L21: Endocrine+Pancreas Flashcards by Jeri Sheldon (AZ PA Mast 20)

Islet of langerhans

endocrine cells in a sea of exocrine tissue (the rest of the pancreas)

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beta cells produce

insulin, amylin

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alpha cells produce

glucagon

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delta cells produce

somatostatin (14 amino acid polypeptide hormone)

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gamma cells produce

pancreatic polypeptide

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epsilon cells produce

ghrelin

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amylin

acts on the CNS to suppress appetite

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somatostatin

inhibits digestive function

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pancreatic polypeptide

putatively reduces appetite and food intake

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ghrelin

appetite stimulating

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Stimulate insulin secretion

GI hormones (incretins)
PNS
Increased blood glucose and amino acid concentration

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Inhibits insulin secretion

Epinephrine

Sympathetic stimulation: alpha-adrenergic

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Cleaved off proinsulin during post-translational processing

C-peptide

a marker of insulin production/beta cell function

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inside of secretory granule of insulin

Insulin
C peptide
small amounts of proinsulin

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how does glucose enter beta cells?

GLUT-2

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once inside beta cells, glucose

is phosphorylated to Glucose-6-phosphate (trapped)

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Oxidation of glucose-6-phosphate yields

ATP

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ATP in beta cells causes

K+ channel to close: decreased K+ flux: depolarization

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depolarization of the beta cell membrane causes

voltage gated calcium channels to open

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Trigger for exocytosis of insulin vesicles

increased intracellular calcium

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effects of insulin on carbohydrates

decrease blood glucose

increase storage

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effects of insulin on lipids

decreased blood fatty acids

increased storage

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effects of insulin on proteins

decreased blood amino acids

increased storage

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glucose is stored as

glycogen

triglycerides

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amino acids are stored as

protein

GLUT1

transports glucose across blood brain barrier

GLUT2

transports glucose in kidney and intestines

GLUT3

transports glucose into neurons

GLUT4

insulin-dependent transporter in adipose tissue and resting muscle cells insulin binds-->second messengers --> GLUT4 brought to surface of cell

HbA1C value which reflects above average blood glucose over previous 3 months

>6.5%

glucosuria

glucose in urine since elevated glucose exceeds what tubular cells can reabsorb causes osmotic diuresis

Polyphagia

increased appetite due to decreased intracellular glucose

Polydipsia

increased thirst

ketone bodies cause metabolic acidosis, the body compensates by

Respiratory ventilation to blow CO2 off and bring pH back up

lack of insulin shifts metabolism towards

more protein catabolism (muscle atrophy), amino acids in bloodstream

excess blood amino acids cause

shift to gluconeogenesis in liver, making hyperglycemia worse

2 ways by which hypoglycemia may occur

1. Insulin overdose | 2. Reactive hypoglycemia

Reactive hypoglycemia

in extreme response to glucose, beta cells release too much insulin

Reactive hypoglycemia shouldn't be treated by

eating sugar, will worsen problem

Glucagon is inhibited by

``` High glucose Somatostatin insulin fatty acids ketoacids ```

Glucagon is stimulated by

``` *Low glucose* Epinephrine (B2) Vagal stimulation CCK fasting exercise increased dietary protein (arginine) in absence of carbs ```

Glucagon

14 amino acid polypeptide

a meal which is a combination of protein and carbs

has no effect on glucagon

Glucagon is produced as

Proglucagon--> glucagon, incretin (GLP1)

Incretin (GLP1)

released from intestine in response to high glucose in intestinal lumen increases insulin release

Glucagon effects

targets liver to stimulate hepatic glucose output opposite of insulin adipose tissue: pro-lipolytic effect

Glucagon effects on carbohydrates and lipids

increased blood glucose, fatty acids, and ketones

Glucagon effects on blood amino acids

minimal hepatic protein degradation is used for gluconeogenesis, not to release amino acids to blood no effect on skeletal muscles

Somatostatin release is stimulated by

High fat, carbs, and protein rich meals

Somatostatin receptors

SSTR2 | found on both beta and alpha cells

Somatostatin effects on pancreas

inhibits release of both insulin and glucagon by hyperpolarizing alpha/beta cells

Somatostatin GI effects

"generalized inhibitory"

Somatostatin on the hypothalamus

brain peptide, released into median eminence Inhibits release of GH by anterior pituitary

which hormone is decidedly not diabetogenic

Thyroid hormone | onset is too slow

Hormones which are diabetogenic

*Glucagon* Epinephrine Cortisol GH+IGF-1

the brain

senses nutrients and hormones (insulin, leptin, GLP-1) associated with nutrient levels

Epi and blood glucose

Increases glycogenolysis, gluconeogenesis Increases glucagon, decreased insulin (a-adrenergic stimulation of beta cells)

Cortisol and blood glucose

Increased gluconeogenesis | Increased glucose sparing (decreased uptake besides brain)

Cortisol on the liver, early stage fasting:

promotes glycogenolysis

Cortisol on the liver, late stage fasting:

promotes glycogen synthesis

Growth hormone effect on blood glucose

glucose sparing

Growth hormone effect on fatty acids

increased lipolysis

Growth hormone effect on amino acids

Increased uptake into cells, decreased blood

Growth hormone effect on muscle protein

Increased synthesis, increased DNA and RNA synthesis | decreased degradation

Growth hormone released during

sleep exercise stress hypoglycemia

brain detects glucose in

Arcuate nucleus

Hypothalamus and glucose homeostasis

Insulin and glucagon secretion Hepatic glucose output Glucose uptake by skeletal muscles