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Physiology 2 > Endocrine Pancreas Physiology > Flashcards

Endocrine Pancreas Physiology Flashcards

1
Q

Exocrine Pancreas

A

Acinar cells and duct cells
Involved in GI function
Secretes enzymes into the lumen of the duodenum

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2
Q

Endocrine Pancreas

A

Organized in islets of langerhans
2-3% of the pancreas
Richly innervated by both vagal parasympathetic system and splanchnic sympathetic fibers

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3
Q

Islets of Langerhans cell types

A

Alpha (20%)- glucagon
Beta (70%)- insulin
Delta (5%) - somatostatin
F (5%) Pancreatic polypeptide

All hormones are involved in glucose metabolism

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4
Q

Insulin

A

A polypeptide hormone produced produced by beta cells in response to hyperglycemia

Like other peptide hormones, is synthesized as a larger molecule inside of the golgi apparatus and packages into secretory granules awaiting secretion

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5
Q

Insulin synthesis and secretion

A
  1. Messenger RNA on the ribosome of the ER binds aa into a peptide chain called a preprohormone. The chain is directed into the ER lumen by a signal sequence of aa
  2. Enzymes in the ER chop off the signal sequence, creating an inactive pro hormone
  3. The pro hormone passes from the ER through the golgi
  4. Secretory vesicles containing enzymes and pro hormone bud off the golgi. The enzymes chop the prohormon into one or more active peptides plus additional peptide fragments
  5. The secretory vesicles releases its contents by exocytosis into he extracellular space
  6. The hormone moves into the circulation for transport to its target
    C peptide and active insulin
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6
Q

Insuline chains

A

A protein consisting of 2 chains (alpha and beta) connected by 2 disulfide bridges

Differences in aa sequences between species are small

  • Cattle, sheep, horses, dogs, and whales differ only in positions 8, 9, and 10 of the alpha chain
  • Porcine differs from Human by 1 aa
  • Bovine from cat by 1 aa
  • Porcine and canine are the same
  • Human from cat by 4 aa
  • Porcine from human by 1 aa
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7
Q

Influences on insulin release

A

Several nutritional, neural, paracrine, and endocrine variables govern insulin release
-secretagogues for insulin vary by species

  • -Glucose in omnivores
    • Amino acids in carnivores
  • -fatty acids
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8
Q

Factors affecting insulin secretion

A

Stimulatory:
Nutrients- Glucose, aa, FA, and ketones
Hormones- Growth Hormone, glucagon

Inhibitory:
Hormones- Adrenocorticosteroids, somatostatin, adrenalin, noradrenalin

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9
Q

Insulin secretion

A

Biphasic secretion kinetics
Acute phase: involves the release of preformed insulin
Chronic phase: involves the synthesis of protein

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10
Q

How is insulin released form B cells

A

Beta cells have a glucose transporter (GLUT2) in the membrane surface
Allows glucose to diffuse freely into the cell
ECF glucose concentration directly affects glucose concentration inside the beta cell
An increase in blood glucose concentration leads to insulin secretion and synthesis

Increase in Glucose into the cell through GLUT 2 leads to increase in ATP production.
This inhibits K ATPase- causes depolarization.
Voltage gated Ca channels open and Ca2+ activates insulin gene expression via CREB. Exocytosis of stored insulin

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11
Q

How does insulin act on target cells

A

After release, insulin binds to a specific membrane receptor on target tissues known as the insulin receptor or insulin receptor tyrosine kinase
2 insulin binds to receptors and form a dimer that activates cell responses

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12
Q

Most important insulin-sensitive tissues

A

Liver
Muscle
Fat

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13
Q

Physiological effect of insulin

A

Lower blood concentration of glucose, fatty acids, and amino acids
Promoting intracellular conversion of these compounds to their storage forms: Glycogen, Triglycerides, Proteins

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14
Q

Insulin Mediated Simulation via GLUT 4

A

Insulin binds to insulin receptor- dimer is formed
Insulin signal pathways activated: effects of protein metabolism, Effects on growth, Effects on lipid metabolism

Also causes translocation of GLUT4 vesicle to the cell membrane to allow glucose to enter the cell

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15
Q

Non-insulin mediated stimulation of GLUT 4

A

Exercise-responsive GLUT 4 containing vesicles

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16
Q

Insulin action of fat

A

Insulin facilitates glucose entry into cells by increasing the number of specific glucose transporters (GLUT 4) in the cell membrane
GLUT 4 is the only insulin sensitive

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17
Q

Insulin action on muscle

A

Smooth, striated and cardiac muscle
Stimulates glycogen synthesis enzymes
-promoting storage of glucose molecules in the form of glycogen
Promotes the use of glucose as a fuel source
-reduces fatty acid oxidation
-in the absence of insulin muscle rely more on fatty acids as a fuel source
Enhances amino acid uptake which promotes muscle growth

Increase glucose transport
Increase glycogen synthesis
Decrease glycogenolysis
Increase aa uptake
Increase protein synthesis
Decrease protein degradation
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18
Q

Insulin action on adipose tissue

A

Increase glucose transport and consequently:
Glycerol formation- combines with fatty acids delivered to adipose tissue to form triglycerides
-fatty acids come from very low density lipoproteins (VLDL) produced in the liver
Glycogen synthesis

Insulin inhibits lipolysis which promotes adipose deposition

Increase glucose transport
Increase glycogen synthesis
Decrease glycogenolysis
Increase lipogenesis
Decrease lipolysis
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19
Q

Insulin action on liver

A

Promotes fatty acid synthesis in hepatocytes
-stimulates incorporation of those fatty acids and triglycerides into lipoprotein-bound vesicles such as VLDL for transport to adipocytes

Increase glycogen synthesis 
Decrease glycogenolysis
Decrease gluconeogenesis
Increase lipogenesis
Decrease lipolysis
Decrease gluconeogenesis
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20
Q

Insulin inactivation

A

Is metabolized mainly by the liver and kidneys
Specific enzymes reduced the disulfide bonds
Chains are subjected to protease activity
-reduce them to peptides and amino acids
Half life is about 10 minutes

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21
Q

Glucose homeostasis summary

A

Consumption of carbohydrate, fat, protein
Insulin release
Carbohydrates main source of energy for cells
Excess stored as glycogen fat (in liver, fat, muscles)
Release of glucagon and epinephrin
Hepatic glycogenolysis
Release of cortisones and GH
Gluconeogenesis- production of glucose from glycerol, aa, and lactate
Reduced glucose uptake on cells- fat is used as energy source except in brain

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22
Q

Which hormones counteract the efforts of insulin

A

Glucagon (acute phase)
Epinephrin/norepinephrin (acute phase)
Cortisol (Chronic Phase)
Growth hormone (Chronic Phase)

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23
Q

Glucagon

A

Is a polypeptide hormone consisting of 29 amino acids produced in the alpha cells of the pancreatic islets
Close relationship with insulin
Considerable homology between species
Half life of 5 minutes

Glucagon is encoded by the proglucagon gene which is located not only in alpha cells but also other cells of the body

  • A large peptide is first produced= proglucagon
  • Proglucagon is cleaves in alpha cells to form glucagon
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24
Q

Glucagon synthesis

A

Mainy stimulated by decreased glucose concentration- hypoglycemia
The secretion is triggered when levels of glucose decline below threshold, which differs between species
Opposed most insulin actions to help maintain blood glucose concentration
-glucagon is one of the counter regulatory hormones

Synthesized in a manner similar to insulin:
Membrane depolarization is independent from K channels
Secretion is promoted via voltage-dependent sodium and calcium channels
-depolarization increased calcium influx
-glucagon is released by exocytosis

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25
Q

G protein coupled receptors

A 
After secretion, glucagon binds to G protein couples receptors in the target tissues
Liver
Adipocytes
Kidney
Heart
Brain
GI tract
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26
Q

Blood glucose

A

Insulin decreases blood glucose

Glucagon increases

27
Q

Glucagon pt 2

A

Glucagon is not always an opposing hormone to insulin
Protein ingestion stimulates both insulin and glucose release
-specially the aa alanine and arginine
-Important feature in obligate carnivores
-Insulin released in response to increased amino acid levels –> lower glucose concentration
-Glucagon promotes rapid conversion of the amino acids to glucose by stimulating gluconeogenesis

28
Q

Glucagon action in the liver

A

Leads to the activation or inactivation of specific liver enzymes
Main effect is centered in the liver and enhances the availability of glucose to other cells of the body
1. decrease glycogen synthesis
–inhibition of glycogen synthase
2. breakdown of liver glycogen-glycogenolysis
–activation of glycogen phosphorylase
3. increase in liver gluconeogenesis
All increase blood glucose

29
Q

Glucagon action in adipose tissue

A

Activates hormone sensitive lipase in adipocytes
Promotes breakdown of fat- lipolysis
Increase availability of fatty acids to tissues (energy source)
Also inhibits storage of triacylglycerol in the liver
-help make additional amounts of fatty acids available for other tissues

30
Q

Activation of hormone sensitive lipases

A

Epinephrin or glucagon binds to GPCR
HSL activates and leads to glycerol and liver gluconeogenesis
HSL also leads to FA which is a source of energy for tissues in the absence of glucose

31
Q

Pancreatic somatostatin

A

Produced by delta cells
-in the same way as other protein hormones
Inhibitory actions
-decreases motility and secretory activity of GI tract
-Inhibits secretion of all endocrine cell types of the islet of langerhans (glucagon is more affected than insulin)

32
Q

Pancreatic polypeptide

A

Produced by F or PP cells
-secretion is stimulated by GI hormones, vagal stimulation and protein ingestion
-Inhibition occurs through somatostatin
Effects are directed toward the GI tract
-Decrease gut motility and gastric emptying
-Inhibits secretion of pancreatic enzymes and the contraction of gallbladder

33
Q

Diabetes Mellitus

A

Lack or deficiency of insulin
Can be absolute or relative
Absolute= absence of insulin= type 1
Relative= insulin is not working properly= type 2

Causes blood glucose to increase. Glucose uptake from insulin sensitive tissues will be compromised

34
Q

Insulin directly inhibits glucagon release by binding to what receptor and cell type

A

Insulin receptor

Alpha cells

35
Q

Diabetes Mellitus affects glucagon

A

Insulin deficiency has effects on glucagon production
Insulin directly inhibits glucagon release by binding to the insulin receptor on alpha cells
Glucagon stimulates insulin secretion directly
-by binding to insulins receptor on the beta cell
-also stimulates indirectly though induction hyperglycemia by glycogenolysis and gluconeogenesis

36
Q

Diabetes Mellitus affects adipose tissue

A

Insulin deficiency causes lipolysis of storage fat and release FFA
The enzyme hormone sensitive lipase (HSL) is strongly activated
-hydrolysis of stored triglycerides occurs releasing large amounts of FFA and glycerol in the blood. FFA will be used as a source of energy in the absence of glucose
-Excess FFA will be converted into phospholipids and cholesterol
-Triglycerides will be formed at the same time in liver. An increase in blood lipids is expected in any diabetic patient

Insulin inhibits HSL while glucagon activates it
HSL is highly expressed in adipose tissue and steroidogenic tissue

37
Q

Dibetes Mellitus

A

Insulin deficiency causes protein depletion and increased plasma amino acids
-catabolism of protein increases and protein synthesis stops
Amino acids in the blood will be used as: a direct energy source in the liver or a substrate for gluconeogenesis

38
Q

Insuline deficiency (absolute or relative)

A

Increase in glucagon
Hepatic gluconeogenesis
Hyperglycemia

Compromised glucose transport in the muscle and adipose tissue
Protein and fat catabolism
AA and glycerol in blood
Hepatic gluconeogenesis
Hyperglycemia
39
Q

Insulin deficiency

A

Glucose does not enter the satiety center: Poliphagia

Catabolic state: weight loss

Increase in blood glucose levels: hyperglycemia
Exceed renal tubular threshold: glycosuria
Osmotic diuresis: Polyuria
Compensatory: Polydipsia

40
Q

Type I diabetes

A

Characterized by permanent hypoinsulinemia
Absolute deficiency
-no increase in endogenous insulin after stimulation; absolute necessity for exogenous insulin to maintain control of glycemic, avoid ketoacidosis and survive
Common in dogs (95% of cases)

41
Q

Cataracts in dogs

A

The most common long term complication
Related with altered osmotic relationships in the lens induced by accumulation of sorbitol and galactitol

Sugar alcohols produced following reduction of glucose and galactose by the enzyme Aldose reductase in the lens
Potent hydrophilic agents causing influx of water
-swelling and rupture of the lens fibers

42
Q

Type II diabetes mellitus

A

Characterized by the resistance to the metabolic effects of insulin
Relative deficiency: it is a combination of impaired insulin action in liver, muscle and adipose tissue (insulin resistance) and beta cell failure
Common in cats (80% if cases)

43
Q

Type II diabetes in cats

A

For diabetes to develop, there must be a beta cell dysfunction
-healthy beta cells can adapt to obesity and insulin resistance by increasing insulin secretion

Amylin (or islet amyloid polypeptid IAPP)

  • it is a polypeptide produced and secreted by beta cells together with insulin secretion
  • increases satiety, decreases gastric empty and reduced glucagon production

Only humans, cats, and non human primates have an amyloidogenic aa structure with the potential to form amyloid depositions within the islets

44
Q

Islets of Langerhans amyloidosis

A

When allying aggregates it forms the amyloid
The amyloid deposition within the pancreatic islets is called amyloidosis
The deposition is toxic to beta cells and leads to beta cell dysfunction

45
Q

Common causes of insulin resistance in cats

A 
OBESITY
cushing
infection
pancreatitis
Hyperthyroidism
renal failure
46
Q

Obese cat insulin resistance

A

Hormone action is compromised
Pancreas will compensate producing more insulin
OVER TIME
Initiates the lost of capacity to compensate (B cell)
Glucose levels cannot be maintained in the normal range
Glucose intolerance
When the levels of insulin start to decrease
Sever hyperglycemia and diabetes mellitus

47
Q

Type 2 diabetes in cats

A 
Clinical remission can occur
Clinical signs disappear, blood glucose concentration normalizes and insulin treatment or other anti diabetic drug can be discontinued
Depends on beta cell dysfunction
Irreversible damage: amyloidosis
Reversible damage: glucotoxicity
48
Q

Diabetic neuropathy

A 
One of the most common chronic complications
Hyperglycemia leads to nerve injury
-in shawn cells and axons of myelinated fibers
-microvascular abnormalities
Pathogenesis is not completely understood
Clinical signs range from mild to severe
-limb weakness
-difficulty jumpin
-base-narrow gait
-ataxia
-muscle atrophy in pelvic limbs
-plantigrade posture
-postural reaction deficits
-decreased tendon reflexes
-irritability when feet are touched
49
Q

What diagnostic methods could we use to detect ketoacidosis in dogs

A

Measuring Beta-hydroxybutyrate in the serum of dogs

Using a urine dipstick to measure acetoacetic acid and acetone

50
Q

Diabetic ketoacidosis

A

Sever complication of diabetes mellitus
Results in unrestrained ketone body formation in the liver, metabolic acidosis, severe dehydration, shock, and possibly death

Before the availability of insulin DKA was fatal

51
Q

Keton bodies

A

Derived from oxidation of free fatty acids by the liver
Used as an energy source by many tissues during periods of glucose deficiency
-oxidation of FFAs leads to the production of acetoacetate
-in the presence of NADH, acetoacetate is reduced to B-hydroxybutyrate
-acetone is formed by the spontaneous decarboxylation of acetoacetate

Excessive production results in ketosis and ketoacidosis

Insulin deficiency increases FFAs release from adipocytes, thus increasing the availability of FFAs to the liver and in turn promoting ketogenesis. Also reduced the peripheral utilization of glucose and ketones

52
Q

Keton bodies synthesis

A

For the synthesis of ketone bodies to be enhances, there must be two major alterations in intermediary metabolism

  1. increased mobilization of FFAs from triglycerides stored in adipose tissue
  2. A shift in hepatic metabolism from fat synthesis to fat oxidation and ketogenesis
53
Q

Counterregulatory hormones

A

The body increases production in response to a wide variety of diseases and stress situations- this response is usually beneficial
Circulating levels are typically markedly elevated in DKA
-insulin resistance
-stimulation of lypolisis and the generation of FFAs
-Shift the hepatic metabolism to fat oxidation and ketogenesis

54
Q

Diabetic ketoacidosis and counter regulatory hormones

A

Glucagon is considered the most influential ketogenic hormone
-epinephrin also stimulates through stimulation of lypolysis
Both glucagon and epinephrin contribute to insulin resistance
-by inhibiting insulin-mediated glucose uptake in muscle
-by simulating hepatic glucose production through glycogenolysis and gluconeogenesis

Cortison and GH
-enhance lipolysis in the presence of insulin deficienct
-block insulin action in peripheral tissues
-potentiate the stimulating effect of glucagon and epinephrin on hepatic glucose output
The combination of insulin deficiency and excess in counter regulatory hormones also leads to protein catabolism
-impairs insulin action in muscle
-provide substrate to drive gluconeogensis

55
Q

Chronic insulin deficiency

A

Increase glucose and ketone bodies
Osmotic diuresis: glycosuria, ketonuria
Loss of water, K, Na, and PO4
Dehydration

Increase glucose and ketone bodies
Decrease in pH: metabolic acidosis- increase anion gap
Hyperventilation, nausea vomiting OR increase K loss
Dehydration

56
Q

Worsening hyperglycemia and ketonemia

A

Leads to acidosis, fluid depletion, and hypotension
Influence the progression of DKA in a self-perpetuating spiral of metabolic decompensation
Coexisting disorders increase the secretion of counter regulatory hormones
-pancreatitis
-infection
-CKD
-hormonal disorders

57
Q

Diabetic ketoacidosis acid base status

A

Acidosis results form excess accumulation of kenos in the blood
-overwhem the bodys buffering system
Increase in H concentration

Failure of kidney to compensate in DKA is partly a result of the physiochemical properties of B hydrocybutyrate and acetoacetate

  • renal threshold is low- the amount exceed the kidney capacity: potentiates loss of water and electrolytes
  • They are relatively strong acids and are excreted mostly as sodium and potassium salts- concomitant loss of bicarb
58
Q

Diabetic ketoacidosis: Sodium

A

Deficit in total body sodium
Excessive urinary loss caused by osmotic diuresis
Insulin enhances renal sodium reabsorption in the distal portion of the nephron
-insulin deficiency increases sodium wasting
glucagon, vomiting, and diarrhea also contribute

59
Q

Diabetic ketoacidosis: potassium

A

Deficit in total body potassium
Increase in plasma and ECF tonicity in DKA leads to shift of water out of the cells and shift of K out of cells
K shift is enhanced by the presence of acidosis and the breakdown of intracellular protein secondary to insulin deficiency
Entry of K into cells is also impaired in the presence of insulinopenia
Osmotic diuresis causes marked urinary losses of K
Secondary hyperalsodteroneism augment the K deficit

60
Q

Diabetic ketoacidosis: phosphate

A

Deficit in total body phosphate
Phosphate along with K, shift from the intracellular to extracellular compartment in response to hyperglycemia and hyperosmolality
Osmotic diuresis also leads to enhanced urinary phosphate loss

61
Q

Hypervolemia and Hemoconcentration

A

Metabolic stress: increase glucagon, cortisol, GH. Increase gluconeogeneis, proteolysis and insulin resistance

Prerenal azotemia: increase H and K concentrations

Hyperviscosity: trombosis, CNS, renal vein

Shock: acute tubular necrosis, lactic acidosis

Increase Aldosterone: K loss

Increase catecholamines: Increase lipolysis, ketogenesis, glucose production, leucocytosis, insulin resistance

62
Q

Insulinoma

A

Malignant functional pancreatic tumors of the pancreatic B cells: occurs primarily in dogs, ferrets, and rare in cats
Neoplastic B cells synthesize and secrete insulin independent of the normal suppressive effect of hypoglycemia
-results in potentially life-threatening periods of hypoglycemia
-remember the brains only energy source is glucose

63
Q

Glucagonoma

A

Neoplasm of alpha cells
Insulin resistance- diabetes mellitus
Sever weight loss
Superficial necrolytic dermatitis

Physiology 2 (12 decks)

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