physiology of pancreas s. sh. sadr md professor of tehran university department of physiology
TRANSCRIPT
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PHYSIOLOGY OF PANCREAS
S. Sh. Sadr MD
Professor of Tehran University
Department of Physiology
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General Informations
W : 50 – 75 gr Langerhans Islet : 0.5 – 1.5 million Histology :
α : 20 – 30 % ; Glucagon (around of islet) β : 60 – 80 % ; Insulin (center of islet) δ : 8 % ; Sumatostatin & Gastrin (between α, β) PP or F : variable ; pancreatic polypeptide)
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Insulin
W : 6000 d 51 aa (A chain = 21, B chain = 30) Pro-insulin : 9000 d, 84 aa (= 51+33)
C-peptide : 33 aa Store : 4 u/kg (in adult = 200 u) Gene on short arm of Chr. 11
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Secretion of Insulin
1- Basal secretion : Continuous, 1 u/h
2- Stimulated secretion : IV Glu. : peak : after 3 – 5 min = 8 – 10 x BS Oral Glu. : peak : after 0.5 – 1 h = 6 – 8 x BS Insulin response to Glu. Infusion shows a rapid
first phase of release followed by a fall and a later slower second phase
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Metabolism of Insulin
Half life : 6 min
When insulin is secreted into the blood, it circulates almost entirely in an unbound form
Each hepatic passage : 40 – 50 % inactivation
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Mechanism of Action
Receptor : W = 300,000 d 2α (extracellular) + 2β(intracellular) Insulin + α subunit → autophosphorilation of β
subunit → tyrosine kinase activity ↓ cAMP ↑ Glycogenesis, lipogenesis and Pr. Synthesis ↓ Glycogelolysis, lipolysis, proteolysis,
gluconeogenesis and ketogenesis
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Effects of Insulin
Metabolism of Carbohydrates : ↑ Glu. Uptake from plasma Facilitates Glu. entrance into cells ↓ rate of release of Glu. From liver by :
By Inhibiting glycogenolysis By Stimulating glycogen synthesis By Stimulating Glu. Uptake By Stimulating glycolysis By indirectly inhibiting glycogenesis via inhibition of fatty acid
mobilization from adipose tissue Insulin is necessary for entrance of Glu. Into the most of cells
(Except of CNS, intestine epithelium, pancreas cells and renal tubul epithelium)
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Effects of Insulin
Metabolism of Carbohydrates : Effect on Liver:
Glu. Uptake from plasma ↑ glycogenesis ↓ glycogenolysis ↓ glyconeogenesis Glu. Converting to fatty acids
Effect on Muscles: Most of day time: fatty acid At rest: glu. resistant during sport: needs glu. for providing energy After meal: rapid glu. Transport into muscle cells
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Effects of Insulin
Metabolism of Proteins: ↑ transport of aa into hepatic and muscle cells (unrelated to glu.
transport but may be related to Na/K pump activity)
Val Leu Ile Tyr Phe
↑ synthesis of protein ↓ proteolysis
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Insulin Promotes Protein Synthesis and Storage.
1 . Insulin stimulates transport of many of the amino acids into the cells
2. Insulin increases the translation of messenger RNA
3. Insulin also increases the rate of
transcription of selected DNA genetic sequences in the cell nuclei
Effect of Insulin on Protein Metabolism and on Growth
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4. Insulin inhibits the catabolism of proteins
5. In the liver, insulin depresses the rate of gluconeogenesis
Insulin Deficiency Causes Protein Depletion and Increased Plasma Amino Acid
Insulin and Growth Hormone Interact Synergistically to Promote Growth
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Effects of Insulin
Metabolism of Lipids: ↓ lipolysis ↑ synthesis of fatty acids in liver
As a result: Insulin is an Anabolic Hormone Effect on growth:
In embryonic life, Insulin is the most important hormone for embryonic growth.
Effect on Glucagon: Insulin refuses glucagon secretion
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The end effects of Insulin
1. Within seconds after insulin binds with its membrane
receptors, the membranes of about 80 percent of the body’s cells
markedly increase their uptake of glucose.
2. The cell membrane becomes more permeable to many of
the amino acids, potassium ions, and phosphate ions,causing
increased transport of these substances into the cell
3. Slower effects occur during the next 10 to 15 minutes to change the activity levels of many more intracellular metabolic
enzymes.
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• 3. Slower effects occur during the next 10 to 15 minutes to change the activity levels of many more intracellular metabolic enzymes
4. Much slower effects continue to occur for hours and even several days. They result from changed rates
of translation of messenger RNAs at the ribosomes to
form new proteins and still slower effects from changed
rates of transcription of DNA in the cell nucleus
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Insulin Secretion
Increased by Decreased byD-glucoseGalactoseMannoseGlyceraldehydeProtein: Arg, Lys, Leu, AlaKetoacidsFree fatty acidsPotassiumCalciumGlucagon
Glucagon-like peptide IGasteric inhibitory polypeptideSecretinCholecystokininVagal activityAcetylcholineβ-adrenergic activitySulfounylurea drugs
FastingExerciseEndurance trainingSomatostatinGalaninPancreastatinInterleukine Iα2-adrenergic activityProstaglandin E2Diazoxide
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Glucagon
Single chain polypeptide 29 aa 3485 d α cells Entro-glucagon:
Larger molecule Half life = 6 min Hepatic and renal metabolizing Glomerule infiltration
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Effects of Glucagon
(Completely against Insulin effects) Metabolism of Carbohydrates :
↑ glycogenolysis in liver ↑ glyconeogenesis (slow process) Inhibition of glycogen synthesis in liver
Metabolism of Lipids : ↑ lipolysis
Other effects: β cell stimulation Catecholamine secretion stimulation ↑ heart muscle contractility ↑ bile and calcitonin secreton
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Glucagon Causes Glycogenolysis and Increased Blood Glucose
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Factors Influencing Glucagon Release
Stimulation Inhibition
Amino acidsGastrointestinal polypeptide hormonesCatecholamine (exercise)Growth HormoneGlucocorticoid
GlucoseInsulinFree fatty acids
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Pancreas Islets Control
Effective agents:
Metabolites
Hormones
Neural factors
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Pancreas Islets Control
Metabolites: Glucose: ↑ insulin, ↓ glucagon and
hypothalamic effects Amino acids: Arg, lys and Leu
aa. amplifies glu. effect on insulin secretion Lipids:
Fatty acids and Ketons: inhibitory effects on α cells and stimulatory effect on β cells.
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Pancreas Islets Control
Hormones: GI hormones:
oral glu. increases insulin more than IV glu. Gastrin Secretin CCK GIP Entroglucagon
Gastrin, CCK and GIP, ↑ glucagon secretion. glucagon Other hormones: GH, Thyroxin, Glucocorticoids, SS
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Pancreas Islets Control
Neural factors:
α2 adrenergic: ↓ insulin
β adrenergic: ↑ insulin
Parasympathetic, dopamine, serotonin and PG : ?
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Somatostatin
δ cells Polypeptide with 14 aa Half life = 2 min All of the factors related to digestion and
absorption stimulates SS. secretion: ↑ glu. ↑ aa ↑ fatty acids ↑ GI hormones
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Effects of Somatostatin
Insulin and glucagon secretion inhibition (local effect)
↓ gastric, duodenal and biliary bladder motility
↓ GI secretions and absorption
GH inhibitor
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Blood Sugar Control
Normal FBS = 70 – 100 mgr/100cc 1 hour after eating = 120 – 140 mgr/100cc Control Mechanism:
Liver Insulin and glucagon Hypoglycemia
Early Late
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Blood Sugar Control
↑ BS:
↑ extracellular osmotic pressure → cellular dehydration
Excretion in urine → osmotic dieresis → polydipsia and polyuria signs → dehydration
↓ BS: Cerebral cells, retina and testicular epithelium
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Diabetes Mellitus (pathophysiology)
↓ insulin : ↓ metabolism of gu. in cells ↑ fatty acids from lipid storages Protein emptying in tissues
Abnormalities: Glu. excretion in urine: > 180 mgr/100cc
Intra and extra cellular dehydration: shock Acidosis and Coma: metabolism changing from
carbohydrate to lipid
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Chronic High Glucose Concentration Causes Tissue Injury
When blood glucose is poorly controlled over long periods in
diabetes mellitus, blood vessels in multiple tissues throughout
the body begin to function abnormally and undergo structural
changes that result in inadequate blood supply to the tissues.
This in turn leads to increased risk for heart attack, stroke,
end-stage kidney disease, retinopathy and blindness, and
ischemia and gangrene of the limbs.
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Chronic high glucose concentration also causes damage
to many other tissues.
Peripheral neuropathy,
( which is abnormal function of peripheral nerves)
Autonomic nervous system dysfunction
These abnormalities can result in impaired cardiovascular reflexes
Impaired bladder control
Decreased sensation in the extremities
Other symptoms of peripheral nerve damage.
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Hypertension
(secondary to renal injury)
Atherosclerosis
( secondary to abnormal lipid metabolism)
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Diabetes Mellitus Causes Increased Utilization of Fats and
Metabolic Acidosis.
Rapid and deep breathing
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Clinical Characteristics of DM type I and type II
Type I Type II
Age at Beginning Usually under 20 Usually above 40
Body Mass ↓ (Thin) abnormal Obese
Plasma Insulin ↓ or empty Normal to ↑ at beginning
Plasma Glucagon ↑ it can be suppressed ↑, resistant to suppression
Plasma Glucose ↑ ↑
Insulin Susceptibility Normal ↓
Treatment Insulin ↓ Weight, Insulin, Drugs*
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Insulin Resistance: Causes
1) Obesity and Overweight
2) Glucocorticoid excess (Cushing syndrome)
3) ↑ GH
4) Pregnancy and GDM
5) PCO
6) Lipodystrophy
7) Insulin Receptor Ab
8) Insulin Receptor Mutation
9) Hemochromatosis
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Metabolic Syndrome
Obesity
Insulin Resistance
Fasting Hyperglycemia
Lipid Disorders (↑ TG and ↓ HDL)
Hypertension
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Obesity, insulin resistance and metabolic syndrome are usually
present before DM II
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