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What is type II diabetes?
What are the functions of glucose?
- Convert to glycogen to store energy
- Converted to fat to store energy
- Oxidized for energy
- Precursor of amino acids C-skeleton
- Prevent Ketosis
How do you get ketosis?
Oxidization of fatty acids without glucose
What organs use glucose for energy?
- Brain, RBCs, mammary gland. getus, spermatogenesis
- NOT the gut (uses AA metabolism for energy)
Can you synthesize glucose from fatty acids?
Where do we get CHO from in our diet?
- Plant-based foods plus milk
What is amylose?
alpha(1-4) chains of glucose
What is amylopectin?
alpha(1-4) chains of glucose with alpha(1-6) branches
What are the three types of fibre?
Soluble, Insoluble, functional
What is soluble fibre?
Forms a gel in water, pectins (found in fruits)
What is insoluble fibre?
- Hemicellulose, cellulose
- Have beta bonds, which we cannot digest
What is functional fibre?
Psyllium added to foods
What are the freatures of soluble fibre?
- Viscous gel
- Delaus gastric emptying
- Glycemic control
- Binds Cholesterol and bile acids
- Fermended by colonic bacteria
- Low GI
What are the features of insoluble fibre?
- Bulk (laxitive effect)
- Delays gastric emptying
- Some glycemic control
- Binds cations
- Minor fermentation by colonic bacteria
How are CHO digested?
- Mouth- salivary amylase
- Small intestinal lumen- pancreatic amylase, glucoamylase
- Small intestinal brush border- sucrase-isomaltase, lactase
What is lactose intolerance?
- Lactose not digested, reaches colon
- Fermentation by bacteria- flatulence (methane, hdrogen, CO2)
- Osmotic diarrhea
- Breath hydrogen test to diagnose
How is lactose intolerance tested?
Breath hydrogen test
Is lactose intolerance an immune disorder?
Not immune related
What is primary lactose non-persistance?
- Decreased lactase production after weaning
- 70% of adults worldwide but varies with population
- Mutation for lactase persistance (autosomal dominance- Single-Nucleotide-Polymorphism in intron)
- Dairy farming cs malaria hypothesis
What is secondary lactose intolerane?
- Caused by some injury to the small intestine
- eg. Parasite infection, celiac disease, pathology, malnutrition
What is congenital lactose intolerance?
- Non-functioning protein
- Infants, lactase-free formula (unable to digest breast milk)
- Same as lactose intolerance after infancy
What is a milk allergy?
- Not the same as lactose intollerance
- Protein, or peptides in milk
- IgE antibodies
- Mast cell degranulation
- Massive histamine response
- Involves immune reaction
How is galactose absorbed?
- SGLT-1 (sodium-glucose transport proteins) and GLUT-2
- First pass removal by liver
- Preferential conversion to glycogen
How is fructose absorbed?
- GLUT5 facilitated diffusion agains concentration gradient into cell
- GLUT5 or GLUT2 to exit cell
- First pass removal by liver (GLUT2)
- Rapid oxidation (faster than glucose)
- Preferential conversion to fatty acids, triglycerides
How is glucose homeostasis maintained?
- Dietary CHO from stomach delivered to small intestine
- Glucose and other monosaccharides transported through the bloodstream to the liver
- Galactose and fructose are converted to glucose
- Blood levels of glucose maintained for brain and other body cells
- Glucose transported to muscle
- Glucose is stored as glygocen in both liver and muscle
- The glycogen stored in the liver maintains blood glucose between meals
- Muscle glycogen provides immediate energy to the muscle during exercise
What stimulates glucose synthesis?
How is glycogen degraded?
- Glycogen Phosphorylase --- glucose-1-P
- Phosphoglucomutase---glucose-6-P (glycolysis)
- glucose-6-phosphatase is only in liver- this means only the liver and kidney can make glucose from glycogen
Why can only the liver and kidney make glucose from glycogen?
Glucose-6-phosphatase (the enzyme that converts glucose-6-P into glucose) is only in the liver and kidney
What is the brains glucose requirement?
What is the hepatic glycogen availability?
What is gluconeogenesis?
production of glucose from non-carbohydrate carbon substrates
What are the precursors for gluconeogenesis?
Amino acids, pyruvate, gycerol
What stimulates gluconeogenesis?
Stimulated by glucagon and glucocorticoids when plasma glucose is low
What happens as a result of gluconeogenesis?
Protein breakdown is high
What is ketogenesis?
- Fatty acid beta-oxidation in the basence of glucose
- No anaplerosis of TCA cycle
- Causes acetyl-CoA to accumulate
- Beta-hydroxybutyrate and acetoacetate are products (ketones)
- Ketone bodies are an alternate fuel for the brain (do have negative impact)
What is ketoacidosis?
- Beta-oxidation of fatty acids in absence of glucose
- TCA cycle intermediates depleted for gluconeogenesis
- Acetyl-CoA accumulates
What are the components and breakdown of total energy expenditure?
- 67%- Basal Metabolic Rate
- 10%- Diet-Induced Thermogenesis
- 23%- Activity
- ?%- Adaptive Thermogenesis
What are the facilitative glucose transporters?
SLC2A1-5- Solute carrier family 2 members 1-5
- GLUT1- RBCs, brain (blood brain barrier), kidney
- GLUT2- Liver, B-cell, kidney, smal intestine
- GLUT3- Brain (neurons)
- GLUT4- Muscle, heart, adipose tissue
- GLUT5- Small intestine (fructose transporter)
How do insulin receptors interact with GLUT4?
- Insulin binds to receptors starts many protein cascades
- Protein cascades result in translocation of GLUT-4 to the plasma membrane
- Influx of glucose
- Glycogen synthesis, glycolsis, and fatty acid sythesis
Why is glucose transport important?
- Glucose-6-phosphatase is only in liver (and kidney)
- Muscle can't export glucose derived from glycogen
- Peripheral cells can't synthesize glucose from glycogen of gluconeogenic precursors
What is the Cori cycle?
- Lactic acid cycle
- Glucose in muscle is converted to 2 pyruvate (uses 2 ATP)
- 2 pyruvate is converted to 2 lactate
- Lactate goes to liver
- 2 lactate is converted back to 2 pyruvate and back into glucose (requires 6 ATP)
How does athletic performance depend on glucose?
- Requireent for gucose increases with exercise intensity
- Marathon: glycogen for 1-3 hours
- CHO loading to maximize glycogen
What is type-I Diabetes mellitus?
- Blood sugar above normal levels- spilled in the urine (glucosuria)
- Cell-mediated autoimmune Beta cell distruction
- Genetic predisposition
- 5-10% of all cases of diabetes
How is T1DM diagnosed?
- Glucosuria/Ketonuia- urinalysis
- Fasting plasma glucose concentration >7.00mmol/L (normal 5mmol/L)
- Oral glucose tolerance test- plasma glucose >11mmol/L
- Glycated hemoglobin (hemoglobin A1c) >6.5% (normal range 3.5-5.5%)
Simplified version of T1DM
- Stomach converts food to glucose
- Glucose enters the blood stream
- Pancreas produces little or no insulin
- Glucose unable to enter body effectively
- Glucose levels increase
What are the consequences of untreated diabetes?
- No glucose in cells- Ketoacidosis
- Hyperglycemia- dehydration
How is T1DM managed?
- Insulin injections (pump, nasal, islet transplant)
- Balance intake, activity, insulin
How is insulin synthesized?
- Signal peptide is translated and translocated into the ER lumen
- Folding, oxidation and signal peptide cleavage
- ER export, Golgi transport, vesicle packaging
- Protease clevage liberatoes C-peptide
- Carboxypeptidase E produces mature insulin
How is insulin secreted?
- GLUT2 allows an influx of glucose
- Glucose and respiration produce ATP
- An increase in the ATP:ADP ratio closes the K-ATP channel, causing depolarisation
- Voltage-gated calcium channels cause an influx of Ca2+
- Ca2+ activate insulin gene expression via CREB (Calcium responsive element binding protein)
- Exocytosis of stored insulin
What is the peak age of T1DM onset?
What is microangiopathy?
- High glucose in some non-insulin sensitive tssues damages cells
- Accumulation of AGEs (advanced glycation end products)
What is nephropathy?
- Thickening of glomerulus
- Results in micralbuminuria
- Dialysis, transplant
What are the risk factors for T2DM?
- Heredity- multigenic disorder
- Obesity (visceral)
- Stomack converts food to glucose
- Glucose enters bloodstream
- Pancreas produces sufficient insulin but it is resistant to effective use
- Glucose unable to enter body effectively
- Glucose levels increase
What happens to GLUT4 peripheral tissues in T2DM?
- Fat-based economy
- Low muscle glycogen
- Increased muscle proteolysis for gluconeogenic AAs
- Cori cycle
What happens in the liver in T2DM?
- Lipogenesis, increased VLDL
- Non-alcoholic fatty liver disease
How is drug treatment used to treat T2DM?
- Metformin (a biguanide)
- Decrases hepatic gluconeogenesis
- Increased peripheral insulin sensitivity
- Increases GLUT4 mediated glucose uptake
- Increases fatty acid oxidation
How does metformin work?
- Metformin activates AMPK (AMP activated protein kinase)
- AMPK increases muscle glucose transport and decreases hepatic glucose production
- AMPK can also decrease acetyl-CoA carboxylase activity, hence decreasing hepatic FA, VLDL synthesis and increasing hepatic FA oxidation
- AMPK also decreases SREMP-1 expression and activity, which results in a decrease in hepatic gene expression and also leads to a decrease in hepatic FA, VLDL synthesis
- All of these pathways resul in a decrease in plasma glucose and plasma triglycerides
How is T2DM monitored?
- Fasting plasma glucose (FPG) and insulin
- Oral glucose tolerance test (OGTT)
- Glycated hemoglobin (HbA1c)
What is a catabolic response to surgery?
- Inflammatory response and neuro-endocrine response can lead to insulin resistane and hyperglycemia
- Insulin resistance and hyperglycemia lead to loss of body protein
- Loss of body suppression can lead to immunosuppression (delayed wound healing) or muscle wasting (delayed convalescence)
How is insulin resistance and hyperglycemia caused by neuro-endocrine response combated during surgery?
How is loss of body protein during surgery combated?