Carb Metabolism In Diabetes Flashcards
Insulin synthesis
. Created equal amounts of insulin and C-peptide
C-peptide levels helps monitor ___ insulin
Endogenous insulin
Endogenous versus exogenous insulin
Endogenous: produces by one’s body
Exogenous: insulin taken as medication
Causative agent of long term damage seen in diabetes type I and II
Chronically high blood sugar
Peripheral neuropathy
. Lack of nerve sensation in extremities
. Can have phantom pains
Nephropathy
. Kidney disease
. kidney tests: BUN and creatinine
. Presence of protein can be indicative of loss of kidney function
Retinopathy
. 95% patients w/ DM develop blindness
. Periodic eye exams done
Atherosclerosis in relation to diabetes
. Poorly controlled DM assoc. w/ high serum triglyceride levels and high cholesterol levels
. Develops at faste rate and with greater severity than if you don’t have DM
. Tests: blood tests for serum lipids
Impaired circulation in relation to DM
. Basement membrane thickening leads to vascular problems, leaky capillaries, and micro aneurysms
Is insulin inductively in GLUT 2?
No
GLUT 4 characteristics
. Found in muscle and fat
. Passive transport
. Insulin inducible
. Direction from blood to cells
SGLT glucose transporter characteristics
. Intestine and renal tubules
. Na glucose cotransporter
. Directions intestinal lumen to cells
High intracellular glucose leads to ___
. Protein glycation and polyglot pathway
Protein glycation (glycosylation)
. Protein + glucose protein:glucose -> advanced glycosylation
. Glycosylated proteins: Hb, lens proteins, collagens, myelin
. Abnormal glycosylation products crosslink abnormally and responsible for basement membrane thickening
Polyol pathway
. Only occurs in cells w/ reductase
. Glucose + NADH -> sorbitol + NAD
. Sorbitol and other sugar alcohols cause osmotic problems for cell
. Cells affected: nerves, retina, lens, aorta, and kidney
Type I diabetes
. Pancreas produces little or no insulin at all (<10%)
Type II diabetes
. Pancreas produces some insulin, but tissues don’t respond to it normally
. Insulin produces more than normal or less than normal depending on disease progression
Gestational diabetes
. Subset of type II
. Occurs during pregnancy, disappears after birth of baby
. Occurs in 9.2% of American pregnancies
. Many women developer type II diabetes later in life
Potential causes for inc. in type II diabetes in youth
. Genetics
. Lack of availability
. Lack of ability to exercise safely
DM 1 vs 2 prevalence in US
1: 10%
2: 90%
DM 1 vs 2 nutritional state
1: thin
2: overweight at diagnosis
DM 1 vs 2 speed of onset
1: fast
2: slow
DM 1 vs 2 acute complications
1: ketoacidosis common
2: hyperosmolar episode (ketoacidosis rare)
DM 1 vs 2 genetic component
1: partial
2: strong
DM 1 vs 2 treatment
1: diet, exercise, insulin
2: diet, exercise, oral hypoglycemic agents, insulin
What type of biological activity of insulin needs the largest amounts of insulin?
Glucose lowering
What biological activity of insulin requires the lowest amounts of insulin?
Anti-lipolysis
Common theories of DM 1 cause
. Autoimmune antibodies to pancreatic beta-cells
. Pancreatic disease/cancer/surgery (causes loss of synthesis ability or tissues that make insulin are removed from body creating DM)
. Genetic defect in insulin/insulin receptor (rare, result in infant death)
Molecular mimicry
. Infectious agents have e valves surface proteins that resemble host proteins
. Enables them to escape detection by host defenses
Role of genetics in DM 1
. Concordance rate is 50% for identical twins
. Some HLA haplotypes are more highly represented in DM 1 and some that are less represented
. Both genetic and environmental factors contribute
DM 2 causes
. Obesity (BMI>30) that accompanies metabolic syndrome
. Secondary to another disease
Metabolic syndrome
. Set of conditions that inc. risk for cardiovascular disease
. Most possess at least 3:
Abdominal obesity (waist >40 in men, 35 in women)
High bp (130/85 or higher)
Fasting blood glucose of 110 or higher
Triglyceride level of 150 of higher
Low HDL cholesterol (<40 men, <50 women
Insulin resistance
. normal to high insulin blood levels but don’t react normally
. Requires 100+ units/day to maintain control (healthy needs 40-50 units)
Role of genetics in DM 2
. Concordance rate 100% for identical twins
. Correlated w/ familial factors
Symptoms of DM 1
. Polyuria . Polydipsia (excessive thirst) . Polyphagia (excessive hunger) . Weight loss (15 lbs or more) . Ketogenesis and ketoacidosis . Fasting blood glucose over 126 (7.0 mM)
Symptoms of DM2
. None
. When present resemble mild symptoms of DM 1 (polyuria, polydipsia, weight loss (over long period)
Results of intensive treatment for DM 2
. Reduced risk for eye, kidney, and nerve diseases
. Inc. risk of hypoglycemic episodes that required assistance
Single most important predictor of diabetes
. Overweight/obesity
Normal, prediabetic, and diabetic ranges for HBA1C
Normal: 2-5.6%
Pre: 5.7-6.4
DM: 6.5-15% (good glycemic control <7%, poor control 9% or higher)
Definitions used to diagnose DM
. Patients who possess fasting glucose of over 126 (7.0 mmol/L)
. Patients who possess classic symptoms of DM in addition to casual plasma glucose over 200 (11.1 mmol/L)
. Patients w/ HBA1C ver 6.5%
. Patients w/ abnormal oral glucose tolerance test (2 hr reading over 200 (11.1 mmol/l using 75g dissolved glucose in wateR)
Oral glucose tolerance test
. Patient given 75g glucose following overnight fast
. Blood samples taken at 30 min, 1, 1.5, 2, 2.5, and 3 hours analyzed for glucose
Prediabetes
Patients have levels of glucose above normal but not high enough to be DM
Brittle diabetes
Poorly controlled diabetes where glucose levels vary widely btw very high and very low
Kussmaul respirations
. Symptoms of diabetes ketoacidosis where patients breath abnormally w/ deep respiration’s
. Compensatory mechanism for high metabolic acid
. Acetone detected on breath
