Diabetes: An Overview Christine Rubie MS, RD, LD

Facts and Figures Currently affects 18.2 million people 5.2 million are undiagnosed 1.3 million new cases per year At the current rate, 1 out of every 3 children born in the year 2010 will get DM in their lifetime

Classifications Type 1 Previously juvenile-onset DM Most cases diagnosed before 30 years of age Autoimmune Beta cell destruction with resulting absolute deficiency of insulin ~10% of DM cases Symptoms: significant weight loss, polyuria, polydipsia

Type 1 Risk in general population: 1:400 to 1:1000 Combination of genes for disease susceptibility and disease resistance 40% of caucasians express the genes, less than 1% develop type 1 DM 50% discordance rate between identical twins

Type 1 A trigger is necessary for gene expression Immunological attack on beta cells and insulin Hyperglycemia and symptoms develop after >90% destruction of the secretory capacity of the beta cell

Type 1 “Honeymoon Period” Noninsulin dependancy Maintains normal glycemia Continued beta cell destruction Insulin required in 3-12 months

Type 2 diabetes 90% of DM cases 30-50% of childhood-onset diabetes 50% of men and 70% of women are obese at diagnosis Insulin resistance Endogenous insulin may be normal, increased,or decreased Frequently asymptomatic at diagnosis

Type 2 30% remain undiagnosed Microvascular complications exist in ~20% at time of diagnosis May be present 6.5 years at time of diagnosis Pima Indians have a 50% prevalence rate

Type 2 Specific defects Beta cell dysfunction resulting in insulin deficiency Insulin receptor abnormalities Postreceptor defects Insulin resistance

Type 2 50% reduction in beta cell mass Abnormal beta cell recognition of glucose Beta cells chronically exposed to hyperglycemia become less efficient in their response

Type 2 Insulin resistance BG is maintained by hepatic glucose production when fasting Insulin suppresses hepatic glucose Type 2: decrease in sensitivity and response Type 2: persistant hepatic glucose production

DM Diagnosis Prediabetes Fasting: mg/dL Random: mg/dL Diabetes Fasting: >126 Random: >200 Confirmed with a second lab test and/or symptoms

Gestational Diabetes Affects 2-14% of pregnancies Glucose intolerance that develops or is first discovered during pregnancy Diagnostic classification changes after pregnancy Increased future risk for type 2 DM 50%-80% within 1 decade

GDM Pregnancy is an insulin resistant state Resistance is progressive and is related to circulating hormones (human placental lactogen, prolactin, estrogen, and cortisol) Parallel to fetal and placental growth

GDM Risk Factors Marked obesity History of GDM Strong family history of DM Glycosuria Ethnic group of high prevalence Hispanic, African American, Mexican, Native American, South or East Asian, Pacific Islands

GDM Screening High risk: as early as possible Average risk: weeks gestation Diagnosis 1 hour 50g load: >140, 3 hour OGTT is scheduled 3 hour 100g load: 2 or more BG’s meet or exceed, GDM is diagnosed Values: Fasting-95 mg/dL, 1 hour-180 mg/dL, 2 hour-155 mg/dL, 3 hour-140 mg/dL

GDM Fetal risks First trimester: congenital malformations Increased endocrine system workload Macrosomia (<9 pounds) Shoulder dystocia and traumatic birth Hyperglycemia at birth

GDM BG Goals Test 4 times daily Fasting, 1 hour postprandial Fasting: <90 1 hour pp: <130

DM Risk Factors Genetics Age (>45 years) Overweight/Obesity Physical Inactivity Ethnicity Prior GDM or babies over 9#

Blood Sugar Testing Varying times per day 1-7 times BG goals: Fasting Preprandial: <110 2 hours postprandial: <140

DM Management Dietary Carbohydrate control Individualized recommendations No standardized menus Total carbohydrates- NOT sugar Use of alternative sweeteners NO SUGARY DRINKS!!!!!!!!!!!!!!!

DM Management Exercise Improved BG control with weight loss of 10% 30 minutes/day as many days as possible Doesn’t have to be consecutive

DM Management Oral Medications Sulfonylureas, Meglitinides, Biguanides, Thiazolidinediones (TZD’s), Alpha- Glucosidase Inhibitors, Amylin Agonists Secretagogues, sensitizers, suppress hepatic glucose production, delay glucose absorption Insulin Rapid-acting to long-acting

Oral Medications Sulfonylureas Glyburide, Glipizide (Glucotrol), Glimepiride (Amaryl) Increase insulin release from the pancreas Can cause hypoglycemia BG < 70

Oral Medication Meglitinides Repaglinide (Prandin) and Nateglinide (Starlix) Increases insulin release but the effect is glucose-dependant and diminishes at low blood glucose concentrations Can cause hypoglycemia

Oral Medications Biguanides Metformin (Glucophage), Glucovance (Glyburide/Metformin), Metaglip (Glipizide/Metformin), Avandamet ( Metformin/ Rosiglitazone) Reduce hepatic glucose production and decrease insulin resistance Not a hypoglycemic agent

Oral Medications Thiazolidinediones (TZD’s) Pioglitazone (Actos), Rosiglitazone (Avandia) Decrease insulin resistance Not a hypoglycemic agent

Oral Medications Alpha-Glucosidase Inhibitors Acarbose (Precose) and Miglitol (Glyset) Inhibit alpha-glucosidase enzymes in the small intestine and pancreatic alpha-amylase Reduces the rate of starch digestion and subsequent glucose absorption

Injectable Medications Symlin and Byetta Synthetic Amylin: hormone secreted by the pancreatic cells in response to hyperglycemia Inhibits gastric emptying and suppresses glucagon secretion Adjunctive therapy

Insulin Basal vs. bolus Variation in peak time and duration Vial and syringe vs. insulin pens Pump therapy

Insulin guidelines Absorbed most readily in the abdomen, followed by the arms, thighs, and buttocks Best injected at room temperature Keep backups in the refrigerator Vials last ~1 month at room temperature, pens last ~2 weeks

Carbohydrate Counting 1500 Rule Weight in kilograms Wt (kg) X 0.6 = TDD (total daily dose).6 (Type 1) – 1.0 (Type 2) 1500/ TDD= BG1 (How much 1 unit of insulin drops the BG) BG1 X.33 = How many grams of carbohydrate is equal to 1 unit of insulin

DM Emotions Anger Fear Depression Denial Acceptance