulin causes movement of GLUT-4 glucose transporters from an intracellular pool -> plasma membrane where they begin to transport glucose -> cells
- Brain doesnt require it since it has GLUT-1 and GLUT-3 glucose transporters in the plasma membrane
- Exercising skeletal muscles are also able to take up glucose
independent of insulin.
- Liver uptake of glucose is by GLUT-2 is also insulin-independent.

2) Stimulate glycogenesis in skeletal muscle and the liver
- This promotes the storage of glucose as glycogen.

3) Inhibit glycogenolysis in the liver
- This prevents the catabolism of glycogen and further promotes glucose storage.

4) Inhibit gluconeogenesis in the liver
- This prevents the formation of glucose from amino acids.

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15
Q

Discuss the effect insulin has on fats? (4) **

A
  1. Enhances the entry of fatty acids into adipose tissue cells
  2. Increases GLUT-4 recruitment in adipose cells to increase glucose uptake for the synthesis of
    triglycerides
  3. Enhances the activity of the enzymes involved in synthesizing triglycerides
  4. Inhibits lipolysis
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16
Q

Discuss the effect insulin has on proteins? (3) **

A
  1. Promotes the uptake of amino acids into all tissues.
  2. Enhances the activity of the enzymes involved in protein synthesis.
  3. Inhibits the degradation of proteins.
17
Q

Using what you have learned so far about the effects of insulin in the body and any trends
you’ve noticed in hormonal regulation, predict how the secretion of insulin might be regulated.

A

Insulin secretion is directly related by the plasma glucose level with a negative-feedback system.

1) An incr of blood glucose stimulates islet B-cells -> secrete insulin. Insulin lowers blood glucose levels and secretion of insulin will stop (in this manner, nsulin promotes anabolism). During the absorptive state and the lack of insulin = catabolism during the postabsorptive state.
2) Insulin release can also be caused by a feedforward system. Gi hormones secreted by the digestive tract stimulate insulin release to prepare for the rise in blood glucose about to happen.

3) The cells of the islets of Langerhans are innervated by the ANS. The presence of food in the digestive system -> activates PNS in a
feedforward manner. The SNS has the opposite effect to decr insulin
secretion (allows blood glucose levels to incr during fight-or-flight or while exercising).

18
Q

What is glucagon?

A

It’s the major pancreatic hormone involved during the postabsorptive state.

19
Q

How is glucagon secretion triggered? Where is its major site of action?

A

The secretion of glucagon is triggered directly by the decr in blood glucose levels.

Its major site of
action is the liver, where its effects are the direct opposite of insulin.

20
Q

Discuss the effects of glucagon on carbs, fats and proteins.

A

Effects on Carbohydrates
- Glucagon incr hepatic glucose production by decr glycogen synthesis, enhancing both
glycogenolysis and gluconeogenesis.

Effects on Fats
- Glucagon promotes lipolysis while inhibiting fat storage. It also enhances the formation of ketone
bodies in the liver.

Effects on Proteins
- Glucagon promotes protein catabolism but only in the liver.

21
Q

True or false: Fluctuations in blood fatty acid concentration result in the same pattern of insulin and glucagon
release as changes in blood sugar concentration.

A

True

However, a rise in blood AA concentration stimulates the release of both insulin and glucagon. B/c the hyperglycaemic effects of glucagon counteract the hypoglycaemic actions of insulin, the net result is maintenance of normal blood glucose level following a high protein, low carbohydrate
meal.