P 2 – Diabetes Type 1

-Ketogenesis and Ketone Bodies

Ketogenesis
• Occurs when there’s a high rate of fatty acid oxidation
(during fasting, starvation & diabetes).
• Takes place in the liver and exported for other tissues.
• Energy source for the brain during fasting.
1. Condensation by a
thiolase.
2. Addition of the 3rd
acetyle CoA by
Insulin -
HMG CoA synthase Glucagon +
(key enzyme)
3. Cleavage of HMG-CoA
by HMG CoA lyase.
4. Acetoacetate:
◦ Decarboxylation
◦ Reduction by
hydroxybutyrate
dehydrogenase
Ketolysis

1. Oxidation by hydroxybutyrate
dehydrogenase
2. Addition of CoA by acetoacetate
succinyl-CoA transferase.
3. Split by thiolase.
Types of DM
1. Type 1.
2. Type 2.
3. Gestational diabetes mellitus.
4. Other specific types:
 Genetic defects of beta cell development or function
 Drug- or chemical-induced e.g. glucocorticoids
 Endocrinopathies such as acromegaly and Cushing’s disease
 Infections e.g. fulminant diabetes
 Uncommon forms of immune-mediated diabetes—”stiff-person” syndrome & anti-
insulin receptor antibodies.
Ribose
 Pentose monosaccharide.
 Forms the back bone of RNA.
 Deoxyribose forms the back bone of DNA.