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Endocrine Signaling and Systems > Pancreas & Fuel Metabolism > Flashcards

Pancreas & Fuel Metabolism Flashcards

1
Q

What is anabolism?

A

[ARNIE]

SYNTHESIS of larger molecules from smaller

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2
Q

What is catabolism

A

DEGREDATION of large molecule into smaller molecules

(through hydrolysis, oxidation)

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3
Q

What is glycogenesis?

A

Glucose → glycogen

CONSEQUENCE = Decrease blood glucose

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4
Q

What is glycogenolysis?

A

Glycogen → glucose

CONSEQUENCE = Increase blood glucose

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5
Q

What is gluconeogenesis?

A

A.a’s → glucose

CONSEQUENCE = Increase blood glucose

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6
Q

What is protein synthesis?

A

A.a’s → protein

CONSEQUENCE = Decrease blood a.a’s

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7
Q

What is proteolysis? (protein degradation)

A

Protein → a.a’s

CONSEQUENCE = Increase blood a.a’s

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8
Q

What is lipogenesis? (fat synth.)

A

Fatty acids & glycerol → triglycerides (fat/lipids)

CONSEQUENCE = Decrease blood fatty acids

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9
Q

What is lipolysis? (fat degradation)

A

Triglycerides (fat/lipids) → fatty acids & glycerol

CONSEQUENCE = Increase blood fatty acids

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10
Q

What is the absorptive (FED) state?

A

UNDER THE INFLUENCE OF INSULIN

Glucose major source of energy.

–excess glucose stored in liver & muscle as glycogen

→HOWEVER, this gets ‘filled up’, THUS rest is converted into fatty acids & glycerol

–excess circulating fatty acids must be incorporated into triglycerides

–proteins are synthesised.

–excess circulating _a.a’_s converted to glucose & fatty acids (ultimately stored as triglycerides)

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11
Q

What is the postabsorptive (FASTED) state?

A

UNDER THE INFLUENCE OF GLUCAGON

Energy stores mobilised to provide energy.

(stops net synth. of glycogen, fat & protein)

–Glycogen degraded to glucose in liver & musle

–Catabolism of triglycerides into fatty acids & glycerol in adipose tissue is increased

–Glycerol reaching liver converted to glucose

–Many cells (e.g. aerobic muscle fibres) catabolise fatty acids (glucose sparing)

–Increased uptake a.a’s into liver, and gluconeogenesis maintains hepatic output of glucose.

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12
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A
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13
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A
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14
Q

What are the 2 (main) types of pancreatic endocrine cells?

A

Beta cells secrete insulin

→ DECREASE blood GLUCOSE

Alpha cells secrete glucagon

→ INCREASE blood GLUCOSE

[Delta (D) cells secrete somatostatin]

→ decrease gastric secretion, inhibit digestion of nutrients

[PP cells secrete pancreatic polypeptide]

→ an effect on appetite, & alterations to GI motility

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15
Q

How does glucose stim. insulin secretion?

A

Glucose entry → 

Oxidative metabolism →

↑ATP →

Inhibition of KATP channels →

depolarisation →

opening of voltage-­‐sensitive Ca2+ channels →

↑[Ca2+]i → 

insulin secretion

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16
Q
A
17
Q

How does the endocrine system regulate blood glucose?

A

When blood glucose lvls decrease, endocrine cells in pancreas SECRETE glucagon to stim. glucose release from liver & decrease secretion of insulin

18
Q

How does the nervous system regulate blood glucose?

A

Neurons in hypothalamus sense glucose lvls, & through nerve connections stim. release of adrenaline

19
Q

How many types of glucose transporters are there (the main types)?

Which are regulated by insulin?

A

GLUT 1-4

–GLUT 1, 2 & 3 are NOT regulated by insulin

–GLUT 4 regulated by insulin

20
Q

What is the function of GLUT 1?

A

Facilitates transport glucose across cell mem. of cells

(e.g. acrodd BBB)

21
Q

What is the function of GLUT 2?

A

Principal transporter for transfer glucose betw. liver & blood, and for renal glucose reabsorption

22
Q

What is the function of GLUT 3?

A

Main transporter of glucose into neurons

23
Q

What is the function of GLUT 4?

A

SKELETAL MUSCLE AND ADIPOSE CELLS

24
Q

What are the 3 main functions of insulin?

A

–Promotes glucose entry into skeletal muscle & adipose cells

–Promotes glucose utilisation

–Liver cells can store excess glucose as glycogen

25
Q

Give a brief summary of insulin’s actions in terms of carbs.

A
  1. Facilitates glucose uptake by most cells
  2. Stim. glucogenesis (liver & muscle)
  3. Inhibits glycogenolysis
  4. Inhibits gluconeogenesis (decreasing availability of a.a’s & inhibiting hepatic enzymes)
26
Q

Give a brief summary of insulin’s actions in terms of fats

A
  1. Increase glucose uptake into adipose
  2. fatty acid uptake into adipose
  3. Increase fatty acid synth. from glucose in adipose
  4. Decrease lipolysis in adipose
27
Q

Give a brief summary of insulin’s actions in terms of proteins

A
  1. Promotes active transport of a.a’s in muscle
  2. Increase protein synth.
28
Q
A
29
Q

What are the main actions of glucagon?

A

– Decreases glycogen synth. and promotes breakdown of stored glycogen within liver.

–Maintains hepatic output of glucose by stim. gluconeogenesis

– Promotes fat breakdown & inhibits triglyceride synth. (in adipose tissue)

–Also increases ketone production (ketogenesis) in liver (fatt acids to ketone bodies)

RESULT = increase blood fatty acid & ketone lvls

– Inhibits hepatic protein synth. & promotes hepatic protein degradation

30
Q

What is type 1 Diabetes Mellitus?

A

[10% people]

Destruction beta cells –>

no insulin secreted –>

chronic fasted state, ketoacidosis, glucosures, polyuria, polydipsia & can lead to coma & death

31
Q

What is type 2 Diabetes Mellitus?

A

[common in older & overweight individuals]

Gradual development insulin resistence (often due to R downregulation) & attenuation of meal-induced insulin secretion

32
Q

What are some complications of Diabetes Mellitus?

A

Microvascular

Macrovascular

–Hypertension (2o to renal failure)

–Atherosclerosis (due to abnormal lipid metabloism)

Peripheral neuropathies & ANS dysfunction

–impared cardiovascular reflexes

–impaired bladder control

–distal sensory neuropathy (decreased sensation in extremeties)

–gastroenteropathy (gastroparesis, constipation with episodes of diarrhoea).

Endocrine Signaling and Systems (7 decks)

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