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Summary Block 1.6 Tutorial cases
- Vak
- Block 1.6
- Instelling
- Maastricht University (UM)
Tutorial cases from block 1.6 Diabetes, Obesity and Lifestyle. Onderwijsgroep (OWG) casussen uit blok 1.6 Diabetes, obesitas en leefstijl
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Voorbeeld 3 van de 23 pagina's
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Case 1Metabolic rate
Fat is most ‘effective’ if we look dat this.
The last values in the tables is what we
have to remember. 1 mol of protein
gives 4,0 kcal etc.
Daily energy balance
Obesity and diabetes are illnesses with a disbalance in calories, more intake of calories than use. Ultimately obesity
is the result of a positive energy balance. Very energy rich food is present and we move less and less. The daily
energy use of an individual can be divided into:
1. basal metabolsim (BMR: basic metabolic rate)
2. thermic effect of food
3. physical activity
BMR: minimum amount of energy that is used to let all chemical reactions in our body proceed, measured in rest.
50-70% of energy use in a sitting individual.
65-70 kcl/hour – male of 70kg, differences are determined by difference in muscle mass
decreases when older and thus more obesity
stimulated by thyroid hormone, GH and fever
decreasing during sleep and vasting
Thermic: all energy we use is converted into heat or stored.
70kg male: 200kcal per day needed to digest food
normal need in our society 2000-2250 kcal (sedetary lifestyle)
NEAT: non exercise activity thermogenesis, meaning our normal daily activities and how much energy they
require (in kcal), can differ a lot between people. NEAT difference contributes to obesity. Twins experiment
one low calorie diet one low calory diet. Children that can increase the BMR do not get fat children that
cannot adapt get obese.
Losing weight is difficult because we increasingly have to diminish our energy intake and also vasting can cause the
BMR to decrease so that helps us nothing to be honest.
Obesity requires more energy, but not much more than you would usually need. Basal metabolic rate is going up.
Metabolism of glucose: insulin
Two states of the body: postabsorptive and….
Digestion = conversion
Polysaccharides monosaccharides
o sucrase
o lactase
o maltase
Take up of glucose and function of insulin
Take-up of glucose: SGLT transporter in the intestines
,In the liver galactose and fructose are converted into glucose. This then can go to tissue where it is used for energy:
Basal glucose uptake in a cell that needs it to FUNCTION (ex. muscle cell) goes via a GLUT 1/3 transporter.
Facilitated glucose uptake goes via GLUT 4 and is insulin dependent.
Liver uptake of glucose is INDEPENDENT of insulin. Then how is the glucose uptake regulated? Mass action as much
glucose as we have in our blood, that much will be taken up by the liver. Low amount available, liver releases glucose
into the blood instead of taking it up. Liver regulates, when too much glucose:
inhibit glycogenolysis (due to also defect of insulin)
inhibit gluconeogenesis (due to also defect of insulin)
Insulin
Polypeptide that consists of two peptide chains that are tied by two disulfide bridges. In the pro-hormone a molecule
named C-peptide connects the two insulin peptide chains. Insulin and C peptide are stored in beta cell granules in
the amount 1:1. The C peptide is removed from the blood by the liver and released in the urine. Can de used to
examine amount of insulin secretion.
Beta cells respond on the insulin concentration and the speed of glucose concentration changes in the blood. They
transport the glucose into the cells via the GLUT2 transporter. Glucokinase enzyme catalyzes the formation of
glucose-6-phosphate out of glucose (this is the only way it can be in the cell) pancreas and liver, more gradual
enzyme. Hexokinase same function in other cells to convert to Glu6p but this one is very rapid. This is the speed
limiting step in glycolysis and the key mediator in beta cells. 3-C parts like glyceraldehyde that are formed
downstream from glucose-6-phosphate are stimulators of insulin release. The secretion of insulin depends on ATP.
The formed ATP in glucose metabolism closes an ATP-dependant K+ channel which causes depolarisation of the cell
followed by voltage dependent Ca2+ influx. Higher intracellular Ca2+ causes exocytosis of insulin/C peptide. The beta
cells contain a ATP-dependant K-channel and a sulfonylurea receptor, diabetes medication bind to that receptor.
, Regulation by amino acids
Anionic amino acids depolarize the membrane and open voltage gated Ca2+ channels, this leads to Ca2+ influx and
insulin secretion.
Regulation by other hormones
Glucagon stimulates insulin release
Somatostatin inhibits insulin release
CCK en GIP en GLP-1 stimulate insulin
o GIP by K cells small intestine
o GLP-1 door L-cellen in het distale ileum en colon.
o GIP en GLP-1 degraded by dipeptidyl peptidases DPPs, vooral de DPP-4
Rise of GLP-1 en GIP after eating (het incretine effect) is less in patiënts with diabetes mellitus type 2 and a attampt
to restore incretine functie can lead to increased glycemisch control and weight loss. (verzadigingsgevoel).
Neural control
Islets of langerhans are innervated PSNS and SNS. N. vagus causes stimulation of beta cells to release insulin
(because more Ca2+ uptake) via Ach. SNS inhibits insulin release via noradrenalin on the alpha 2 adrenergic
receptors on the beta cells.
Insulin effect
Insulin causes uptake of glucose by muscle and fat tissue. Also it causes the uptake of amino acids, Mg+, K+ and
PO43-. The secondary effect is that glucose oxidation, lipid and glycogen synthesis are stimulated in insulin-sensitive
tissues. This is because the speed determining reaction (to Glu6P) is stimulated directly due to over availability of
glucose. The overal effect is to provide glucose as energy, storage of too much carbohydrates and fat and highten
the protein synthesis.
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