Diabetes

Question 0

Type 2 or non insulin dependant diabetes

Answer 0

• insulin secretion still OK but insulin action is depressed. Related to reduced tissue receptor numbers or action
• can be controlled with diet

Question 1

Type 1 insulin dependant

What is it?

Answer 1

• problem with insulin formation (islet cells are damaged).

- means individual is dependant on multiple daily injections of insulin

Question 2

Why does blood glucose need to be so tightly controlled?

Answer 2

-obvious need for glucose dependant tissue so plasma glucose must be maintained
-also plasma glucose is harmful of the is a chronic elevation for 3 reasons
A) hyperglycaemia leads to glucose loss In the urine and so water loss (dehydration)
B) chronic hyperglycaemia leads to glycosylation of proteins- chemical reaction with amino acid side chains and resulted protein dysfunction
C) chronic hypoglycaemia leads to sorbitol accumulation in nervous tissue (including the eye) resulting in peripheral nerve damage and cataracts

Question 3

What are the effects of insulin?

Answer 3

-membrane transport- entry of glucose into cells particularly with GLUT 4 (adipose tissue and muscle). Also aa entry into cells
-metabolism of glucose- insulin activates all pathways which metabolise glucose ie glycolysis, glycogenesis, non essential aa biosynthesis and lipogenesis. The basic mechanisms for this are:
A) insulin tends to promote ‘dephosphorylation’ of enzymes under control of the c-amp cascade ie PFK , glycogen synthase, glycogen phosphorylase, acetylCoA carboxylase, citrate cleavage pathway, transaminases.
C) insulin promotes anabolic actions such as protein synthesis and fat synthesis which need ATL and so an energy sink is provided which means more glucose is oxidised for ATP supply.

Question 4

What happens when there is an absence of insulin?

Answer 4

The absence of insulin response a strongly catabolic state expressed.

• increased rate of hepatic glycogenolysis (glycogen mobilisation) due to covalent regulation of enzyme activity via stimulation of the c-AMP axis
• increased hepatic rates of gluconeogenesis- increased gene expression of gluconeogenic enzymes plus c-AMP induced covalent regulation at PFK2 and so PFK-/ fructose 1,6 bisphosphatase axis. Glycogenolysis and gluconeogenesis obviously antagonise the hyperglycaemia
• increased rates of lipolysis via C-amp induced activation of hormone sensitive lipase. The increased in lipid mobilisation is sufficiently large in the more serious type1 diabetes to cause pathological ketone body production
• decreased protein synthesis and increased protein breakdown means tissues mobilise amino acids (muscle wasting) for conversion to glucose in liver pl
• basically insulin is a major anabolic signal within the animal and in its absence the body enters uncontrolled catabolism