Endocrine and hormones

Question 1

Explain the protein structure of insulin – disulphide bonds, chains,
What’s the half-life of insulin and why?
What is cleaved off proinsulin to form insulin?

Answer 1

B-chain and A-chain, c-peptide. 3 disulphide bonds and an intradisulphide bond within the a chain
half life of insulin: 5-9 mins (short) as it’s not bound to plasma protein and so easily broken down by proteases

Proinsulin, c-peptide is cleaved off

Question 2

In insulin production, Ribosomes make [blank]. In RER is the [blank]. Transported to Golgi and cleaved to form [blank].

Answer 2

preproinsulin
proinsulin
insulin

Question 3

What are the 3 enzymes involved in conversion of proinsulin to insulin?
What are the cleavage points?

Answer 3

Proconvertase 1 (PC1) - 32,33
PC2 - 65,66
CPH - 64,65 of c -peptide

Question 4

Solubility of proinsulin and insulin? What ion is required in the secretory granules? What’s the structure?
What’s required for the exocytosis?

Answer 4

proinsulin is highly water soluble, insulin less so, precipitates out with zinc ions.

forms a crystalline core

exocytosis involves Ca2+ and ATP

Question 5

How does a rise in blood glucose change the ATP:ADP ratio? What happens as a result? What channel opens and what happens?

Answer 5

rises ATP:ADP ratio, results in closure of ATP-sensitive K+ channels, membrane depolarisation, opening of voltage-gated Ca2+ channels –> increased IR

Question 6

2 adrenoceptors are present for beta-cells. What are they? Which is dominant? What’s the overall effect of activation of sympathetic nervous system?

Answer 6

beta adrenoceptors - increases insulin release
alpha -2 adrenoceptor reduces IR

dominant receptor - alpha-2-adrenoceptor so predominant effect is to reduce insulin release if sympathetic is activated

Question 7

What does activation of the PS NS do? What receptor is involved?

Answer 7

parasympathetic - muscarinic increases IR (insulin release)

Question 8

What cells release GLP-1 and GIP?

Answer 8

GLP-1 = secreted by L cells

GIP cells = secreted by K cells

Question 9

What are the potentiators? When are they released? What do they do?

Answer 9

Gut hormones and glucagon
they are released when food is present in the gut
increases IR

Question 10

What are some effects of insulin?

Answer 10

promote growth and development, cellular uptake of K+
Promote uptake and utilisation of glucose in skeletal muscle and adipose
Promote fuel storage (ANABOLIC) increases rate of synthesis and storage of energy reserves (glycogen and fats) and of protein

Question 11

Glucagon secretion stimulated by both SNS and PSNS. T/F?

Answer 11

TRUE

Question 12

What cells secrete glucagon?
What other things stimulate glucagon?
What inhibits glucagon?

Answer 12

Islet alpha-cells

stimulated by low blood glucose and amino acids
Inhibited by high blood glucose, insulin and somatostatin

Question 13

What are the 3 main actions of glucagon?

Answer 13

raise blood glucose
stimulate hepatic glycogenolysis
stimulate hepatic gluconeogenesis
stimulate lipolysis

Question 14

what kind of hormone is somatostatin? What cell releases it? Where is it released from?

Answer 14

peptide hormone
islet delta-cells
hypothalamus and GIT

Question 15

How does the somatostatin released by the pancreas different to that released by CNS and GIT?

Answer 15

could hold a physiological role in islet

Question 16

What is the function of somatostatin?

Answer 16

inhibits glucagon and insulin secretion

Question 17

What’s the normal range of blood glucose?

Answer 17

4-8mmol/L

Question 18

What hormones raise blood glucose in prolonged hypoglycaemia? In severe hypoglycaemia

Answer 18

cortisol and GH raise in prolonged hypoglycaemia

in severe use adrenaline