Endocrine Pancreas Flashcards
(25 cards)
Insulin receptors are inc in ….& dec in….
Starvation
Obesity
GLUT4 move in cell membrane independent of insulin in response to……
Exercise
The major insulin independent organs are……
Brain, liver, RBCs, epithelial cells of kidney & intestine
Describe effects of insulin on CHO metabolism
- Facilitation of glucose transport into the cells of insulin-senisitive tissues
- Stimulation of glycogenesis by activating glycogen synthase
- Inhibition of gluconeogenesis & glycogenolysis (by inhibiting glycogen phosphorylase
How does insulin inc liver glucose uptake?
Induces glucokinase which induces phorphorylation of glucose so free glucose remains low facilitating glucose entry into cells.
Describe effects of insulin on fat metabolism
- Lowers blood fatty acids
- Promotes triglyceride storage (by inc glucose transport to adipose tissue forming a-glycerol phosphate, inc transport of FFA from blood to adipose tissue by activating lipoprotein lipase)
- Inhibits lipolysis by inhibiting intracellular HSL
Describe effects of insulin on protein metabolism
- Lowers blood amino acids level
- Inc protein synthesis (inc AA uptake & incorporation in proteins by stimulating cell’s protein-synthesizing machinery
- Inhibits protein catabolism
THUS, essential for normal growth
With respect electrolytes, insulin causes…….
K+ entry to cells
Describe principal actions of insulin on muscle
- Inc glucose entry & glycogenesis, dec glycogenolysis
- Inc AA uptake & protein synthesis, dec degradation
- Inc K+ entry to cells
Describe principal actions of insulin on liver
- Inc glucose entry & glycogenesis, dec glycogenolysis & gluconeogenesis
- Inc AA uptake & protein synthesis, dec degradation
- Inc K+ entry to cells
- Inc lipid synthesis, dec ketogenesis
Describe principal actions of insulin on adipose tissue
Inc glucose entry
Inc synthesis of glycerol phosphate, triglycerides & fatty acids.
Activate LPL, inhibit HSL
Inc K+ entry to cells
The primary control of insulin secretion is……
Direct -ve feedback system between B-cells & conc of blood glucose
Metabolism of pyruvate via TCA causes inc……, explain its effects on insulin
Glutamate, appears to act on 2nd pool of secretory granules committing them to the releasable form, it may act by dec pH which is a necessary step in secretory granules maturation, thus it is responsible for prolonged phase of insulin response to glucose (2nd messenger).
AAs that stupimulate insulin
Arginine & lysine
L-arginine also by NO
Mention the “incretins” & their role
They ar degraded by….
GIP, GLP-1
They enhance the rate of insulin release from pancreatic B cells to inc plasma glucose level, they cause anticipatory inc in blood insulin in preparation for glucose & AAs to be absorbed from the meal.
DPP-4
Describe effect of ANS on insulin secretion
Parasympathetic stimulatory to insulin by M4
Sympathetic inhibitiry by a2 (b2 is present & stimulatory but its effect is weaker than a2, thus net effect is inhibition)
Describe effects of other hormones on insulin
- Glucagon inc it by inc cAMP in B cells & also by caused by hyperglycemia
- Somatostatin is inhibitory
- Cortisol, GH, estrogen & progesterone diretly either inc insulin secretion or potentiate its glucose stimulus.
Describe effects on insulin of each:
1. Leptin
2. cAMP
- Dec food intake & inhibit insulin release
- Inc insulin secretion, caused by b-agonists, glucagon, theophyline
Describe phases of hypoglycemia & its treatment
- Sympathetic overactivity (less than 70mg%): tremors, nervousness, tachycardia, palpitations, sweating, dilated pupil, in BP
- CNS symptoms (less than 40mg%): due to neuroglycopenia: confusion, weakness, dizziness & convulsions
- Brainstem phase (less than 20mg%): coma
TTT: IV/oral glucose + IV glucagon
Mention metabolic functions of glucagon
- Hyperglycemia by glycogenolysis & gluconeogenesis
- Lipolytic, inc FFA & glycerol release & inc ketoacid formation
- Inc ureagenesis due to inc gluconeogenesis
- Other: enhance myocardial contractility, facilitates secretion of GH, inuslin & pancreatic somatostatin
Describe control of glucagon secretion
- Dec in blood glucose inc secretion & vice versa
- AA inc stimulates it esp alanine & arginie
- Hormones:
Somatostatin, secretin, insulin: inhibit
CCK, gastrin: stimulate - Vagal stimulate, sympathetic stimulate (a2 & b2 are present but b2 are predominant)
- Exercise: can inc 4 or 5-fold by b-adrenergic stimulation
- Infections, toxemia, burns, surgery are stimulatory (symoathetic activity)
I/G molar ratio is…..in balanced diet, …..in 3 days of starvation, ……in continuous glucose infusion.
2.3
0.4
25
Describe actions & mentions stimulants of pancreatic somatostatins
- Inhibit insulin & glucagon secretion
- Dec GIT secretion & delays gastric emptying
Stimulated by high blood glucose & AAs, glucagon, CCK.
Describe effects of the following on glucose homeostasis:
1. CAs
2. Glucocorticoids
- Inhibit insulin & inc glucagon, stimulate glycogenolysis & gluconeogenesis
- Stimulate gluconeogenesis & cause insulin resistance