DIABETES MELLITUS TYPE 1

Pathogenesis
1. Destruction of -cell is quite variable.
2. Fasting hyperglycemia can rapidly change to
severe hyperglycemia or ketoacidosis (in
infection or other stress).
3. Manifestation little or no insulin secretion
low or undetectable C-peptide
 Pathophysiology
Insulin deficiency
increased glucose production by the liver and
kidney and
impaired peripheral glucose utilisation
hyperglycaemia

Increase anti insulin hormones

Lipolysis ketonaemia and metabolic acidosis
DIABETES MELLITUS TYPE 2
 Pathophysiology
Beta-cell dysfunction
Insulin resistance
In the progression from normal to abnormal glucose
tolerance, postprandial blood glucose levels
increase first. Eventually, fasting hyperglycemia
develops as suppression of hepatic
gluconeogenesis fails.
 Genomic factors
Single-Nucleotide Polymorphisms (SNPs) have
identified a number of genetic variants that are
associated with beta-cell function and insulin
resistance.
 Amino acid metabolism
The risk of future diabetes was at least 4-fold
higher in normoglycemic individuals with high
fasting plasma concentrations of 3 amino
acids (isoleucine, phenylalanine, and tyrosine).
Concentrations of these amino acids were
elevated up to 12 years prior to the onset of
diabetes.
Gestational Diabetes
 Pathophysiology
Insulin resistance in pregnancy because of :
Increase of fat deposits in mother
Increase hormones in pregnancy (HPL,
progesterone, cortisol, and prolactin)