Physiology notes
Enzymes go into the small intestine (duodenum) via the pancreatic
duct. Within the pancreas: islets of Langerhans.
Islets of Langerhans exist out of different cells.
- Alpha cells secrete the hormone glucagon
- Beta cells secrete insulin and co-hormone amylin
o Amylin is co-secreted with insulin
- D cells secrete somatostatin (inhibitor of GH)
o Somatostatin is a general inhibitor
Insulin
- Transports glucose from the blood over the cell membrane into
insulin-sensitive tissues (have a receptor)
- Decrease blood glucose, increases glucose in storage tissues
- Is released at high blood glucose levels
- Take care of removing glucose from the blood
- Insulin-dependent and insulin-independent tissues (brain takes
up glucose independently). Active muscle is also insulin-independent
(fight-flight)
Glucagon
- Takes glucose from the storage cells into the blood (when blood
glucose is low)
- Increases glycogenolysis and lipolysis (increases FFA’s in blood
more glucose in brain).
- Higher blood glucose and FFA levels
- Released at low blood glucose levels.
Balance between glucagon and insulin: in fed state, blood glucose goes up
insulin dominates higher glucose oxidation & synthesis, fat synthesis,
protein synthesis.
In fasted state: glucagon dominates higher glycogenolysis,
gluconeogenesis, ketogenesis. Glucose only goes to brain and active
muscle.
Exocrine pancreas = produces digestive enzymes
Endocrine pancreas: = responsible for regulation of carbohydrate
metabolism (blood glucose). Islets of Langerhans are located here.
Brain anticipates when glucose comes in (parasympathetic) = pre-
absorptive insulin release/cephalic phase. Lack of anticipation
higher disturbance by glucose. Atropine can block the receptors no
anticipation.
Artificial sweetener like saccharin makes insulin levels rise bc of the taste
lower glucose hunger.
Factors that stimulate insulin release:
- Glucose, amino acids, FFA’s (all energy substrates)
- Parasympathetic stimulation (anticipation)
, - Gut hormones: incretins (digestive factors) (GLP-1, CCK) and
feedforward effect (food is going to come in insulin release).
Anticipatory responses reduce the glucose to get glucose homeostasis.
Sympathetic stimulation inhibits insulin release
- Only insulin-independent tissues receive glucose
- = brain and exercising muscle
Hypoglycaemia = low blood sugar
Diabetes
Shortage of insulin.
Baseline blood glucose levels are already elevated when not eating. When
eating, blood sugar rises even more than in non-diabetics. Kidney cannot
handle filtering the blood anymore sweet urine.
Pre-diabetes = glucose intolerance. When you are
pre-diabetic, dieting/exercising etc. can prevent
diabetes.
Glucose measurement for diabetes diagnosis
- Measurement of glucose in urine
- Measurement of glucose in blood
- Measurement of HbA1c (long term regulation)
HbA1c = haemoglobin type A1c
Hyperglycaemia glycosylation of molecules. Haemoglobin binds to
glucose and is sensitive for glycosylation. Haemoglobin molecules live 2-3
months content of glucose in the HbA1c molecule may be used as an
indication for the average blood sugar.
Advantage: provides info on the long-term situation.
Disadvantage: missing of hypoglycaemic/hyperglycaemic peaks. Some
people suffer on extremes.
Type 1 Diabetes = Insulin dependent (autoimmune)
Enzymes go into the small intestine (duodenum) via the pancreatic
duct. Within the pancreas: islets of Langerhans.
Islets of Langerhans exist out of different cells.
- Alpha cells secrete the hormone glucagon
- Beta cells secrete insulin and co-hormone amylin
o Amylin is co-secreted with insulin
- D cells secrete somatostatin (inhibitor of GH)
o Somatostatin is a general inhibitor
Insulin
- Transports glucose from the blood over the cell membrane into
insulin-sensitive tissues (have a receptor)
- Decrease blood glucose, increases glucose in storage tissues
- Is released at high blood glucose levels
- Take care of removing glucose from the blood
- Insulin-dependent and insulin-independent tissues (brain takes
up glucose independently). Active muscle is also insulin-independent
(fight-flight)
Glucagon
- Takes glucose from the storage cells into the blood (when blood
glucose is low)
- Increases glycogenolysis and lipolysis (increases FFA’s in blood
more glucose in brain).
- Higher blood glucose and FFA levels
- Released at low blood glucose levels.
Balance between glucagon and insulin: in fed state, blood glucose goes up
insulin dominates higher glucose oxidation & synthesis, fat synthesis,
protein synthesis.
In fasted state: glucagon dominates higher glycogenolysis,
gluconeogenesis, ketogenesis. Glucose only goes to brain and active
muscle.
Exocrine pancreas = produces digestive enzymes
Endocrine pancreas: = responsible for regulation of carbohydrate
metabolism (blood glucose). Islets of Langerhans are located here.
Brain anticipates when glucose comes in (parasympathetic) = pre-
absorptive insulin release/cephalic phase. Lack of anticipation
higher disturbance by glucose. Atropine can block the receptors no
anticipation.
Artificial sweetener like saccharin makes insulin levels rise bc of the taste
lower glucose hunger.
Factors that stimulate insulin release:
- Glucose, amino acids, FFA’s (all energy substrates)
- Parasympathetic stimulation (anticipation)
, - Gut hormones: incretins (digestive factors) (GLP-1, CCK) and
feedforward effect (food is going to come in insulin release).
Anticipatory responses reduce the glucose to get glucose homeostasis.
Sympathetic stimulation inhibits insulin release
- Only insulin-independent tissues receive glucose
- = brain and exercising muscle
Hypoglycaemia = low blood sugar
Diabetes
Shortage of insulin.
Baseline blood glucose levels are already elevated when not eating. When
eating, blood sugar rises even more than in non-diabetics. Kidney cannot
handle filtering the blood anymore sweet urine.
Pre-diabetes = glucose intolerance. When you are
pre-diabetic, dieting/exercising etc. can prevent
diabetes.
Glucose measurement for diabetes diagnosis
- Measurement of glucose in urine
- Measurement of glucose in blood
- Measurement of HbA1c (long term regulation)
HbA1c = haemoglobin type A1c
Hyperglycaemia glycosylation of molecules. Haemoglobin binds to
glucose and is sensitive for glycosylation. Haemoglobin molecules live 2-3
months content of glucose in the HbA1c molecule may be used as an
indication for the average blood sugar.
Advantage: provides info on the long-term situation.
Disadvantage: missing of hypoglycaemic/hyperglycaemic peaks. Some
people suffer on extremes.
Type 1 Diabetes = Insulin dependent (autoimmune)
