Flashcards in Diabetes & eating disorders Deck (292)
Discuss the flow of glucagon and insulin post-prandially in T2DM.
Glucagon stays high during meals, as it is not inhibited by the insulin release as in healthy subjects
Insulin release is delayed and reduced.
What are the anabolic actions of insulin in glucose metabolism?
o Glucose transport into muscle and adipose tissues (GLUT4)
o Glycolysis --> energy
What are the anabolic actions of insulin in lipid metabolism?
o Lipogenesis (TG in adipose tissues and synthesis of FFAs in liver)
o Lipoprotein lipase activity (LPL; adipose tissue)
What are the anabolic actions of insulin in protein and electrolyte metabolism?
o Transport of amino acids
o Protein synthesis
o Potassium enters into the cell
What are the actions of insulin in glucose metabolism that decrease catabolism?
o Decreased gluconeogenesis (liver)
o Decreased glycogenesis (liver and muscle)
What are the actions of insulin in lipid metabolism that decrease catabolism?
o LPL (muscle)
o Fatty acid oxidation (liver)
What are the actions of insulin in protein metabolism that decrease catabolism?
Decreased Protein catabolism
Explain how glucose stimulates insulin release in healthy people.
Glucose enters the beta cells with GLUT2 --> To glucose-6-phosphate by glucokinase --> glycolysis to pyruvate --> TCA cycle --> ATP --> K channels shut --> Ca 2+ channels open --> insulin storage granules go to membrane --> insulin release
Insulin secreted as pro-insulin (Insulin + P-peptide)
Discuss the 2 phases of insulin secretion and how it relates to diabetes
First phase insulin
• The initial burst of insulin, 5-10 minutes after Beta cells are exposed to a rapid increase in BG (5-10 min after meal)
• “uncontrolled” flux of release
• Important to decrease glucagon, decrease hepatic gluconeogenesis, decrease lipolysis and prepare target cells for the action of insulin
Second phase insulin
• Lasts longer than phase 1
• After the acute response (first phase), insulin secretion rises more gradually and is directly related to the degree and duration of the stimulus
--> Diabetic patients do not have the first phase = problem
The second phase is better preserved in type 2 diabetes (= lasts longer)
What are 2 incretins and where are they produced?
- GLP-1 is secreted from proglucagon in the enteroendocrine L-cells (ileum and colon)
- GIP is derived from proGIP in the K-cells of the jejunum
Both are released in the presence of nutrient ingestion
Diabetes is the cause of __% of strokes
Diabetes is the cause of __% of heart attacks
Diabetes is the cause of __% of kidney failure requiring dialysis
Diabetes is the cause of __% of non-traumatic leg and foot amputations
Diabetes is the cause of __% of blindness
What is LADA?
Latent autoimmune diabetes of adults;
Type of type 1 diabetes diagnosed in adulthood, often with a slower course of onset than type 1 diabetes diagnosed in juveniles (islet failure, not insulin resistance)
What is MODY?
Maturity onset diabetes of the young" (MODY) refers to any of several hereditary forms of diabetes mellitus caused by mutations in an autosomal dominant gene disrupting insulin production
Explain the onset of T1DM in a person.
1. Genetic predisposition (100% of B cells present and functional)
2. Silent insulin/B cell destruction (% B cells goes down. This process can take years) – Autoimmune
3. 30% of B cell function = alterations in glucose tolerance
4. 15% of B cells – diagnostic --> clinical diabetes
Who has the highest chance of developing T1DM:
Offspring of affected mother?
Offspring of affected father?
Offspring of affected mother: 1 in 50
Offspring of affected father: 1 in 14
Incidence of type 1 diabetes increases with time, while type 2 has stabilized. Why?
- Genetics? HLA, DR3, DR4
- Infection? Coxsackie virus
- Alimentation (Cow’s milk?)
Seasonal variations in T1DM: vitamin D?
What proportion of people with T1DM get diagnosed during adulthood?
42% (almost half) of people with type 1 diabetes were diagnosed between age 31 and 60. People often assume they have type 2 diabetes.
What proportion of B-cell loss is needed for pre-diabetes? For diabetes diagnosis?
Loss of 50% of B cell mass/function = pre-diabetes
Loss of 80% of B cell mass/function = type 2 diabetes diagnosis
Name 6 possibilities for insulin resistance in non-diabetic people
• Children in puberty
• People with type 2 diabetes
• Late term pregnant women
• People ill with an infection
• People on steroids
• People experiencing high stress levels
What are the 4 values for diabetes diagnosis and when are they used for diagnosis?
FPG >= 7.0 mmol/L (need 2 measurements if asymptomatic)
o Fasting = no intake for at least 8h
A1C >= 6.5% (in adults)
o Not for suspected T1DM
2hPG in a 75g OGTT >= 11.1 mmol/L
Random PG >= 11.1 mmol/L
What are the 3 values for pre-diabetes diagnosis?
Postprandial glycemia (or post load) ≥ 7.8 mmol/L = IGT
FPG ≥ 5.6 mmol/L = IFG
A1C 6.0-6.5% = Prediabetes
What is the recommended macronutrient distribution in diabetes? Fiber? Trans fat? SFA?
Protein 15-20% (or 1.0-1.5 g/kg BW)
Fiber: Increased to 30-50g/d; > 1/3 (10-20g/d) from viscous soluble fiber (e.g oats, barley, psyllium, konjac mannan, pulses, F&V)
Avoid trans fats; reduce SFA to < 9% of kcals; replace with PUFAs from mixed n-3/n-6 sources (e.g. nuts, canola oil, soybean oil, flaxseed), MUFAs from plant sources (e.g. extra virgin olive oil, high oleic oils, avocados), whole grains, or low GI CHO
What can a weight loss of 5-10% accomplish in people with diabetes and BMI≥25?
Nutritionally balanced, calorie reduced diet should be followed to achieve and maintain a lower, healthier BW
Weight loss of 5-10% of initial BW = improved insulin sensitivity, glycemic control, BP control, lipid levels
What should people with diabetes replace SFA with?
Polyunsaturated fatty acids (PUFAs) from mixed n-3/n-6 sources (e.g. nuts, canola oil, soybean oil, flaxseed)
Monounsaturated fatty acids (MUFAs) from plant sources (e.g. extra virgin olive oil, high oleic oils, avocados),
Whole grains, or
What is the first step for management of hyperglycemia after diagnosis of T2DM? What if not at target? What is the time goal for attainment of A1C?
1. Initiate intensive healthy behaviour interventions or E restriction and increased PA to achieve and maintain healthy BW (+ Provide counselling on a diet best suited to the individual based on the values, preferences, and treatment goals)
2. If not at target: Add pharmacotherapy
Timely adjustments to healthy behaviour interventions and/or pharmacotherapy should be made to attain A1C within 2-3 months for healthy behaviour interventions alone or 3-6 months for any combination with pharmacotherapy