regulation of glucose Flashcards
what are endocrine cells
-cells which are embedded in the pancreas called islets of langerhans
-endocrine tissue is only 1-2%
what are the islets main secretory cells
- beta (65%)
-alpha (20%)
-sdelta (10%)
what are other single/grouped endocrine cells
-F (PP/gamma) cells
-ε cells
-enterchromaffin cells
what are the secretory products of endocrine tissues
-beta cells- insulin (peptide hormone), proinsulin, C peptide, amylase (IAPP)
-alpha cells- glucagon
-delta cells- somatostatin
-F (PP) cels- pancreatic polypeptide
-ε cells- gherkin protein
-beta cells are most important as they secrete insulin
-glucagon has reversed effects of insulin
-together, insulin and glucagon regulate glucose, fatty acid and AA in blood
-somatostatin controls release of other hormones
-pancreatic polypeptide decreases exocrine pancreas secretion
-grehlin stimulates hunger
-serotonin very involved in blood hormone regulation
how does communication and control get controlled humorally
-small arteries enter islet core, distribute blood via fenestrated capillaries
-vascular arrangement- venous blood of one cell type bathes the other (paracrine as well as endocrine)
-richly perfumed with blood- metabolically active/ hormone release/ nutrient sensing
-vascular arrangement allows vein out of blood of one cell to bathe others
-metabolically active because they secrete large amounts of secretions
how does communication and control get controlled cell to cell
-gap junctions between beta and alpha cells
-delta cells send dendrite-like processes to beta cells
how does communication and control get controlled neurally
-islets are innervated by adrenergic, cholinergic and peptidergic neurones
-have sympathetic nerves coming in and parasympathetic
-ACh are mediators pf the nerve
-VIP is an example of peptidergic neurones
how is insulin secretion regulated
-regulated by islets beta receptors
-high blood glucose stimulates synthesis and secretion, low levels inhibits
-neural control- islets richly innervated:
=sympatehtic stimulation- beta-adrenergic increase secretion, alpha-adrenergic decrease (in exercise- prevents hypoglycaemia)
=parasympathetic (vagus- ACh) causes an increase release
-humoral factors, GIP (K cells of SI), amylase (beta cells), somatostatin (GI , pancreas, CNS, hypothalamus)
-drugs e.g. sulphoylureas action on Katp channels increasing secretion of insulin
how does a secretion go beta cells occur
-influx of calcium that triggers movement of vesicles which contain insulin towards membrane to fuse with membrane then it can leave via exocytosis
-secondary pathway= exocytosis o vesicles as well
-negative sign near somatostatin
how does insulin act as a receptor
-heterotetramer- alpha/beta and IC tyrosine kinase
-receptor activaation initaites a cascade of phosphorylation events substrates to activate or inhibit: PKC, phosphates, phospholipase, or G protein
-range of downstream effects- cell growth, proliferation, gene expression
-autophosphylates
-insulin- receptor complex internalised- downregulated
-high insulin levels leads to down regulation of receptors
how does insulin action help with blood glucose level
-decreases blood glucose concentration
-increased glucose transport into target cells by insertion of GLUT4
-GLUT4 fuse with membrane therefore now inserted
why is insulin known as the ‘ hormone of plenty’
-all body cells are targets but the liver and muscle tissues especially targeted to store glucose as glycogen (glycogenesis)
-increase glucose uptake into cells, when glycogen stores replenished, excess glucose converted into fat called lipogenesis
what’s insulin action like on the liver
-promotes formation of glycogen from glucose (glycogenesis)
-inhibits glycogenolysis
-inhibits gluconeogenesis
what’s insulin action like on muscle
4 major effects:
-promotes glucose uptake (increases GLUT4 transporters to plasma membrane )
-promotes glycogen synthesis from glucose
-promotes glycolysis and carbohydrate oxidation (little or no gluconeogenesis)
-promotes protein synthesis (anabolic) and inhibits protein breakdown, decreases blood AA concentration and increases uptake
what’s insulin action like on adipocytes
-increases GLUT4 transporters expression- rapid glucose uptake
-glucose converted to fatty acids- stored as triglycerides
-increase in lipoprotein lipase- liberates fatty acids for triglyceride synthesis
-insulin inhibits mobilisation and oxidation of fat stores
-therefore decreases circulating levels of fatty acids and keto acids
