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δcell
α cell
β cell
Diabetes Mellitus
Type I Type II
Classification of Diabetes Mellitus
by Etiology
Type 1 -cell destruction—complete lack of
insulin
Type 2 -cell dysfunction and insulin
resistance
Hyperglycemia
Other Symptoms:
Polyphagia
recurrent infection
Diabetes Mellitus
Type I Type II
Age of onset Usually during Frequently after
childhood or puberty the age of 35
Symptoms develop Symptoms
rapidly develop
gradually
Nutritional Frequently Obesity usually
status at the undernourished present
time of disease
onset
Type I Type II
Genetis
+
Glucose toxiity
Decline of beta cell function
Free fatty acids
Type 2 diabetes
Metabolic changes
• Due to deficiency of insulin
• Profoundly affect three tissues
Liver
Muscle
Adipose tissue
Hyperglycemia and ketoacidosis
•Elevated levels of blood glucose and ketones are
hallmarks of untreated diabetes mellitus
Hyperglycemia and ketoacidosis
Increased hepatic production and diminished
peripheral utilization of glucose –
hyperglycemia
Glucagon
1 Fatty Acids
Epinephrine Hormone
Glucocortic-
oids
Sensitive
Lipase Albumin -oxidation 3
+ Acetyl Co A
Glycerol
TCA
Cycle
Fatty Acids Fatty
Acids Ketone
Bodies
NORMAL DIABETES
Cataract
Glucose
Sorbitol
Hypercholesterolemiaemia
Laboratory investigation
• Blood Glucose level
• Complete lipid profile
• Blood urea and creatinine
• Microalbuminuria
• Glycated hemoglobin (HbA1c)
Diagnosis
Oral glucose tolerance test
The Miracle
of Insulin
www.urmc.rochester.edu/neuroslides
www.urmc.rochester.edu/neuroslides
Biology of
Macrovascular Complications
Metabolic injury to large
vessels
Advanced glycation
Glycated proteins Sorbitol and fructose
end products (AGEs)
(eg, A1C)