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Metabolic syndrome and diabetes.
Obesity is what bmi?
Underweight = <18.5
Normal weight = 18.5–24.9
Overweight = 25–29.9
Obesity = 30 or greater
Obesity has what risks?
CVD, Metabolic disorders, respiratory problems.
Metabolic syndrome. the 5 conditions.
High blood pressure (> 130/85 mmHg)
High blood glucose (fasting blood glucose ≥ 110 mg/dL)
Central/visceral adiposity (waist circumference: men > 40 in; women > 35 in)
High triglycerides (≥ 150 mg/dL)
Low HDL cholesterol (men < 40 mg/dL; women < 50 mg/dL)
How many of the conditions needed for metabolic syndrome?
atleast 3 out of 5
Metabolic syndrome risks.
Atherosclerosis
Coronary heart disease, heart attack, stroke
Type 2 diabetes
Kidney disease
Nonalcoholic fatty liver disease
MOA of insulin. Action on glucose level, glucose uptake into cells, other energy substrates, and energy storage.
Allows uptake of glucose into cells
Cells use glucose to make ATP
Lowers blood glucose
Uptake of fatty acids and amino acids
Nutrient storage & use
Excess glucose → glycogen
Fatty acids → triglycerides
Amino acids → proteins
gluconeogenesis, glycogenesis, glycogenolysis, lipolysis, lipogenesis, protein anabolism, protein catabolism
gluconeogenesis-metabolic process that creates glucose from non-carbohydrate sources like fat and protein
glycogenesis-the metabolic process where the body converts excess glucose into glycogen, a storage form of glucose, primarily in the liver and muscles, to be used later for energy.
glycogenolysis-the process of breaking down glycogen into glucose
lipolysis-the metabolic process where triglycerides (stored fat) are broken down into glycerol and free fatty acids
lipogenesis-the metabolic process where your body converts excess carbohydrates and other substrates into fatty acids and then stores them as triglycerides (fats)
protein anabolism- building new proteins
protein catabolism-breakdown of protein
What is diabetes?
a disease in which the body’s ability to produce insulin or respond to insulin is impaired, resulting in abnormal metabolism of carbohydrates and elevated levels of glucose in the blood and urine
Type 1 vs type 2 diabetes
Type 1 is lack of insulin production
Type is poor responding to insulin.
Type 1 diebetes.
5-10% of diabetes
Peak age of diagnosis: 14 yo
Absolute insulin deficiency
Treatment: insulin
Type 2 diabetes.
Insulin resistance: cells do not respond to insulin
Causes initial hyperinsulinemia (prediabetes)
Leads to progressive loss of beta cell insulin secretion and hyperglycemia (type 2 diabetes
HOMA-IR: test for insulin resistance (uses fasting glucose and fasting insulin)
Treatment goal: increase insulin sensitivity
Physical activity
Weight loss
Proper diet/nutrition
Stress reduction
Proper sleep
FPG, OGTT, A1C, HOMA-IR
What is each diagnostic for?
Fasting plasma glucose test (FPG)
Oral glucose tolerance test (OGTT)
Glycated hemoglobin A1c (A1C)
—Measure of long-term glucose control past 120 days.
HOMA-IR: test for insulin resistance
Chronic complications of diabetes.
Neuropathy
Foot ulcers and amputations
Retinopathy
Nephropathy
Cardiovascular disease
DKA Pathogenesis.
Occurs when the body cannot use glucose as fuel and uses fat instead (more common in type 1)
Breakdown of fat produces ketones (acidic)
Hyperosmolar Hyperglycemic State pathogenesis.
Most in type 2, underlying condition (infection), elderly
Profound hyperglycemia → glucosuria → polyuria → severe dehydration → serum hyperosmolarity
Hyperosmolar Hyperglycemic State. Symptoms and labs.
Profound hyperglycemia ( > 600 mg/dL) lab
Dehydration (up to 9 L)
Serum hyperosmolarity lab
Nonketotic lab.
Alterations in consciousness
Mortality 5-20%
DKA lab and symptoms.
Glucose, ketone, BUN labs.
Excessive thirst
Frequent urination
Dry mouth and throat
Fatigue
Nausea and vomiting
Abdominal pain
Confusion and lethargy
Coma
Fruity-smelling breath
Deep, rapid breathing
Blurred vision
Weakness
Weight loss
Headache
