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Questions and Answers
What primarily differentiates Type 1 diabetes mellitus (T1D) from Type 2 diabetes (T2D)?
What primarily differentiates Type 1 diabetes mellitus (T1D) from Type 2 diabetes (T2D)?
- Type 1 occurs more frequently in older adults.
- Type 1 is characterized by insulin resistance.
- Type 1 is an autoimmune condition that leads to insulin deficiency. (correct)
- Type 1 is mainly caused by lifestyle choices.
Which of the following factors is most commonly associated with insulin resistance in Type 2 diabetes?
Which of the following factors is most commonly associated with insulin resistance in Type 2 diabetes?
- Age-related decrease in beta-cell function.
- Obesity and adipose tissue remodeling. (correct)
- High physical activity levels.
- Genetic mutations affecting insulin production.
Which process is primarily affected by insulin deficiency in Type 1 diabetes?
Which process is primarily affected by insulin deficiency in Type 1 diabetes?
- Glycolysis.
- Hepatic gluconeogenesis. (correct)
- Lipolysis.
- Glycogenolysis.
What is the role of GLUT4 in insulin signaling?
What is the role of GLUT4 in insulin signaling?
What is a primary goal of diabetes treatment?
What is a primary goal of diabetes treatment?
What primarily leads to the release of insulin from beta cells during glucose metabolism?
What primarily leads to the release of insulin from beta cells during glucose metabolism?
Which type of diabetes is primarily characterized by autoimmune destruction of beta cells?
Which type of diabetes is primarily characterized by autoimmune destruction of beta cells?
What is the role of GLUT2 in glucose metabolism?
What is the role of GLUT2 in glucose metabolism?
What is a common feature of both type 1 and type 2 diabetes mellitus?
What is a common feature of both type 1 and type 2 diabetes mellitus?
In type 2 diabetes, what typically contributes to the development of insulin resistance?
In type 2 diabetes, what typically contributes to the development of insulin resistance?
How do fatty acids influence glucose metabolism in diabetes?
How do fatty acids influence glucose metabolism in diabetes?
Which hormonal response is triggered by low blood glucose levels?
Which hormonal response is triggered by low blood glucose levels?
What is the primary function of insulin in glucose metabolism?
What is the primary function of insulin in glucose metabolism?
What condition indicates a random blood glucose level of 200 mg/dL or higher?
What condition indicates a random blood glucose level of 200 mg/dL or higher?
What HbA1c level is considered diagnostic for diabetes?
What HbA1c level is considered diagnostic for diabetes?
During the glucose tolerance test, what blood glucose level indicates diabetes at the 2-hour mark?
During the glucose tolerance test, what blood glucose level indicates diabetes at the 2-hour mark?
What is the range for normal fasting blood sugar levels?
What is the range for normal fasting blood sugar levels?
What HbA1c level range suggests prediabetes?
What HbA1c level range suggests prediabetes?
What condition is indicated by a fasting blood sugar level of 126 mg/dL or higher?
What condition is indicated by a fasting blood sugar level of 126 mg/dL or higher?
What is a common procedure in the glucose tolerance test?
What is a common procedure in the glucose tolerance test?
What blood glucose level at the 2-hour mark suggests prediabetes?
What blood glucose level at the 2-hour mark suggests prediabetes?
What type of receptor is involved in insulin signaling in the liver?
What type of receptor is involved in insulin signaling in the liver?
Which primary pathway is activated by glucagon signaling?
Which primary pathway is activated by glucagon signaling?
What effect does insulin have on gluconeogenesis?
What effect does insulin have on gluconeogenesis?
What condition is primarily associated with excessive glucagon action in Type 2 diabetes?
What condition is primarily associated with excessive glucagon action in Type 2 diabetes?
What type of damage is caused by the accumulation of Advanced Glycation End Products (AGEs)?
What type of damage is caused by the accumulation of Advanced Glycation End Products (AGEs)?
Which of the following complications is NOT associated with AGEs and their receptor RAGE?
Which of the following complications is NOT associated with AGEs and their receptor RAGE?
Which of the following statements regarding glucose and protein interaction is true?
Which of the following statements regarding glucose and protein interaction is true?
What is the overall effect of insulin on blood glucose levels?
What is the overall effect of insulin on blood glucose levels?
What does the presence of glucose in the urine indicate?
What does the presence of glucose in the urine indicate?
Which test is used to measure levels of β-Hydroxybutyrate (BHB) to indicate fat metabolism?
Which test is used to measure levels of β-Hydroxybutyrate (BHB) to indicate fat metabolism?
What is the significance of C-peptide levels in blood testing?
What is the significance of C-peptide levels in blood testing?
Which treatment regimen typically involves 2-3 daily injections?
Which treatment regimen typically involves 2-3 daily injections?
What is the most common complication of insulin therapy?
What is the most common complication of insulin therapy?
Which individuals should avoid tight control in diabetes management?
Which individuals should avoid tight control in diabetes management?
What lifestyle changes are recommended for initial management of T2D?
What lifestyle changes are recommended for initial management of T2D?
What type of oral antihyperglycemic agent decreases hepatic gluconeogenesis?
What type of oral antihyperglycemic agent decreases hepatic gluconeogenesis?
In intensive treatment for T1D, what is the typical HbA1c level target?
In intensive treatment for T1D, what is the typical HbA1c level target?
Which of the following indicates a higher risk of hypoglycemia?
Which of the following indicates a higher risk of hypoglycemia?
What primarily leads to the misidentification of β cells in Type 1 diabetes?
What primarily leads to the misidentification of β cells in Type 1 diabetes?
What metabolic change is characterized by increased hepatic glucose production and reduced peripheral utilization?
What metabolic change is characterized by increased hepatic glucose production and reduced peripheral utilization?
Which of the following symptoms is associated with Diabetic Ketoacidosis (DKA)?
Which of the following symptoms is associated with Diabetic Ketoacidosis (DKA)?
What is the relationship between Type 2 diabetes (T2D) and insulin resistance?
What is the relationship between Type 2 diabetes (T2D) and insulin resistance?
In Type 1 diabetes, what does the mobilization of fatty acids lead to?
In Type 1 diabetes, what does the mobilization of fatty acids lead to?
Which hormonal imbalance is primarily caused by defects in β-cell function?
Which hormonal imbalance is primarily caused by defects in β-cell function?
What complication can occur in 25-40% of newly diagnosed Type 1 diabetes cases?
What complication can occur in 25-40% of newly diagnosed Type 1 diabetes cases?
How does Type 1 diabetes affect metabolic processes in tissues?
How does Type 1 diabetes affect metabolic processes in tissues?
Flashcards
Type 1 Diabetes
Type 1 Diabetes
An autoimmune disease where the body's immune system attacks and destroys insulin-producing cells in the pancreas, leading to a lack of insulin.
Type 2 Diabetes
Type 2 Diabetes
A chronic disease where the body doesn't properly use or make enough insulin, often linked with obesity and insulin resistance.
Hyperglycemia
Hyperglycemia
High blood sugar levels, a defining characteristic of diabetes that can harm various organs over time.
Insulin Deficiency
Insulin Deficiency
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Insulin Resistance
Insulin Resistance
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What are the trigger factors for Type 1 Diabetes?
What are the trigger factors for Type 1 Diabetes?
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How does genetic predisposition affect T1D?
How does genetic predisposition affect T1D?
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What role do HDL genes play in T1D?
What role do HDL genes play in T1D?
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What are the metabolic changes in T1D?
What are the metabolic changes in T1D?
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What is hyperglycemia and how does it occur in T1D?
What is hyperglycemia and how does it occur in T1D?
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What is ketonemia and how does it occur in T1D?
What is ketonemia and how does it occur in T1D?
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What is Diabetic Ketoacidosis (DKA)?
What is Diabetic Ketoacidosis (DKA)?
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What is the impact of T1D on tissues?
What is the impact of T1D on tissues?
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Insulin Receptor Type
Insulin Receptor Type
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Glucagon Receptor Type
Glucagon Receptor Type
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Insulin's Effect on Gluconeogenesis
Insulin's Effect on Gluconeogenesis
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Glucagon's Effect on Gluconeogenesis
Glucagon's Effect on Gluconeogenesis
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AGEs Formation
AGEs Formation
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AGEs and Inflammation
AGEs and Inflammation
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RAGE Receptor
RAGE Receptor
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RAGE Signaling
RAGE Signaling
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Insulin's Role in Glucose Metabolism
Insulin's Role in Glucose Metabolism
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Intertissue Relationships in T2D
Intertissue Relationships in T2D
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What Happens When Insulin is Released?
What Happens When Insulin is Released?
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Glucose Entry into Systemic Circulation
Glucose Entry into Systemic Circulation
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Portal Circulation's Role
Portal Circulation's Role
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Hyperglycemia's Effect on Glucagon
Hyperglycemia's Effect on Glucagon
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Type 1 vs. Type 2 Diabetes
Type 1 vs. Type 2 Diabetes
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Random Blood Glucose Test
Random Blood Glucose Test
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Fasting Plasma Glucose Test
Fasting Plasma Glucose Test
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Oral Glucose Tolerance Test (OGTT)
Oral Glucose Tolerance Test (OGTT)
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HbA1c (Glycated Hemoglobin)
HbA1c (Glycated Hemoglobin)
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What is the connection between HbA1c and diabetes?
What is the connection between HbA1c and diabetes?
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Prediabetes
Prediabetes
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What are the blood glucose values associated with prediabetes?
What are the blood glucose values associated with prediabetes?
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What is inflammation's role in tissue damage?
What is inflammation's role in tissue damage?
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Glycosuria
Glycosuria
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Ketones in Urine
Ketones in Urine
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C-Peptide
C-Peptide
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Standard T1D Treatment (Injection Regimen)
Standard T1D Treatment (Injection Regimen)
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Intensive T1D Treatment (Injection Regimen)
Intensive T1D Treatment (Injection Regimen)
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Hypoglycemia Unawareness
Hypoglycemia Unawareness
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Exercise and T1D
Exercise and T1D
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Tight Control for T1D
Tight Control for T1D
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Initial T2D Treatment
Initial T2D Treatment
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Study Notes
Diabetes Mellitus Overview
- Diabetes mellitus (DM) is a chronic metabolic disease caused by elevated blood glucose levels.
- DM leads to serious damage to the heart, blood vessels, eyes, kidneys, and nerves over time.
- Three main types of DM: type 1, type 2, and gestational diabetes.
Type 1 Diabetes (T1D)
- Pathophysiology: Autoimmune attack on pancreatic islet beta cells, leading to insulin deficiency.
- Symptoms: Develop rapidly (weeks), including polyuria, polydipsia, polyphagia, fatigue, and blurred vision.
- Beta-cell loss: Gradual destruction over years, symptoms appear after 80-90% loss.
- Trigger factors: Environmental stimuli (e.g., viral infections) and genetic predisposition.
- Metabolic changes: Increased hepatic glucose production, ketone production, and potential diabetic ketoacidosis (DKA).
- Intertissue relationships: Reduced glucose uptake in muscle and adipose tissue, increased ketone body production, and potentially abnormal lipid metabolism in visceral adipose tissues.
- Diagnosis & tests: Elevated blood glucose levels, HbA1c, and glucose tolerance tests.
- Treatment: Insulin injections/pump therapy. Tight control is goal to minimize long-term complications.
Type 2 Diabetes (T2D)
- Pathophysiology: Insulin resistance combined with impaired beta-cell function.
- Symptoms: Develop slowly (several years), including increased thirst, frequent urination, and blurred vision.
- Beta-cell dysfunction: Initially compensatory with increased insulin levels for a duration before inadequate insulin secretion.
- Metabolic differences: Milder metabolic alterations compared to Type 1.
- Insulin resistance: Reduced ability of target tissues (muscle/adipose tissue) to respond to insulin. Increased hepatic glucose production, adipose lipolysis increase free fatty acids.
- Diagnosis & tests: Elevated blood glucose levels, HbA1c, and glucose tolerance tests.
- Treatment: Lifestyle modifications (nutrition, weight loss, exercise), medical nutrition therapy, and potential for oral medications and insulin if needed.
Insulin Receptor Signaling
- Insulin binds to insulin receptors on target cells, triggering phosphorylation (activation)
- Leads to GLUT4 translocation, increasing glucose uptake into cells.
- Type 1 Diabetes: Lack of insulin severely disrupts signaling.
- Type 2 Diabetes: Insulin resistance impedes GLUT4 translocation, leading to decreased glucose uptake and hyperglycemia.
Diabetic Complications (T1D & T2D)
- Hyperglycemia & AGEs: Elevated blood glucose leads to advanced glycation end products (AGEs) causing oxidative stress, inflammation, and vascular damage. They can promote inflammatory pathways, causing tissue damage
- RAGE Receptor: A receptor on endothelial cells, neurons, and immune cells, triggers inflammation and oxidative stress upon AGE binding.
- Diabetic complications: retinal problems, nephropathy (kidney failure), neuropathy (nerve damage), and vascular damage, leading to cardiovascular issues.
- Chronic inflammation: Exacerbates tissue damage.
Diabetes Diagnosis & Tests
- Hyperglycemia: Elevated blood glucose levels, diagnosed via random, fasting, or oral glucose tolerance tests.
- Glycated hemoglobin (HbA1c): Measures average blood glucose levels over 2-3 months, used for diabetes diagnosis and monitoring.
- Oral glucose tolerance test (OGTT): Assesses how the body processes glucose. A 2-hr glucose level > 200mg/dl confirms diabetes. Fasting glucose level > 126 mg/dL or higher may indicate diabetes .
- Glycosuria: Glucose in urine, indicates high blood glucose levels.
- Ketones: Measured in blood or urine, indicating potential diabetic ketoacidosis (DKA).
- C-peptide levels: Indicates how much insulin the pancreas is producing. High levels suggest type 2 diabetes; low levels may suggest type 1 diabetes.
Diabetes Treatment
- T1D: Involves insulin therapy (injections or pump therapy) aiming for tight control.
- T2D: Lifestyle changes are initial approaches: Weight reduction, regular exercise, and dietary modifications (low carbohydrate diet). Oral medications and insulin may be needed.
- Intensive Therapy: Aggressive treatment aiming for tight glucose control to prevent long-term complications, may not be suitable for all patients (e.g. children, elderly)
Adipose Tissue & Insulin Resistance
- Visceral white adipose tissue (WAT) is highly metabolically active, and excess WAT is linked to insulin resistance. Chronic weight gain and high fat intake are risks.
- The adipose tissue influence the immune system and may potentially influence the metabolism and overall inflammation in the body.
- Adipokines, released by adipose tissue, play roles in metabolism and inflammation; altered adipokine secretion can contribute to insulin resistance, chronic inflammation, and other complications.
- Changes in adipose tissue structure and function can influence signaling and metabolism to increase the risk of Type 2 Diabetes.
Hepatic Gluconeogenesis
- Lack of insulin leads to unregulated gluconeogenesis (production of glucose in the liver).
- Unopposed glucagon stimulates gluconeogenesis further, resulting in hyperglycemia.
- Different mechanisms are involved in gluconeogenesis/glycogenolysis in T1D vs T2D. Mechanisms influencing the signaling will have different results in each type of diabetes.
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Description
Test your knowledge on the key differences between Type 1 and Type 2 diabetes mellitus. This quiz covers various aspects including insulin resistance, the role of glucose transporters, and the metabolic processes affected by insulin. Determine your understanding of diabetes treatment goals and hormonal responses.
