Sugar metabolism example PDF

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ASSESSMENT COVERSHEET S T U D E N T D E TA I L S Student ID

25989006

Surname

Gough

First Name

Georgina

A S S E S S M E N T D E TA I L S Unit Code

PHY2032

Unit Title

Endocrine Control Systems

Assignment Title

Sugar Metabolism

Lecturer name

Farshad Mansouri

Tutor’s name

Tutorial Day

Tuesday

Tutorial Time

10am

Has any part of this assignment been previously submitted as part of another unit/course? Is this an authorised group assessment?

Y

Y

N

N

For group assessment, each student must attach their own signed coversheet to the assignment

Due Date

21.8.2017

Date Submitted

21.8.17

E X TE N S I O N O F W O R K All work must be submitted by the due date. For late assignment submission http://www.med.monash.edu.au/policies/docs/assessment-late-submission-policy-v6.pdf

policy

see:

Intentional plagiarism or collusion amounts to cheating under Part 7 of the Monash University (Council) regulations.

Plagiarism: Plagiarism means taking and using another person’s ideas or manner of expressing them and passing them off as one’s own. For example, by failing to give appropriate acknowledgement. The material used can be from any source (staff, students or the internet, published and unpublished works). Collusion: Collusion means unauthorised collaboration with another person on assessable written, oral or practical work and includes paying another person to complete all or part of the work. Where there are reasonable grounds for believing that intentional plagiarism or collusion has occurred, this will be reported to the Associate Dean (Education) or delegate, who may disallow the work concerned by prohibiting assessment or refer the matter to the Faculty Discipline Panel for a hearing. Client/Patient Confidentiality: Where a patient/client case study is undertaken informed consent from the individual/s studied must be obtained. Care must be taken to ensure confidentiality is maintained at all times. Failure to obtain a signed, original Consent Form or other unethical behaviour in the performance of a case study (such as putting the subject's real name on the report, or otherwise breaking confidentiality) will result in a mark of zero being given for the assignment. Consent form templates are available at: http://www.med.monash.edu.au/current/student-forms.html Student Statement:  I have read the university’s Student Academic Integrity Policy and Procedures.  I understand the consequences of engaging in plagiarism and collusion as described in Part 7 of the Monash University (Council) Regulations http://adm.monash.edu/legal/legislation/statutes  I have taken proper care to safeguard this work and made all reasonable efforts to ensure it could not be copied.  No part of this assignment has been previously submitted as part of another unit/course.  I acknowledge and agree that the assessor of this assignment may for the purposes of assessment, reproduce the assignment and: i. provide to another member of faculty and any external marker; and/or ii. submit it to a text matching software; and/or iii. submit it to a text matching software which may then retain a copy of the assignment on its database for the purpose of future plagiarism checking.  I certify that I have not plagiarised the work of others or participated in unauthorised collaboration when preparing this assignment.  I have retained a copy of my work. Georgina Isabel Gough Date: 21.8.17 Student Signature: * delete (iii) if not applicable Privacy Statement: The information on this form is collected for the primary purpose of assessing your assignment and ensuring the academic integrity requirements of the University are met. Other purposes of collection include recording your plagiarism and collusion declaration, attending to course and administrative matters and statistical analyses. If you choose not to complete all the questions on this form, it may not be possible for Monash University to assess your assignment. You have a right to access personal information that Monash University holds about you, subject to any exceptions in relevant legislation. If you wish to seek access to your personal information or inquire about the handling of your personal information, please contact the University Privacy Officer: [email protected]

PHY2032 2016 Sugar Metabolism Worksheet Submit an individual electronic version of this worksheet to the Moodle drop box. Due Friday 21/08/2017 at 2pm GRAPHS An excellent tutorial on how to organise your data in excel and graph it using Graphpad Prism specifically for this practical is available here: https://www.alexandriarepository.org/reader/virtual-practical-class-sugar-metabolism/28224. Use the data in the class excel data file available on MOODLE, construct and provide the following 2 graphs: 

Line graph: The mean blood glucose concentration (± standard error of the mean, SEM) for each experimental group for each time point (time 0, 30, 60, 90, and 120 min). Hint: GraphPad Prism can automatically calculate SEM but to do it manually: divide the standard deviation by the square root of the number of samples (n) in the group, i.e. SEM = STDEV(#) / SQRT(COUNT(#)).

 

Bar graph: The mean ± SEM change in peak blood glucose concentration of each group. The change in blood glucose concentration is the difference between the maximum blood glucose concentration (the highest blood glucose concentration after consumption of the sugar drink) and the basal blood glucose concentration.

Create your graphs in GraphPad Prism and insert them in the space below. For a graph to be informative it must have:  A Figure Legend BELOW the graph with an informative title, an explanation of what each symbol, line, colour or shading means, what statistics are shown, treatments, times etc.. All the information required to understand the Figure completely on its own independent of what is written in the results or main text. (HINT: Look at a recent manuscript in Journal of Physiology Figure legend for guidance).  Both axes are appropriately labelled with units used,

  

Different line types and/or symbols used for different experimental groups which are easily distinguishable from each other, A legend (key) in the top right or left hand corner showing what the different symbols and/or line types used for the different plots in the graph stand for. and Appropriate font sizes (12 point for labels and figure legend, at least 10 pt for axes).

Mean Blood Glucose Concentration (mM) of the Different Experimental Groups for Each Time Point Blood Glucose Concentration (mM)

10

Legend Glucose Rest

8

Glucose Exercise 6

Fructose Rest Glucose Sip & Spit Rest

4

2

12 0

90

60

0

30

0

Time (mins)

Change in Peak

Graphical representation of mean blood glucose concentration (mM) of each experimental group (glucose rest, glucose exercise, fructose rest and glucose sip & spit rest) measured at five different time points. Initially the basal level was obtained (0mins) after subjects fasted for a minimum of 3hours. Participants then consumed either glucose or fructose (approximately 50g) to initiate the experiment. Progressive blood glucose concentrations were obtained across 30minute intervals for 120mins. The blue line represents blood glucose concentration whilst remaining rested throughout the period. The red line represents blood glucose concentration whilst exercising for at least 5 minutes between recording times. The green line represents blood glucose concentration of those that consumed a fructose drink whilst remaining rested throughout the period. The purple line represents the blood glucose concentration of the participant who didn’t consume the glucose drink but rather sipped and spit the entirety of fluid and then also remained rested throughout the experimental period. 1

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Experimental Group

Graphical representation of the peak blood glucose concentration (mM) of each experimental group (glucose rest, glucose exercise, fructose rest and glucose sip & spit rest) across the five time points. The peak blood glucose points observed originate from subtracting the basal blood glucose concentration from the maximum blood glucose concentration for each experimental group. The blue line represents peak blood glucose concentration whilst remaining rested throughout the period. The red line represents peak blood glucose concentration whilst

PRE-PRAC CONSIDERATIONS 1.

Why is it necessary to fast before taking the glucose load?

To have a valid baseline for comparison, insulin and glucose levels would be inconsistent due to different individual’s ingestion times/types. Ultimately, it’s important for accuracy. 2.

Why would it be more accurate to measure the glucose concentration in the blood rather than in the urine?

Taking blood is an easy and rapid representation of glucose levels because individuals only excrete glucose when it’s in high concentrations. Also, the kidney reabsorbs glucose, sends it back to the blood and then it is filtered again, ultimately taking a long time to pass as urine. ORAL GLUCOSE TOLERANCE TEST 3. Referring to your figure, what happens to the concentration of glucose in the blood during the first hour after ingestion of the glucose load? Why?

Within the first 30minutes the concentration increases and hits its peak, and then progressively across the next 90minutes decreases approaching the basal level. This is due to the production of insulin from the pancreas. Insulin prevents blood sugar levels getting too high or too low by converting the glucose to energy or storing for future use. 4.

When does the blood glucose concentration reach a maximum? Why is this amount of time required?

At 30minutes. Because it takes the body approximately 30mins to produce enough insulin to start working. Working being defined as countering the effects of glucose and converting the glucose to energy or moving to storage.

5.

What makes the blood glucose concentration fall again? (Discuss the physiology)

Insulin is secreted from storage granules in the islets of Langerhans (pancreatic islets), more specifically beta cells. Insulin is vital for organic metabolism; its plasma concentration increases during the absorptive state and decreases during the post absorptive state as it responds to differing plasma glucose levels. The stimulation of insulin release occurs via the activation of the parasympathetic neurons which occurs after consuming a form of glucose. Alternatively, activation of the sympathetic neurons to the islets increase the release of adrenalin inhibiting insulin secretion. Insulin is a peptide hormone, that induces its effects by binding to certain receptors on plasma membranes of target cells. The binding activates signal transduction pathways that influence the plasma membrane transport proteins and intracellular enzymes of the target cell. In response to the influx of glucose, the parasympathetic neurons activate the secretion of insulin for approximately 10-15mins (phase 1). This increases the glucose uptake and utilisation from muscle cells and adipocytes. Predominantly, it also increases the net glycogen synthesis in muscle and liver cells and decreases the gluconeogenesis. Some other reactions occur throughout these cells also however. Once reaching the peak (at 30minutes) the secretion of adrenalin via the sympathetic neurons in the islets of Langerhans is what causes a decrease in glucose uptake and utilisation in muscle cells and adipocytes and an increase in glucose release due to removal of inhibitory effects on glycogen catabolism and gluconeogenesis, working to restore normoglycaemia. Phase 2 is what occurs until basal glucose levels are achieved again and is what is occurring to make the blood glucose concentration fall and get closer to basal levels across the 2 hour time period. GLUCOSE VS FRUCTOSE 6.

What happens to the concentration of glucose in the blood for the first hour after ingestion of the FRUCTOSE? How does this compare with ingesting glucose?

There was a slight increase and after 30mins levels started to decrease progressively back to basal levels. The ingestion of glucose initiated a rapid and large spike, this wasn’t seen for fructose. The same effect was seen (a spike and max reached after 30mins and then progressive decrease until normoglycaemia) however glucose ingested was much more significant.

7.

When does the blood glucose concentration reach a maximum? How does this compare with the group that ingested the glucose load?

After 30 minutes. The peak was reached at the same time as the group that ingested the glucose, however not as substantial. It was within the same time frame as glucose. This would suggest that despite the chemical differences in structure the body acts in similar time frames

EXERCISE VS RESTING 8.

Explain the differences between the basal glucose and glucose exercise groups before and after the ingestion of the sugar drink. That is, does exercise have any effect on the change in blood concentration of glucose? Why might this be?

After consumption of the glucose drink both groups reached their peak/maximum at 30minutes. The exercise group however wasn’t as high as the control. Muscle contraction is vital during exercise and for this to occur large quantities of fuel must be mobilised. During constant exercise activation of the sympathetic nervous system (increased secretion of adrenalin, cortisol and growth hormone) occurs decreasing the release of insulin. However, constant exercise does stimulate the secretion of glucagon from the liver for energy synthesis. Whilst our results mimic those of the resting results just at lower values, it is largely due to the energy demands from muscle cells for contraction during the exercise periods that would uptake plasma glucose levels immediately. However, the remaining 25minutes between measurements (not exercising) would also work with the parasympathetic system and secretion of insulin to work towards normoglycaemia via glucagon synthesis and glucose uptake. 9.

The exercising subjects sometimes show variable responses to this glucose load. Why might this be?

Many other factors may impact a cells ability to uptake or convert glucose to energy whilst exercising, which in turn effects the amount of insulin required to be secreted to counter the effects of raised glucose levels. Some examples include, gender, age, fitness, muscle mass, cardiac output and heart rate during the exercise. Each factor may impact how quickly glucose is utilised or converted by insulin. Furthermore, individual’s performance within the practical may be quite different, some group members may have been pushing to reach max heart rate whilst others may have just been strolling along. CLINICAL APPLICATIONS 10.

In a clinical setting, when would you administer an oral glucose tolerance test (OGTT)?

When the results of fasting or a random blood glucose are ambiguous. That being after fasting blood glucose levels are between 5.5 and 6.9mmol/L, or random between 5.5 and 11mmol/L diabetes is uncertain and the OGTT should be administered. Any levels equal to or above 7.0mmol/L after fasting or above or equal to 11.1mmol/L at random diabetes is likely. Both scenarios warrant the OGTT test for predicted diagnosis of diabetes. The OGTT should be performed in a laboratory under stringent guidelines, such as duration of fasting, type of food ingested, time of day, activity throughout the test. Furthermore, the test should occur at least twice under these settings for near accuracy of diagnosis.

11.

You are consulting a person diagnosed with Type 2 diabetes (Mellitus) on their diet. How would you describe to the person the expected changes in their blood glucose concentration after consumption of a sugary meal compared to a non-diabetic person? Discuss the underlying physiology.

Type two diabetes occurs when insulin resistance begins usually due to poor diet and lack of exercise. As a result of the insulin resistance the pancreatic islet cells (beta cells) respond by producing greater amounts of insulin, to try and manage glucose levels. As this occurs over a large amount of time the beta cells ‘wear out’ depleting a large amount of production cells. It is a combination of ineffective insulin and not enough of insulin. Early in diagnosis an individual that with diabetes that consumes a sugary meal will have a larger basal glucose level, larger spike in blood concentration and a larger amount of insulin circulating and trying to achieve normoglycaemia. The diabetic will also take a much longer time to try and re-establish their basal glucose concentration....