Heat balance + bone and minerals

Question 1

66. The heat balance, and the effect of the environmental temperature.

Answer 1

• Factors affecting Heat Balance:
   Time of day
   Feed intake
   Muscle activity, motility
   Sexual cycle, parturition
   Age
• Effect of the environmental temperature:
  *Hypothermia – Body temp decr below the controllable range.
   Metabolism slows down
   Heart/respiratory frequency drops
   Circulatory failure:
  *Hypercapnia–Too much CO2 in blood
  *Hypoxia–Too little dissolved CO2
   Disorders of digestion, absorption and kidney functions
   Fainting
   Occasionally: ventricular fibrillations
   E.g. Newborn animals or clipped sheep
  *Hyperthermia – Insufficient operation of heat dissipating mechanisms
   Metabolism slows down
   Corruption of circulation -> Overheating shock
   Hypercapnia
   Hypovolemia
   Loss of salts and water
   Muscle seizures
  -Fever is also a type of regulated hyperthermia, caused by infections, inflammations, tissue damage and other diseases.
  -Acclimatisation: shift of thermoneutralzone to a higher or lower level

Question 2

67. Heat balance regulation

Answer 2

-Defence against COLD
•Heat conservation:
•Diminishing heat loss by behavioural change. Eg. living in groups (penguins).
•Incr muscular activity: Induces heat prod, Incr in tonicity (voluntary), Shivering
•Metabolic heat prod: Fat burnin, Chem heat prod of the skeletal muscle
- Sympathetic excitation: Effect of adrenaline/noradrenaline, long term thyroxine effects
- Calorigenic effect of thyroid hormones: Prolonged effect on heat prod.
-Brown adipose tissue: Extra source of heat in newborn animals since they have a high ratio of surface to volume.
- Defence against HEAT
*Behavioural defence reactions
*“Dry” heat loss
*Conduction – By direct contact with surrounding objects
*Convection – By air or water touching the body
*Radiation – By electromagnetic radiation
*“Humid” heat loss: evaporation
-Body temp controlled through hypothalamic centre:
*Warm – 2 systems
Superficial skin layer: Precapillary sphincters open.
Deep system: Major veins contract. Supf. veins dilate.
*Cold – 2 systems
Superficial skin layer: Precapillary sphincters close.
Deep system: Major veins dilate. Supf. veins contract.

Question 3

68. Thermogenesis at the cellular level

Answer 3

• Mechanisms to incr heat prod at a cellular level:
  1. Mitochondrial heat prod in brown adipose tissue. May be effective in other tissues also.
  2. Fish experiments – Modified “heat cells” differentiated from muscle cells. May have important thermogenic functions all around the body.
  1. CELLULAR LEVEL: BROWN ADIPOSE TISSUE
• Uncoupling of ATP synt in brown adipose tissue
• UCP Thermogenin (uncoupling protein) is prod as a response to thyroid hormones. Settles in inner membrane of mitochondria.
• Epinephrine generates FFA in the cells -> Opens thermogenin channel & becomes transparent to protons.
• No ATP synthesis, just heat prod.
  2. CELLULAR LEVEL: HEATER CELLS, FUTILE CYCLE
• Operating the Ca2+ pump of SR w/ø muscle contraction.
• The heater cells are modified muscle cells.
• A modified ryanodine receptor allows leakage of Ca from SR. This continuously activates Ca2+ pumps -> High heat prod.
• In mammals, skeletal muscle incr Ca pump activity (heat production) due to thyroxine and epinephrine stim.
• This is called the “futile cycle” process as the pump is being “abused”.

Question 4

69. Role of calcium and phosphorus, absorption, distribution and excretion

Answer 4

• Calcium:
• Hemostasis
• Muscle contraction
• Excitability
• Effects on cardiac muscle
• Capillary permeability
• Membrane stabilisation
• Enzyme activation
• Shaping the form
• Calcium as a signal
• Phosphorus:
• Intermediary metabolism
• Storage of energy
• Rigidity of bone
• Nucleic acids
• Buffer systems
• Membrane composition
• Regulation of absorption:
• Mainly depends on actual needs – Lactation will lead to a higher abs of Ca2+ from feed.
• Vitamin-D (D-hormone) is a determining factor for the utilisation of calcium.
• Need for Caa and P decr w. age, therefore abs decr
• Incr and decr intestinal factors.

Question 5

70. The role of the osteoblast, osteoclast and osteocyte

Answer 5

• OSTEOBLAST:
• Calcium Concentrations
• Ca Pathways
• Calcium Mobilisation
• D-Hormone Effect
• OSTEOCYTE:
• Develop from osteoblasts and are not involved in osteogenesis or osteolysis to a great extent.
• Maintain normal metabolism in the bone.
• Involved in resorption.
• Trophic activity.
• Metabolite elimination.
• OSTEOCLAST:
• Under indirect control of PTH, activated by Vitamin A.
• PTH induces production of a group of peptides: Osteoclasts, facilitating their bone resorbing activity.
• Two Processes:
  1. Production & release of collagenase enzyme increases.
  2. By facilitation of a proton pump and glycolytic activity in the cell, local pH decr and hydroxyapatite crystals are dissolved.
• These two processes converge to the resorption of both organic and inorganic components of bone.
• The osseous debris from resorption is taken up by phagocytosis and diffusion and appears on the plasma side.
• Hydroxyproline can be detected in the urine as a result of intensive collagenolysis (collagen is rich in proline).

Question 6

71. The role of the PTH, calcitonin, and the D-hormone in the Ca balance

Answer 6

• PARATHYREOIDEHORMONE:
• Secr. is exclusively determined by Ca level in serum
• Low: stim synthesis & secretion of PTH.
• High: inhibits synthesis & secretion of PTH.
• PTH in turn incr serum Ca level in both direct and indirect way: bone, kidneys, mammary glands & intestines.
• Bone: PTH incr Ca permeability (Osteoclast)
• Kidneys: PTH incr plasma Ca level by decr renal excretion of Ca.
• Mammary Gland: PTH decr excreted Ca in milk. Can also incr plasma Ca level by inhib Ca being let down into milk.
• Intestines: PTH facilitates Vitamin-D -> D-Hormone transformation, thus incr Ca abs from intestinal tract.
• D-HORMONE: Influences Ca metabolism of bone, kidneys and intestinal tract.
• Bone: Incr Ca pump activity of osteoblast layer: Ca resorption.
• Kidney: Tubular resorption of Ca is incr.
• Intestines: Facilitation of CaBP; Calcium Binding Protein synt. Leads to incr Ca abs.
• CALCITONIN:
• Causes drastic reduction of plasma calcium.
• Calcitonin is synt. and released when plasma Ca level incr. Therefore it acts as an antagonist to PTH.
• Bone: Ca cannot be transported from bone to blood.
• Calcium deposition is incr, plasma Ca level decr.
• Kidneys:Calcium resorption decreases.