seminar blood glucose regulation
TRANSCRIPT
Regulation of Blood Glucose Level
Dr. Shabeena Patel
What goes wrong when the concentration decreases?
Hypoglycaemia
The symptoms associated with low blood sugar are:
tiredness, confusion, dizziness, headaches, mood swings, muscle weakness, tremors, irreversible CNS damage, coma, death
What goes wrong when the concentration increases too far?
Hyperglycaemia
The symptoms include:
Excessive thirst; frequent urination;
fatigue; unexplained weight loss;
vision problems, such as blurring;
increased susceptibility to infections
Dibetes mellitus
We eat food containing carbohydrates
Fundamental regulation / Autoregulation
• Hormones:
• Insulin
• Glucagon
Organs: Liver
Skeletal muscles
Pancreas
Adipose tissue
ROLE OF
LIVER
Role of liver and Sk muscle
Role of the Pancreas
1. Digestion – secretes digestive enzymes
2. Metabolism• Regulation
• Carbohydrates
• Lipids
• Proteins
• Produces primary messengers (hormones)• Insulin
• Glucagon
Role of adipose tissue
Organ Glucose transporter Classification
Brain GLUT1 Glucose dependent
Erythrocyte GLUT1 Glucose dependent
Adipocyte GLUT4 Insulin dependent
Muscle GLUT4 Insulin dependent
Liver GLUT2 Glucose sensor
GK - cell GLUT2 Glucose sensor
Gut GLUT3-symporter ---- Sodium dependent
Kidney GLUT3-symporter ---- Sodium dependent
Glucose transporters
• 51 amino acids
• 2 chains linked by disulfide bonds
• 5800 Dalton molecular weight
MECHANISM OF INSULIN SECRETION
ADIPOSE TISSUE AND
MUSCLES
insulin stimulates the synthesis of an enzyme (glucokinase) (low affinity to glucose) [ in the liver] •Required to ‘trap’ glucose in the cell (only when glucose concentration is high)
Insulin Control
Muscle Glucose uptake Glycogen synthesis
Liver Glucose uptake Glycogen synthesis Fatty acid synthesis Glucose synthesis
BrainNo effect
PancreasBeta cells
Gastrointestinalhormones
Feedback
aminoacids
glucose
triglyceridesAdipose Glucose uptake Glycerol production Triglyceride breakdown Triglyceride synthesis Insulin
Most Cells Protein synthesis
Amino acids
Bloodglucose
Glucagon Control
Liver Glycogen breakdown Glucose synthesis Glucose release
BrainNo effect
PancreasAlpha cells
Exercise
Feedback
Adipose Triglyceride breakdown Triglyceride storage
Blood glucose
Fatty acids
Epinephrine(stress)
Amino acids
Glucocorticoids• 1)Increase blood glucose:
• i) Peripheral tissues :increase protein catabolism
• Decrease uptake and utilization of glucose
• ii)Liver : Increase amino acid uptake
• Increase the transaminase activity
• Increase gluconeogenesis
• + Pyruvate carboxylase
• + PEP carboxykinase
• + Fructose -1,6-biphosphatase
• +Glucose-6- phosphatase
• 2)Liver: Increase liver glycogen
• + glycogen synthase activity
Glucocorticoids are catabolic to the peripheral tissues but anabolic to the liver
+ ACTH synthesis
Glucocorticoid syn
Anterior pituitary hormones
• 1)Growth hormone:
• i)Decreases glucose uptake in tissues
• ii)Increase liver gluconeogenesis
• Chronic administration may lead to diabetes mellitus due to stimulation and exhaution of beta cells
• 2)ACTH: Stimulates glucocorticoids synthesis
• Raise blood glucose level
Thyroid hormones
• Raise blood glucose levels
• i)Increase hepatic glycogenolysis
• ii)Increase sensitivity of tissues to catecholamines
• iii)Increases destruction of insulin
• iv) Increase absorption of hexoses from intestine
• v) Increase peripheral tissue protein catabolism
Adipose tissue as endocrine gland
Causes of hyperglycemia
• 1)Diabetes mellitus
• 2)Hyperactivity of thyroid, pituitary and adrenals
• 3)Emotional stress
• 4)diffuse pancreatic diseases
• 5)Sepsis
• 6)Asphyxia
Hypoglycemia
• 1)Overdosage of insulin
• 2)Insulinoma
• 3)Hypoactivity of thyroids –myxodema,cretinism
• Pituitary gland
• Adrenals- Addisons disease
• 4)Severe liver diseases
• 5)Glycogen storage diseases