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20 Cards in this Set
- Front
- Back
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Regulation of Blood Glucose
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-regulated most by hormones from pancreatic islets
-istlet alpha cells = glucagon, which increases blood glucose -islet beta cells = produce insulin which decrease blood glucose |
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Carbohydrates Influence on Blood
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-carb broken down by enzymes in intestine to glucose and other sugars
-all tissues can use glucose for fuel -brain requires glucose -glucose easily goes from blood into many tissues -fat & muscle require insulin to take up glucose -insulin also increases fat storage and inhibit lipolysis -insulin stimulates glycogen synthesis in liver and muscle -glycogen is a collection of glucose assembled in branched tree like configuration |
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Foods that contain most glucose:
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1. Starch: bread, pasta, rice, cereal, potato
2. Fruit: glucose + fructose + sucrose 3. Sucrose (table sugar) = glucose + fructose 4. milk = glucose + galactose |
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If carb not available
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-blood glucose decreases
-insulin decreases -stimulus to make and store glycogen disappears -stimulus to store fat disappears -as blood glucose falls further, glucagon secreated |
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Starvation
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-glucagon stimulates liver glycogen breakdown (glycogenolysis)
-Glucagon stimulates liver to convert other molecules (aa) into glucose -more glucose enters circulation -epi stim. lipolysis and free FA enter circulation |
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Insulin & Glucagon Receptors
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-peptides hormones can't be given orallys, interact w/ surface cell receptor
-insulin receptor: insulin binding initiates P of receptor and many additional P -glucagon receptor: G-protein linked receptor, glucagon binding results in increased cAMP & additional rxns |
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Glucose Entry Into Tissues
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-requires glucose transporter protein (GLUT) on cell surface
-fat and muscle cells contain GLUT 4 -insulin bind to its receptor cause GLUT 4 to move from inside fat and muscle cells to the cell surface so glucose can enter |
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Diabetes Mellitus
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-disorder of glucose metabolism result in hyperglycemia due to insulin deficiency or abnormal insulin secretion & action
-2 majory types: 1. Type1 DM (insulin deficiency) 2. Type 2 DM (abnormal insulin secretion & action) |
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Symptoms of Diabetes Mellitus
Diagnosis of DM |
-polyuria (excess urination)
-Polydipsia (excessive thirst) -polyphagia (excessive food intake) -weight loss -random plasma glucose >200 mg/dl w/ classic symptoms -fasting plasma glucose >126 mg/dl (normal = 70-100) not enough insulin to control gluconeogenesis & glycogenolysis in fasting state -oral glucose tolerance test: glucose level at 2 hrs after standard glucose load >200mg/dl (normal <140); can't secrete enough insulin to dispose of glucose -Hemoglobin A1C >6.5%: indicates susteained hyperglycemia |
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Pre-Diabetes
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-fasting plasma glucose 101-125 mg/dl
-oral glucose tolerance test: glucose levels of 141-199 mg/dl after 2 hrs -pre-diab not always progress to DM -progression can be delayed by: calorie reduction + exercise, drugs decrease gluconeogenesis, drugs that increase muscle sensitivity to insulin |
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Type I DM
Type II DM |
-autoimmune desctruction of pancreatic beta cells (usually childhood)
-absolute insulin deficiency -arises in genetically susceptible individuals exposed to a triggering factor -often lean, die w/o insulin -40-50% concordance rate in twins -occurs because of defects in insulin action (insulin resistance) and inadequate insulin secretion -primary defect probably varies by population -failure to compensate for primary defect ultimately leads to hyperglycemia -beta cells defective, not totally destroyed -strong genetic predisposition -environmental risk factors: obesity, again, decrease exercise, poor fetal and postanatal nutrition -95% of diabetes -usually obese adults, adolescents -can survive w/o added insulin -95-100% concordance rate in twins |
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Causes of Insulin Resistance
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Pre-receptor defects (rare)
-abnormal insulin -antibody to insulin Receptor defects (not very often) -decrease # of insulin receptors -antibody to insulin receptor -mutation in insulin receptor Post-receptor defects (most) -abnormality w/ insulin signal transmission |
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Treatment of Diabetes
Tools to Combat Hyperglycemia |
Type I DM: provide insulin
Type II DM: increase insuline sensitivity and/or increase insulin supply Food, Exercise, Drugs |
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Type II DM: sources of Hyperglycemia
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-intestine glucose absorption
-increased liver glucose production -decreased muscle uptake -pancreas, inadequate insulin secretion |
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Diet & Exercise for Diabetes
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-calorie restriction increases insulin sensitivity
-no specific "diabetes diet" -low carb diet decrease need for insulin, best = balanced diet -exercise increases insulin sensitivity -muscles take up more glucse -if pat very symptomatic don't use diet & exercise alone |
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Incretins
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-peptides such as glucagon like peptide 1 (GLP-1) are produced by intestine when glucose increases after carb meal
-stimulate beta cell insulin secretion -inhibit alpha cell glucagon secretion -some delay stomach emptying -drugs: analoges of glucagon-like peptide1 (GLP-1) also cause wieght loss & drugs that inhibit DDP4 (enzyme that degrades GLP1 |
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Insulin Therapy
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-for T1 & T2 DM
-try to mimic normal insulin secretion -basal background insulin -bursts of insulin with meals |
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Causes of Hypoglycemia
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High insulin states:
-administration of too much insulin -drugs that induce insulin secretion -insulinoma (islet cell tumor produce excess insulin) Low insulin states: -liver failure (no gluconeogenesis) -Malnutrition (no glycogen stores) -excessive alcohol (interferes w/ gluconeogensis) -GH or cortisol deficiency (less insulin resistance) |
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Symptoms & Signs of Hypoglycemia
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Due to Epi secretions (adrenergic symptoms)
-sweating, rapid heart rate, palpations, anxiety, agitation, hunger Due to low brain glucose (neuroglycopenia) -lethargy, inappropriate bxr, impaired thinking, seizures, coma, death After 5 years of diabetes, no glucagon response to hypoglycemia -somewhat no epi response so no aware hypoglycemic |
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Treatment of Hypoglycemia
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Immediate:
-ingest glucose takes ~ 20min to reach blood -if swallow impaired, give intramuscular glucagon (stim glycogenolysis) or intravenous glucose Long Term: -change does or timng of diabetic treatment -if not diabetic, treat underlying disease |
