Pancreas Flashcards
(26 cards)
Blood glucose levels
▪️4-8 mmol/l - hardly fluctuates
▪️Over 8= hyperglycaemia
▪️Under 4= hypoglycaemia (uncommon as brain always needs glucose- evolution)
Glycolysis
▪️Glucose is taken up by cells
▪️Glucose is converted into Glucoe-6-phosphate (cannot leave cell).
▪️G6P is converted to fructose1,6-bisphosphate which is cleaved to 2 three-carbon units.
▪️ATP is made from phosphorylation of three-carbon units.
▪️Pyruvate made is transported into mitochondria and oxidised into actetyl-CoA.
Krebs cycle
▪️Acetyl-CoA enters the cycle and through oxidation and decarboxcilation, NADH and FADH2 is produced.
▪️ATP and CO2 is also produced
Electron transport chain
▪️NADH and FADH2 donate electrons to transport chain on inner membrane of mitochondria.
▪️As the elctrons pass down the chain, H+ ions are pumped into intermembrane space creating concentration gradient.
▪️ATP-synthase then uses the movement of H+ ions down its concentration across membrane to make ATP.
▪️Water is made from oxygen and H+ ions.
GLUT 1
▪️Brain ▪️Erythrocytes ▪️Placenta and Fetal tissue ▪️High affinity for binding to glucose (even when conc. are low) ▪️Low Km (~1mM) - 1st priority cells
GLUT 2
▪️Liver ▪️Kidney ▪️Gut ▪️Pancreatic beta-cells ▪️ Lower affinity receptor- glucose entry is proportional to blood glucose levels
GLUT 3
▪️Brain
▪️High affinity
▪️Low Km (~1mM) - 1st priority cells
GLUT 4
▪️ Muscle and adipose tissue
▪️Found in cytoplasm and is translocates to membrane when insulin binds to receptor.
▪️ Insulin sensitive
▪️Medium Km (2.5-5mM)
Glucose uptake form gut and kidney
▪️Na+ dependent glucose transporters
▪️Na+ gradient is needed for glucose uptake (co-transported)
Insulin stimulation
▪️Stimulated by high blood glucose and PSN.
▪️Gastric inhibitory polypeptide (GIP) and Glucagon-like peptide (GLP1) released after ingestion (incretins).
Insulin affect on glucose uptake
1️⃣ Insulin binds to tyrosine kinase receptors on tissue cells.
2️⃣ Signal induces a cascade of reactions leading to GLUT 4 receptors to move to membrane.
3️⃣ Receptors fuse with membrane and allow transport of glucose molecules into the cell.
Insulin action in metabolism
▪️⬆️ Glucose uptake into fat and muscle ▪️⬆️ Glycogen synthesis ▪️⬆️ Lipogensis ▪️⬆️ Protein synthesis ▪️⬇️Gluconeogenisis
Insulin in stimulating glycogen synthesis
▪️1️⃣ Insulin increases uptake of blood glucose into liver by GLUT 2
▪️2️⃣ Stimulates production of G6P in the cell.
▪️3️⃣ As G6P levels rises, glycogen stores build up.
Effects of feeding on metabolism
▪️Liver and Muscle ⬆️Glycogen synthesis ⬇️Gluconeogenesis ⬆️Protein synthesis -Muscle cells switch to carbohydrate oxidation. ▪️Fat ⬆️Lipogenesis ⬇️Lipolysis
Glucagon effects on metabolism
▪️G-protein coupled receptor and cAMP. ▪️⬆️Glycogen breakdown ▪️⬆️Lipogensis ▪️⬆️Gluconeogenesis ▪️⬆️Blood glucose levels
Effects of fasting on metabolism
▪️Liver and Muscle ⬇️Glycogen synthesis ⬆️Gluconeogenesis ⬇️Protein synthesis -Muscle cells switch to lipid oxidation. ▪️Fat ⬇️Lipogenesis ⬆️Lipolysis ▪️Blood ⬆️Ketones ⬇️Amino acids- made but used by gluconeogenesis ▪️Brain ⬆️Ketone useage
Effects of fasting on metabolism
▪️Liver and Muscle ⬇️Glycogen synthesis ⬆️Gluconeogenesis ⬇️Protein synthesis -Muscle cells switch to lipid oxidation. ▪️Fat ⬇️Lipogenesis ⬆️Lipolysis ▪️Blood ⬆️Ketones ⬇️Amino acids- made but used by gluconeogenesis ▪️Brain ⬆️Ketone useage
What is diabetes?
▪️Raised blood glucose
▪️ Due to deficiency of insulin or resistance to its action.
Type 1 diabetes
▪️Autoimmune of beta-cells
▪️Lack of insulin
▪️Common in children and young adults
Type 1 and 2 diabetes effects on metabolism
▪️Liver and Muscle ⬇️Glycogen synthesis ⬆️Gluconeogenesis ⬇️Protein synthesis -Muscle cells switch to lipid oxidation but is incomplete due to low insulin. ▪️Fat ⬇️Lipogenesis ⬆️Lipolysis ▪️Blood ⬆️Ketones ⬆️ Glucose ⬆️Glucagon
▪️ Hyperglycaemia, ketoacidosis, eventual coma and death if untreated.
Hypoglycaemia
▪️Excess of insulin due to treatment of diabetes (poorly controlled)
▪️Rare insulin secreting pancreatic tumour.
▪️Blood glucose lower than 2mmol/l
▪️Sympathetic response- sweating, tachycardia, hunger
▪️Confusion and coma
Type 2 diabetes
▪️Insulin resistance- tissues unresponsive to insulin, more insulin is needed to keep glucose levels normal (hyperinsulinaemia)- eventually lead to deficiency.
▪️Insulin deficiency- pancreas does not make enough insulin, fat deposits, defective incretins response.
▪️Related to obesity and physical inactivity
▪️Appears in older people (over 40)
▪️ Can take around 8 years from hyperglycaemia to diabetes- progressive and can go undetected.
▪️85%-95% of all people with diabetes.
How does being overweight lead to diabetes?
▪️Fat cells have reduced response to insulin
Pancreas location and parts
▪️Lobulated, elongated organ
▪️Head, neck, body, tail
▪️Uncinate process- hook like part behind superior mesenetric vessels.
▪️Retroperitoneal-plastered on posterior wall (apart from tail)
▪️In epigastic region and upper left quadrant- tail extends to spleen.
