week3-L6-intro to Diabetes Mellitus Flashcards
GLUT4
highly insulin responsive common in muscle and adipocytes, recruited by insulin to uptake glucose
effects of insulin of cell metabolism
fed state
increase protein synthesis and inhibit protein breakdown and gluconeogenesis
effects of glucagon on cell metabolism
fasting state
opens channels to allow transport of pyruvate lactate
increase breakdown of proteins
increase gluconeogenesis
fuel stores
carbohydrate, fat and proteins
effects on insulin of adipocytes
increase activity of LPL lipoprotein lipase
increase Glycerol and NEFA intake to form triglyceride and inhibit triglyceride breakdown
NB cortisol and GH breakdown triglyceride during fast state
why short responsive time?
due to double circulation of the GI and hepatic portal circulation
gluconeogenesis
contribute to 25% hepatic glucose output HGO 10h after fasting
triglyceride into Gly-3P to glucose
brain fuel
glucose or ketone bodies
ketone bodies regulation
insulin inhibition
glucagon stimulate conversion of fatty acyl CoA into ketone bodies due to low glucose present for brain supply
hepatic glycogenolysis
conversion of liver glycogen store to glucose to increase the HGO
difference between glycogen in liver and muscles
only liver glycogen store can be broken down to glucose
hormone acting of muscle cells
cortisol and GH inhibit the glucose uptake but insulin hormone increase the uptake of glucose
fasted state process
increase lipolysis, proteinolysis glycogenolysis and gluconeogenesis to increase the HGO and prolonged state results in increase ketogenesis; low insulin to glucagon
fed state process
increase lipogenesis, protein synthesis and glycogen store
decrease proteinolysis and gluconeogenesis
high insulin to glucagon ratio
diabetes
too high blood glucose the the body cannot overcome
diagnosis of diabetes tests
fasting tests random glucose oral glucose HbA1c requires 2 positive test or 1 positive and 1 osmotic symptoms
fasting glucose
> 7.0mmol/L
random glucose
morning glucose, 11.1mmol/L
oral glucose tolerance test
any point of the day, fasting 75g load
HbA1c
average glucose for the last 3 months based on haemoglobin turnover
types 1 Diabetes
autoimmune condition, where no insulin is produced at all
resulting in diabetic ketoacidosis
pH< 7.3
signs and symptoms of T1DM
weight loss, hyperglycaemia, glycosuria with osmotic symptoms, ketones in blood and urine
Diagnostic test of T1DM
antibodies GAD and IA2
c-peptide
presence of ketones
too much insulin administered
hypoglycaemia, no glucose output from liver
too much glucose muscles
conterregulatory response to hypoglycaemia
increase HGO by glycogenesis and gluconeogenesis and increase lipolysis
impaired awareness to hypoglycaemia
reduced ability to recognise symptoms
Loss of counter regulatory response
Recurrent hypoglycaemia
signs and symptoms
autonomic: sweating, pallor, palpitations and shaking
neuroglycopenic: slurred speech, poor vision, confusion, seizures, loss consciousness
severe hypoglycaemia
need 3rd party assistance
type 2 diabetes
insulin resistance in liver, muscle and adipose tissues
suppress ketogenesis and proteolysis
clinical symptoms of insulin resistnace
high triglyceride and low HDL, inflammatory state and energy expenditure, hypertension BP > 135/80
waist circumference men>102 and women >are 88
fasting glucose >6.0mmol/L
type 2 diabetes signs
hyperglycaemia, overweight, dyslipdaemia, less osmotic symptoms, insulin resistance and later deficiency
type 2 diabetes risk factors
age, high BMI family heritability, inactivity and ethnicity
dietary recommendations and education
healthy eating and diet; calories control and reduce fat, reduce refined carbohydrate and increase complex ones
increase soluble fibres and decrease sodium
type 1 diabetes management
exogenous insulin and self monitoring of glucose.
structured education and technology
type 2 diabetes management
diet oral medication
structured education and insulin needs
both type 1 and type 2 management
monitor and prevent retinopathy, neuropathy, nephropathya and cardiovascular
