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Organisation of the Body

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Regulation of blood glucose levels   Utilised by all body tissues Brain especially sensitive to low glucose Stress response hormones increase blood glucose e.g. fight or flight, cortisol Insulin is the only hormone which decreases blood glucose  
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Anatomy of the pancreas   Derived from the developing endoderm of the foregut Islets make up 1% of pancreatic mass Islets distinguishable in human embryo from 12th week Surrounded by lots of vessels so is hard to operate on Behind the stomach  
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Innervation   Innervated by both sympathetic and parasympathetic nerves Via myenteric plexus  
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Islets of Langerhans   Clusters of 1000 endocrine cells 1 million islets in a human Different islet endocrine types; alpha (glucagon), beta (insulin), delta (somatostatin), PP-cells (pancreatic polypeptide) and epsilon (Ghrelin)  
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Insulin   Gene located on chromosome 11 Expressed as preproinsulin and processed to make mature insulin Cleavage of C-peptide occurs in the golgi Mature insulin stored in secretory vesicles - 8fg per granule 10000 granules per beta cell  
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Glucose sensing in beta cells   Increase in glucose moving in through GLUT1/2 Converted to ATP through oxidative metabolism ATP blocks potassium ATP channels Cell depolarises opening CVGGs Leads to exocytosis of vesicles  
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Biphasic secretion of insulin   Initial rapid rise in insulin conc following glucose consumption Continues to increase over the next 2 hours as glucose moves into cells  
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Insulin action   Stimulated by increased blood glucose Inhibits release of glucose from the liver Promotes uptake of glucose into muscle and fat  
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Factors affecting insulin secretion   Increased blood glucose PSNS Amino acids Fatty acids Glucagon Gastrointestinal hormones SNS and Somatostatin inhibit  
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Insulin receptor   Tyrosine kinase Dimerises on activation and auto phosphorylates Inserts GLUT4 into membrane Enzymes involved in metabolic pathways are activated or inactivated  
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Main actions of insulin   Carbohydrate metabolism - GLUT4, glycolysis, glycogenesis, inhibits gluconeogenesis and glycogenolysis Protein metabolism - stimulates AA uptake and protein synthesis Lipid metabolism - Stimulates lipogenesis and inhibits lioplysis  
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Action of insulin on K   Insulin shifts potassium into cells by activating the sodium hydrogen transporter Promotes sodium entry Activates NA K pump Causes electrogenic influx of K  
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Glucose transporters   GLUT1 - plasma membrane of all cells - glucose, galactose and mannose GLUT2 - intestine, kidney etc - glucose and fructose GLUT3 - everywhere - glucose GLUT4 - muscle - glucose GLUT5 - gut - fructose  
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Sodium coupled glucose transporters   SGLT1 - intestine and kidneys = (2 NA for 1 glucose) SGLT2 kidney - (1 Na for 1 glucose)  
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Incretin hormones   GLP-1 and GIP Enhance insulin secretion - more insulin when glucose given orally than IV Appetite regulation Peripheral insulin sensitivity Secreted from small intestine  
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Healthy vs diseased beta cells   Healthy - incretin hormones are responsible for glucose secretion Diseased - K atp channels responsible for glucose secretion GIP pathway not active in diabetics - explains why metformin has no effect on healthy cells  
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Release of incretin hormones   Stimulated by glucose, AAs and FAs K cells are glucose dependant and secrete GIP L cells are nutrient regulated and secrete GLP1, peptide YY and oxyntomodulin  
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How does GLP1 lower glucose   Inhibits glucagon secretion Stimulates insulin secretion Decreases appetite Inhibits gastric emptying  
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Production and degradation of GLP1   Glucagon - pro-glucagon - GLP1 by prohormone convertase 1/3 secreted GLP1 - small peptides - amino acids by dipeptidyl peptidase IV  
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Alpha cells and glucagon   Highly redundant Preproglucagon processed into a large number of active proteins Converted to hormone, glucagon etc Cam mobilise glucose or promote glucose uptake Different processing gives different role  
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Factors affecting glucagon synthesis   Decreased blood glucose SNS AAs GI hormones inhibited by somatostatin and insulin  
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Glucagon receptors   Gas coupled GPCRs Mostly expressed on hepatocytes and adipocytes Mechanism of action involves adenylate cyclase activity and increase in cAMP Affects both gene expression and post translational modifications  
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Somatostatin   Inhibitory polypeptide found in brain, GI tract and islets Cleaved from prosomatostatin - 14aas in brain and 28 aa in islets Pancreatic inhibitor of insulin and glucagon secretion - brake on islet cell activity Inhibitory Gas GPCR  
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Diabetes mellitus   Urine output increases Urine contains raised amounts of glucose Caused by lack of glucose Type 1 - lack of insulin Type 2 - resistance to insulin and collapsing b cell function More than one cause of type 2  
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Normal blood glucose   Normal fasting plasma glucose - 3.5-5.5 mM Considered hypoglycaemic if <4 mM Diagnosis of diabetes if > 7 mM Normal individuals clear glucose in 2 hours diabetic >11.1 mM after 2 hours  
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Causes of diabetes mellitus   Type 1 - immune destruction of B cells Neonatal - mutations in K atp channels Type 2 - impaired b cell function and defective insulin signalling in metabolic syndrome Gestational diabetes Maturity onset diabetes of young people - mutations in 6 genes  
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Type 1 Diabetes   Insulin dependent Immune destruction of beta cells Complete lack of insulin signals starvation increasing gluconeogenesis and glycolysis Ketogenesis is upregulated Peak incidence 12-14 Genetic and environment play a role  
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Type 2 diabetes   Non-insulin dependent Adult onset and associated with diabetes Combo of insulin resistance and b cell failure No ketogenesis but hyperglycaemia seen Presents as polyuria and polydipsia Can be non-symptomatic at <11.1 mM  
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Complications of diabetes   Gangrenous foot - poor blood and nerve supply Neuropathy in retina leading to blindness Kidney damage - primary cause of death Albumin detected in urine due to podocyte damage Results from glycosylation of proteins in high plasma glucose  
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Glycosylated haemoglobin   A form of haemoglobin measured to identify the average plasma glucose concentration over prolonged periods of time HbA1c formed in non-enzymatic glycosylation on exposure to plasma glucose Marker of high glucose over a long period  
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Glycation   A result of covalent bonding of a protein or lipid with sugars like fructose and glucose A haphazard process that impairs function of targets  
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