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UTTAM MEMORIAL COLLEGE PATELPALI RAIGARH
{C.G}
• SUBMITTED BY NIKITA JAISWAL
• CLASS MSC ZOOLOGY 2ND SEM
• TOPIC CALCIUM METABOLISM
GUIDED BY DAYA MAHANT
MAM
SYNOPSIS
• INTRODUCTION OF CALCIUM METABOLISM
• DIFINITION OF METABOLISM
• ROLE OF PARATHYROID HORMONE ON CA++ METABOLISM
• VITAMIN D SYNTHESIS
• ACTION OF PTH AND D3 ON CA++ METABOLISM
• ACTION OF CALCITONIN ON CA++ METABOLISM
• FUNCTION OF CA++ IN OUR BODY
• DISODERS OF CA++
• CONCLUSION
• REFERENCES
INTRODUCTION OF CALCIUM METABOLISM
• CALCIUM METABOLISM IN OUR BODY IS NOTHING BUT THE MOBILIZATION OF THE CALCIUM IN AND
OUT THROUGHOUT THE BODY, WETHER ITS BETWEEN THE INTRA AND EXTRACELLULAR SPACE OR
BETWEEN THE BONE
• THE LEVEL OF CALCIUM IS REGULATED BY THE HORMONES SUCH AS PARATHYROID, CALCITONIN,AND
AND ACTIVATED VITAMIN D3 ,PARATHYROID HORMONE IS RELESED BY THE CHIEF CELLS OF
PARATHYROID GLAND, CALCITONIN BY THYROID GLAND VIA PARAFOLLICULAR CELLS,VITAMIN D3 GETS
SYNTHESIZED,VIA THE SUN
TISSUES LIKE BONE,KIDNEY,AND INTESTINES ARE INVOLVED IN THIS PROCESS
DIFINITION OF METABOLISM
• METABOLISM IS THE CELLULAR ACTIVITY WHICH OCCUR IN CHEMICAL WAY, THIS IS THE PROCESS
WHERE ENERGY PRODUCTION TAKES PLACE OR BUILDING THE GENERAL LIFE BLOCKS LIKE
PROTEIN,FATS,AND LIPIDS,AND CARBOHYDRATES
• IT CAN BE DIVIDED INTO 2 TYPES
1. CATABOLISM THE PROCESS WHERE THE BIG FOOD MOLECULES LIKE CARBS PROTEIN AND FATS ARE
BROKEN DOWN INTO SMALL ER MOLECULES,LIKE GLUCOSE ,AMINO ACID,AND Glycerol
2. ANABOLISM IS THE BUILDING UP PROCESS WHERE SMALL MOLECULES ARE
ASSEMBLE TO BIGGER MOLECULE FOR EXAMPLE AMINO ACIDS ARE ASSEMBLED
TOGETHER TO FORM POLYPEPTIDE CHAIN OR PROTEIN
ROLE OF PARATHYROID ON CALCIUM METABOLISM
• PTH IS A HORMONE WHICH GETS RELEASED VIA THE
CHIEF CELLS OF PARATHYROID GLAND AND PLAYS AN
REALLY IMPORTANT ROLE ON THE CALCIUM
METABOLISM,WHEN THE BLOOD CALCIUM LEVEL
DROPS IT, ACTIVATES CERTAIN PATWAYS TO REABSORBS
CALCIUM INTO THE BLOOD,
• FIRST WHEN THE CALCIUM LEVEL GOES DOWN IN THE
BLOOD IT SENDS SIGNAL .TO PARATHYROID GLAND IT
RELESES PTH HORMONE IT ACTS ON BONE AND
KIDNEY,TO REABSORBS CALCIUM FROM THE BONE AND
PCT OF KIDNEY
VITAMIN D SYNTHESIS
• VITAMIN D3 SYNTHESIS DOES OCCUR IN THE LAYER OF
SKIN
• INACTIVATED FORM OF VITAMIN D IS PRESENT IN THE
SKIN IN THE FORM OF 7 HYDROXYCHOLESTEROL THAT
CONVERTS INTO CHOLECALCIFEROL
• LIVER HAS A SPECIAL ENZYME IN IT CALLED 25-
HYDROXYLASE THAT CONVERTS CHOLECALCIFEROL
INTO 25-OH- CHOLECALCIFEROL
• IN KIDNEY 1-ALPHA HYDROXYLASE CONVERTS 25-OH-
CHOLECALCIFEROL INTO ACTIVATED FORM OF VITAMIN
D3
ROLE OF D3 IN CALCIUM METABOLISM
• When blood calcium level is down, d3 acts on 3 tissue
I. Bone
II. Pct of kidney’
III. Intestine
bone:- d3 directly acts on bone by reabsorbing calcium into the blood
Pct:- d3 acts on kidney to reabsorbs calcium into the blood
Intestine:- d3 acts on mucosa to reabsorb calcium into the blood
PROCESS OF CALCIUM METABOLISM BY THE HELP OF PTH
AND D3
• There are three type of bone cell
I. osteocyte
II. Osteoblast
III. Osteoclasts
osteoblast:- in osteoblasts there are receptors are present for d3 and pth when that receptors binds to the d3 and pth it
activates certain things such as
 Proliferation of osteoblasts
 Rank l (rank ligand ) which are present In osteoblasts there is a protein called osteoprotegrin which binds with rank l and
inhibits the further binding of rank l to osteoclasts because of pth an d3 it inhibits the osteoprotegrin to bind with rank l
 Rank l can now bind to osteoclasts
Osteoclasts :- when rank ligand binds with the osteoclasts it activates more proliferation until its done that osteoclast is known
as pre osteoclasts, after that it releases hcl to make ca++ out of bone and reabsorbs it into the blood
ROLE OF CALCITONIN
• When the concentration of calcium rises, the parafollicular cells of the
thyroid gland increase their secretion of calcitonin, a polypeptide
hormone, into the blood. At the same time, the parathyroid glands
reduce the secretion of parathyroid hormone (PTH), also a polypeptide
hormone, into the blood. The resulting high levels of calcitonin in the
blood stimulate osteoblasts in bone to remove calcium from blood
plasma and deposit it as bone.
• The reduced levels of PTH inhibit removal of calcium from the
skeleton. The low levels of PTH have several other effects: there is
increased loss of calcium in the urine, but more importantly, the loss of
phosphate ions through urine is inhibited. Phosphate ions will therefore
be retained in the plasma where they form insoluble salts with calcium
ions, thereby removing them from the ionized calcium pool in the
blood. The low levels of PTH also inhibit the formation of calcitriol (not
to be confused with calcitonin) from cholecalciferol (vitamin D3) by the
kidneys.
• The reduction in the blood calcitriol concentration acts (comparatively
slowly) on the epithelial cells (enterocytes) of the duodenum, inhibiting
their ability to absorb calcium from the intestinal contents.[2][5][28][29] The
low calcitriol levels also act on bone causing the osteoclasts to release
fewer calcium ions into the blood plasma.
FUNCTION OF CA++
• Voltage gated sodium channels
• The voltage gated sodium ion channels in the cell membranes of nerves and muscle are particularly
sensitive to the calcium ion concentration in the plasma.[6] Relatively small decreases in the plasma
ionized calcium levels (hypocalcemia) cause these channels to leak sodium into the nerve cells or axons,
making them hyper-excitable (positive bathmotropic effect), thus causing spontaneous muscle spasms
(tetany) and paraesthesia (the sensation of "pins and needles") of the extremities and round the
mouth.[7] When the plasma ionized calcium rises above normal (hypercalcemia) more calcium is bound
to these sodium channels having a negative bathmotropic effect on them, causing lethargy, muscle
weakness, anorexia, constipation and labile emotions.[7].
FUNTIONS
• Intracellular signalling
• Because the intracellular calcium ion concentration is extremely low (see above) the entry of minute
quantities of calcium ions from the endoplasmic reticulum or from the extracellular fluids, cause rapid,
very marked, and readily reversible changes in the relative concentration of these ions in the cytosol.
This can therefore serve as a very effective intracellular signal (or "second messenger") in a variety of
circumstances, including muscle contraction, the release of hormones (e.g. insulin from the beta cells in
the pancreatic islets) or neurotransmitters (e.g. acetylcholine from pre-synaptic terminals of nerves)
and other functions.
FUNCTIONS
• Muscle
• In skeletal and heart muscle, calcium ions, released from the sarcoplasmic reticulum (the endoplasmic
reticulum of striated muscles), bind to the troponin C protein present on the actin-containing thin
filaments of the myofibrils. The troponin's 3D structure changes as a result, causing the tropomyosin to
which it is attached to be rolled away from the myosin-binding sites on the actin molecules that form
the back-bone of the thin filaments. Myosin can then bind to the exposed myosin-binding sites on the
thin filament, to undergo a repeating series of conformational changes called the cross-bridge cycle, for
which ATP provides the energy. During the cycle, each myosin protein ‘paddles’ along the thin actin
filament, repeatedly binding to myosin-binding sites along the actin filament, ratcheting and letting go.
In effect, the thick filament moves or slides along the thin filament, resulting in muscle contraction. This
process is known as the sliding filament model of muscle contraction.
• Bone storage
• Calcium flow to and from the bone may be positive, negative, or neutral. When it is neutral, about 5–10
mmol is turned over a day. Bone serves as an important storage point for calcium, as it contains 99% of
the total body calcium. Calcium release from bone is regulated by parathyroid hormone in conjunction
with calcitriol manufactured in the kidney under the influence of PTH. Calcitonin (a hormone secreted
by the thyroid gland when plasma ionized calcium levels are high or rising; not to be confused with
"calcitriol" which is manufactured in the kidney) stimulates incorporation of calcium into bone.
DISORDERS
• Hypocalcemia (low blood calcium) and hypercalcemia (high blood calcium) are both serious medical
disorders. Osteoporosis, osteomalacia and rickets are bone disorders linked to calcium metabolism
disorders and effects of vitamin D. Renal osteodystrophy is a consequence of chronic kidney failure
related to the calcium metabolism.
• A diet adequately rich in calcium may reduce calcium loss from bone with advancing (post-menopausal)
age.[30] A low dietary calcium intake may be a risk factor in the development of osteoporosis in later
life; and a diet with sustained adequate amounts of calcium may reduce the risk of osteoporosis.
CONCLUSION
• AS WE HAVE SEEN HOW THE CALCIUM DOES SOME REALLY IMPORTANT WORK ON OUR BODY, FOR
EXAMPLE CELL SIGNALING, INTESTINIAL REABSORBSON,IN BLOOD PLASMA LEVEL,IN MUSCLE
CONRACTION, BONE, AND STORAGE, THESE ALL THINGS ARE POSSIBLE BECAUSE OF CA++
• METABOLISM OF CA++ IS REALLY IMPORTANT FOR THE REGULATION OF ALL THESE PROCESS
• CELL TO MAKE AN ADHESIVE BRIGDE BETWEEN THEMSELVES THERSE ARE ALL POSSIBLE DUE TO CA++
• EXAMPLE CADHERIN IS AN CA++ DEPENDENT CELL ADHESION MOLECULE OF PROTEIN THAT MAKE CELL
TO CELL BRIDGE BY THE HELP OF CA++ TO COMMUNICATE BETWEEN THEMSELVES
REFERENCES
• WIKIPEDIA
• ENDOCRINOLOGY BY NICHOLAS D WOLFWOOLD
• MOLECULAR CELL BIOLOGY BY KARP

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CALCIUM METABOLISM-1.pptx

  • 1. UTTAM MEMORIAL COLLEGE PATELPALI RAIGARH {C.G} • SUBMITTED BY NIKITA JAISWAL • CLASS MSC ZOOLOGY 2ND SEM • TOPIC CALCIUM METABOLISM GUIDED BY DAYA MAHANT MAM
  • 2. SYNOPSIS • INTRODUCTION OF CALCIUM METABOLISM • DIFINITION OF METABOLISM • ROLE OF PARATHYROID HORMONE ON CA++ METABOLISM • VITAMIN D SYNTHESIS • ACTION OF PTH AND D3 ON CA++ METABOLISM • ACTION OF CALCITONIN ON CA++ METABOLISM • FUNCTION OF CA++ IN OUR BODY • DISODERS OF CA++ • CONCLUSION • REFERENCES
  • 3. INTRODUCTION OF CALCIUM METABOLISM • CALCIUM METABOLISM IN OUR BODY IS NOTHING BUT THE MOBILIZATION OF THE CALCIUM IN AND OUT THROUGHOUT THE BODY, WETHER ITS BETWEEN THE INTRA AND EXTRACELLULAR SPACE OR BETWEEN THE BONE • THE LEVEL OF CALCIUM IS REGULATED BY THE HORMONES SUCH AS PARATHYROID, CALCITONIN,AND AND ACTIVATED VITAMIN D3 ,PARATHYROID HORMONE IS RELESED BY THE CHIEF CELLS OF PARATHYROID GLAND, CALCITONIN BY THYROID GLAND VIA PARAFOLLICULAR CELLS,VITAMIN D3 GETS SYNTHESIZED,VIA THE SUN TISSUES LIKE BONE,KIDNEY,AND INTESTINES ARE INVOLVED IN THIS PROCESS
  • 4. DIFINITION OF METABOLISM • METABOLISM IS THE CELLULAR ACTIVITY WHICH OCCUR IN CHEMICAL WAY, THIS IS THE PROCESS WHERE ENERGY PRODUCTION TAKES PLACE OR BUILDING THE GENERAL LIFE BLOCKS LIKE PROTEIN,FATS,AND LIPIDS,AND CARBOHYDRATES • IT CAN BE DIVIDED INTO 2 TYPES 1. CATABOLISM THE PROCESS WHERE THE BIG FOOD MOLECULES LIKE CARBS PROTEIN AND FATS ARE BROKEN DOWN INTO SMALL ER MOLECULES,LIKE GLUCOSE ,AMINO ACID,AND Glycerol 2. ANABOLISM IS THE BUILDING UP PROCESS WHERE SMALL MOLECULES ARE ASSEMBLE TO BIGGER MOLECULE FOR EXAMPLE AMINO ACIDS ARE ASSEMBLED TOGETHER TO FORM POLYPEPTIDE CHAIN OR PROTEIN
  • 5. ROLE OF PARATHYROID ON CALCIUM METABOLISM • PTH IS A HORMONE WHICH GETS RELEASED VIA THE CHIEF CELLS OF PARATHYROID GLAND AND PLAYS AN REALLY IMPORTANT ROLE ON THE CALCIUM METABOLISM,WHEN THE BLOOD CALCIUM LEVEL DROPS IT, ACTIVATES CERTAIN PATWAYS TO REABSORBS CALCIUM INTO THE BLOOD, • FIRST WHEN THE CALCIUM LEVEL GOES DOWN IN THE BLOOD IT SENDS SIGNAL .TO PARATHYROID GLAND IT RELESES PTH HORMONE IT ACTS ON BONE AND KIDNEY,TO REABSORBS CALCIUM FROM THE BONE AND PCT OF KIDNEY
  • 6. VITAMIN D SYNTHESIS • VITAMIN D3 SYNTHESIS DOES OCCUR IN THE LAYER OF SKIN • INACTIVATED FORM OF VITAMIN D IS PRESENT IN THE SKIN IN THE FORM OF 7 HYDROXYCHOLESTEROL THAT CONVERTS INTO CHOLECALCIFEROL • LIVER HAS A SPECIAL ENZYME IN IT CALLED 25- HYDROXYLASE THAT CONVERTS CHOLECALCIFEROL INTO 25-OH- CHOLECALCIFEROL • IN KIDNEY 1-ALPHA HYDROXYLASE CONVERTS 25-OH- CHOLECALCIFEROL INTO ACTIVATED FORM OF VITAMIN D3
  • 7. ROLE OF D3 IN CALCIUM METABOLISM • When blood calcium level is down, d3 acts on 3 tissue I. Bone II. Pct of kidney’ III. Intestine bone:- d3 directly acts on bone by reabsorbing calcium into the blood Pct:- d3 acts on kidney to reabsorbs calcium into the blood Intestine:- d3 acts on mucosa to reabsorb calcium into the blood
  • 8. PROCESS OF CALCIUM METABOLISM BY THE HELP OF PTH AND D3 • There are three type of bone cell I. osteocyte II. Osteoblast III. Osteoclasts osteoblast:- in osteoblasts there are receptors are present for d3 and pth when that receptors binds to the d3 and pth it activates certain things such as  Proliferation of osteoblasts  Rank l (rank ligand ) which are present In osteoblasts there is a protein called osteoprotegrin which binds with rank l and inhibits the further binding of rank l to osteoclasts because of pth an d3 it inhibits the osteoprotegrin to bind with rank l  Rank l can now bind to osteoclasts Osteoclasts :- when rank ligand binds with the osteoclasts it activates more proliferation until its done that osteoclast is known as pre osteoclasts, after that it releases hcl to make ca++ out of bone and reabsorbs it into the blood
  • 9. ROLE OF CALCITONIN • When the concentration of calcium rises, the parafollicular cells of the thyroid gland increase their secretion of calcitonin, a polypeptide hormone, into the blood. At the same time, the parathyroid glands reduce the secretion of parathyroid hormone (PTH), also a polypeptide hormone, into the blood. The resulting high levels of calcitonin in the blood stimulate osteoblasts in bone to remove calcium from blood plasma and deposit it as bone. • The reduced levels of PTH inhibit removal of calcium from the skeleton. The low levels of PTH have several other effects: there is increased loss of calcium in the urine, but more importantly, the loss of phosphate ions through urine is inhibited. Phosphate ions will therefore be retained in the plasma where they form insoluble salts with calcium ions, thereby removing them from the ionized calcium pool in the blood. The low levels of PTH also inhibit the formation of calcitriol (not to be confused with calcitonin) from cholecalciferol (vitamin D3) by the kidneys. • The reduction in the blood calcitriol concentration acts (comparatively slowly) on the epithelial cells (enterocytes) of the duodenum, inhibiting their ability to absorb calcium from the intestinal contents.[2][5][28][29] The low calcitriol levels also act on bone causing the osteoclasts to release fewer calcium ions into the blood plasma.
  • 10. FUNCTION OF CA++ • Voltage gated sodium channels • The voltage gated sodium ion channels in the cell membranes of nerves and muscle are particularly sensitive to the calcium ion concentration in the plasma.[6] Relatively small decreases in the plasma ionized calcium levels (hypocalcemia) cause these channels to leak sodium into the nerve cells or axons, making them hyper-excitable (positive bathmotropic effect), thus causing spontaneous muscle spasms (tetany) and paraesthesia (the sensation of "pins and needles") of the extremities and round the mouth.[7] When the plasma ionized calcium rises above normal (hypercalcemia) more calcium is bound to these sodium channels having a negative bathmotropic effect on them, causing lethargy, muscle weakness, anorexia, constipation and labile emotions.[7].
  • 11. FUNTIONS • Intracellular signalling • Because the intracellular calcium ion concentration is extremely low (see above) the entry of minute quantities of calcium ions from the endoplasmic reticulum or from the extracellular fluids, cause rapid, very marked, and readily reversible changes in the relative concentration of these ions in the cytosol. This can therefore serve as a very effective intracellular signal (or "second messenger") in a variety of circumstances, including muscle contraction, the release of hormones (e.g. insulin from the beta cells in the pancreatic islets) or neurotransmitters (e.g. acetylcholine from pre-synaptic terminals of nerves) and other functions.
  • 12. FUNCTIONS • Muscle • In skeletal and heart muscle, calcium ions, released from the sarcoplasmic reticulum (the endoplasmic reticulum of striated muscles), bind to the troponin C protein present on the actin-containing thin filaments of the myofibrils. The troponin's 3D structure changes as a result, causing the tropomyosin to which it is attached to be rolled away from the myosin-binding sites on the actin molecules that form the back-bone of the thin filaments. Myosin can then bind to the exposed myosin-binding sites on the thin filament, to undergo a repeating series of conformational changes called the cross-bridge cycle, for which ATP provides the energy. During the cycle, each myosin protein ‘paddles’ along the thin actin filament, repeatedly binding to myosin-binding sites along the actin filament, ratcheting and letting go. In effect, the thick filament moves or slides along the thin filament, resulting in muscle contraction. This process is known as the sliding filament model of muscle contraction.
  • 13. • Bone storage • Calcium flow to and from the bone may be positive, negative, or neutral. When it is neutral, about 5–10 mmol is turned over a day. Bone serves as an important storage point for calcium, as it contains 99% of the total body calcium. Calcium release from bone is regulated by parathyroid hormone in conjunction with calcitriol manufactured in the kidney under the influence of PTH. Calcitonin (a hormone secreted by the thyroid gland when plasma ionized calcium levels are high or rising; not to be confused with "calcitriol" which is manufactured in the kidney) stimulates incorporation of calcium into bone.
  • 14. DISORDERS • Hypocalcemia (low blood calcium) and hypercalcemia (high blood calcium) are both serious medical disorders. Osteoporosis, osteomalacia and rickets are bone disorders linked to calcium metabolism disorders and effects of vitamin D. Renal osteodystrophy is a consequence of chronic kidney failure related to the calcium metabolism. • A diet adequately rich in calcium may reduce calcium loss from bone with advancing (post-menopausal) age.[30] A low dietary calcium intake may be a risk factor in the development of osteoporosis in later life; and a diet with sustained adequate amounts of calcium may reduce the risk of osteoporosis.
  • 15. CONCLUSION • AS WE HAVE SEEN HOW THE CALCIUM DOES SOME REALLY IMPORTANT WORK ON OUR BODY, FOR EXAMPLE CELL SIGNALING, INTESTINIAL REABSORBSON,IN BLOOD PLASMA LEVEL,IN MUSCLE CONRACTION, BONE, AND STORAGE, THESE ALL THINGS ARE POSSIBLE BECAUSE OF CA++ • METABOLISM OF CA++ IS REALLY IMPORTANT FOR THE REGULATION OF ALL THESE PROCESS • CELL TO MAKE AN ADHESIVE BRIGDE BETWEEN THEMSELVES THERSE ARE ALL POSSIBLE DUE TO CA++ • EXAMPLE CADHERIN IS AN CA++ DEPENDENT CELL ADHESION MOLECULE OF PROTEIN THAT MAKE CELL TO CELL BRIDGE BY THE HELP OF CA++ TO COMMUNICATE BETWEEN THEMSELVES
  • 16. REFERENCES • WIKIPEDIA • ENDOCRINOLOGY BY NICHOLAS D WOLFWOOLD • MOLECULAR CELL BIOLOGY BY KARP