2. CHROMIUM, COBALT and COPPER

3. Chromium Cr At. No. 24 Atomic mass 52

5. Functions
Potentiates the action of insulin , Promotes utilization of glucose and is Involved in Glucose Tolerance.

6. Distribution Widely distributed in all tissues.
Element is present since birth
Total body content is up to 6mg.

7. Safe and adequate requirement
Minimal daily intake of 1 g/gram of food
An optimal adult intake of 50 – 200 g

8. Dietary sources Poor sources Rich sources Leafy vegetables Yeast
Polished rice
Table sugar
Rich sources
Yeast
Meat products
Cheese
Whole grains and condiments

9. Absorption & Metabolism
2 – 5% of dietary chromium is absorbed through GIT
Rapidly disappears from blood and is stored in tissues
Released from tissue with ingestion of glucose

10. Absorption & Metabolism
Level appears to decrease with age and with diabetes
Marginal deficiency states have been observed in old age, pregnancy and PCM

11. Cobalt Co At. No. 27 Atomic mass 59

13. Functions Cobalt forms an integral part of vitamin B12 .
It is required as a constituent of this vitamin.

14. Functions Role in Formation of Cobamide Enzyme :
In the formation of cobamide coenzyme (Adenosyl co-enzyme), cobalt of B12 undergoes successive reduction.
Reduction occurs in series / steps.
Catalyzed by the enzyme "B12 reductase",
It requires NADH and FAD.

15. Functions Bone marrow Function:
Cobalt is required to maintain normal bone marrow function and required for development and maturation of red blood cells.
A deficiency of cobalt results in decreased B12 supply which leads to Nutritional Macrocytic Anemia.

16. Functions
Role as Cofactor: Cobalt may act as a cofactor for enzyme like glycyl-glycine dipeptidase of intestinal juice.

17. DIETARY SOURCES Major source: Foods from animal source.
Not present in vegetables.

18. Requirements 1 to 2 µg of Cobalt / day
Normal average diet contains about 5 to 8 µg of cobalt which is far more than the RDA.
Vitamin B-I2 contains approximately to 0.09 ug of cobalt.

19. Absorption and Excretion
About 70 to 80% of the dietary cobalt is absorbed readily from the intestine.
Cobalt is stored mainly in the liver being the principal storage site.
Only trace amount present in other tissues.

20. EXCESS
Excess of cobalt results in overproduction of red blood cells causing polycythaemia.
The polycythaemic effect may be due to inhibition of certain respiratory enzymes viz. cytochrome oxidase, succinate dehydrogenase etc. leading to Relative Anoxia.

21. Cobalt Deficiency
Cobalt deficiency is considered to results in anorexia, fatty liver, macrocytic anaemia, wasting and haemosiderosis of spleen.

22. Copper

24. Copper Cu At. No. 29 Atomic mass 63.5

25. Functions Required for a variety of functions Hb. Formation
Normal bone development
Maintenance of myelin in nervous system
Phospholipid synthesis
Melanin pigment formation
Electron transport

26. Important roles
Cells use copper to help destroy molecules called free radicals that contribute to aging and cancer.
Blood requires copper to clot properly.
Skin requires copper to form collagen and melanin .

27. Cells cannot absorb iron without copper.
Embryos cannot grow and develop without copper.
Copper imbalances have even been implicated in Alzheimer's disease, although the evidence is preliminary.

28. Functions As a component of many enzymes
Involved in fatty acid oxidation
Purine metabolism and energy production

29. Dietary sources
The mineral is found abundantly in shellfish, legumes, nuts, seeds and chocolate.

30. Dietary sources MILK: Human: 0.15 – 1.05 mg/litre Cow’s: poor source

31. Recommended dietary allowances
Not precisely determined
0 – 0.5 years = 0.5 – 0.7 mg
0.6 – = 0.7 – 1.0 mg
1 – = 1.0 – 1.5 mg
4 – = 1.5 – 2.0 mg
7 – = 2.0 – 2.5 mg
= 2.0 – 3.0 mg
Safe adequate dietary intake 2 – 3 mg

32. IMPORTANT FACTS Tissue level of Cu remains constant in adults
Fetus stores Cu during gestation
Hepatic level in newborns 5 – 10 times that found in adult
Levels falls slowly during 1st year of life

33. Distribution Copper is present in all tissues.
Highest conc. is in liver and brain
Adult human body contain 100 – 150 mg of Cu

34. Absorption Mostly from stomach and small intestine
80 – 90% is bound to protein ceruloplasmin
5 – 20% is loosely bound to albumin and amino acid.
Being in bound form, not readily excreted in urine.
Almost all is excreted in feces (via bile into intestine)

37. Related Deficiency Diseases
Dietary Cu deficiency is rare
Deficiency can occur under a variety of conditions
In newborns it is linked to prematurity, LBW, Maternal mal nutrition

38. Related Deficiency Diseases
Low blood levels of Cu is observed in subjects with
Kwashiorkor
Sprue
Mal-absorption
Nephrotic syndrome

39. Related Deficiency Diseases
Bone disease may result from Cu deficiency
Minke’s kinky – hair syndrome – rare inherited
Cu – malabsorption from intestine
De-pigmentation of skin and hair

40. Deficiency signs and symptoms
Hypothermia
Seizures
Cerebral degeneration
Defective arterial walls
Are all due to the impaired activity of copper
containing enzymes

41. Related Deficiency Diseases
As Cu is intimately involved in Fe metabolism,
deficiency results in impaired release of Fe into plasma from Ferritin stores in intestinal mucosal cells
Plasma level of Fe falls  Hb synthesis is depressed  Iron deficiency Anemia

42. Wilson’s Disease
Characterized by markedly reduced serum Cu & ceruloplasmin levels.
Not due to nutritional Cu deficiency but due to abnormal Cu hepatic storage and impaired ceruloplasmin metabolism
Most of Cu in blood remains loosely bound to albumin Therefore is transferred more readily to tissue

43. Wilson’s Disease
In this disease liver and lenticular nucleus of the brain contain abnormally large amount of Cu.
There is also an excessive urinary excretion of this element

44. LOW LEVEL OF COPPER copper deficiencies in adults can trigger
Brain defects
Heart enlargement
Visual impairment,
Anemia (low iron),
Skin and hair breakdown and
Other organ damage.

45. The Duke team studied copper absorption in sept,2006
They identified, for the first time, the cellular gateway through which copper passes in mice.
An identical gateway is present in humans, as well as in other animals and plants.

46. The gateway is a copper "transporter" , a specific pore on the surface of intestinal cells that funnels copper inside the intestinal walls.
From there, copper is absorbed by the bloodstream and distributed throughout the body to serve as an engine to jump-start the activity of dozens of proteins that carry out essential functions.

47. In searching for the mechanism for copper absorption in cells, the researchers focused on a protein called Ctr1, a binding site or "receptor" that sits on the surface of cells in the intestine.
Duke had previously implicated Ctr1 as important in copper metabolism.

48. To further investigate its role, the researchers genetically manipulated pregnant mice so their developing fetuses lacked the gene that controls production of Ctr1 in the intestines. When the offspring were born, they could not absorb copper and dispatch it via the bloodstream throughout the body, the scientists found.

49. Giving copper supplements to adults has proven more effective in alleviating their symptoms, but scientists have been unclear as to what controls copper absorption in the first place.

50. Babies born without the ability to absorb and transport copper,develop a disorder called Menkes disease -- die in childhood.
Because injecting the mineral into children with Menkes has not proven beneficial, because cells may lack the ability to utilize it properly.