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Diabetes Mellitus is usually associated with wide spread biochemical disturbances. Till
date many trace elements have been proposed in etiopathogenesis of diabetes mellitus and its short and long term complications.
Role of Magnesium ions
Magnesium is a key factor in oxidative phosphorylation in step wise carbohydrate
metabolism and is also proposed to have some effect on action of insulin. Yet its status in diabetes mellitus is largely enigmatic.
In IDDM with DKA there is gross urinary loss of magnesium particularly during intensive
insulin and fluid therapy. This loss is reported in more than 55% of patients after initiation of therapy. Leading to hypomagnesemia. On the other hand some studies show raised magnesium level in diabetic patients with poor renal function.
Causes of Hypomagnesemia in DM.
1. Fluid and insulin therapy : In patients with IDDM and DKA there is gross urinary loss of
magnesium due to osmotic action of hyperglycemia in association with decrease renal tubular handling of increase magnesium delivery which is a direct consequence of high fluid infusion.
2. Hyperadrenalism : In IDDM there is a increased level of counter regulatory hormones,
Which add to reduced magnesium levels in such patients.
3. Hyperaldosteronism
Effects en magnesium deficiency in DM
1. Hypmagnesemia is associated with life threatening cardiac arrhythmia's with
concomitant hypokalemia.
2. Increased risk of development of retinopathy.
3. Increased risk of coronary disease due to increased atherogenesis due to platelet
reactivity.
4. High risk for development of nephropathy.
Role of magnesium supplementation.
1. To prevent arrhythmia's.
2. To improve glycemic control : Both by oxidative nietabolism as well asw increased
insulin sensitivity.
3. Prevention of atherosclerosis.
4. Prevention of retinopathy : It has been consistently found -that hypomagnesemia is
associated with high incidence of diabetic retinopathy. So magnesium supplementation
in association with strict glycemic control can prevent a delay progression of
retinopathy.
Zinc ion (German : of unknown origin) described by Liborins a traveler who also
mentioned that Zinc was discovered in India.
Introduction
Zinc is an essential factor for more than 90 enzymes of which at least 20 are metallo
enzymes. The key metabolic regulatory and catalytic function.
Absorption : Zinc is actively absorbed in small intestine mainly duodenum against a
concentration gradient of which almost 50% is available in circulation from dietary sources.
In Plasma 60% is albumin bound rest is bound to amimoacids and serum globulin's.
Sources
Richest sources are sea foods, oyster meat, nuts etc.
Excretion is mainly through faeces.
Role in Carbohydrate metabolism
1. Zinc causes in vitro release of insulin from pancreas during glucose stimulation.
Mechanism of this is not known.
2. Crystallization of insulin in hexameric from is essential for basal insulin level in blood
which causes prolonged glycemic control. So zinc deficient individuals have less stable
hexameric form, so rapid degradation of insulin occurs leading to glucose intolerance in
previously well controllled diabetics.
3. Zinc is an integral part of pancreatic carboxy peptidase essential in intestinal protein
metabolism.
Other roles of Zinc
1. Insulin storage in B-cells is mainly in hexameric form. These crystals are released into
portal venous circulation and variation in zinc insulin molecular ratio have been crystals
are released into this property, so in efficient storage as well as defective release of
insulin occurs.
2. Zinc enhances hepatic insulin binding by increased expression of GLUT-2 receptors on
liver cells.
3. Zinc stimulates lipogenesis in adipose tissue. In diabetes mellitus
Zinc deficiency is seen more commonly in NIDDM / MODY than IDDM.
Causes of Zinc deficiency in Diabetes are following :-
1. Increased urinauy loss of zinc due to glycosuria leading to osmotic effect on zinc
excretion.
2. Polygenic role : Family relatives of diabetes mellitus heavy zincurea than control.
Without having overt symptoms of diabetes. Suggesting a genetic predisposition.
3. Aminoacid urea can increased zinc excretion possibly through competition with serum
proteins for zinc binding and resultant increase in ultra filtrated fraction of zinc. This is
seen after aminoacid infusion zinc excretion was increased upto 100%.
4. Disturbed metabolism of zinc metalloenzymes have been suggested as possible cause.
In effective zinc deficiency in diabetic is a result of increased zinc excretion in urine which
is not compensated by increased intestinal absorption.
Effects of Zinc deficiency
1. Impaired glucose tolerance
2. Blunted insulin action due to rapid degradation and decrease sensitivity.
3. Impaired wound healing.
4. Acrodermatitis enteropathica.
5. Hypogonadism
Chromium
In 1970 it was approved that Chrominm is a essential trace element for normal glucose
and lipid metabolism recent years the role chromium has emerged as exciting advancement in management of diabetes.
Chemical role : Chromium is an integral part of so called Glucose Tolerance Factor
(GTF) a chromium nicotinate complex which enhances insulin efficiency through increased number of insulin receptors and enhanced binding. And post receptor events intracellularly.
Sources : Rich sources are organ meats, mushrooms, wheat germs, and processed meats etc.
Absorption: Chromium is mainly absorbed from small intestine 30- 40% of oral dose is
available in circulation.
Daily Recommendation : Infants 10-60 microgram/day. Children 20- 80 microgram/day
(1 to 3 years), 4-6 years 30-120 microgram/day, 6-11 years 50-200 microgram/day. Adults 50-200 microgram/day.
Chromium is used mainly as
1. Chromium Chloride (brewer's yeast)
2. Chromium Picolinate
3. Chromium Nicotinate
All the three salts contain trivalent Cr3+ ions.
Causes of Chromium deficency
1. Nutritional : Most of then people have got less than 50 microgram Chromium per day as
compared to normal 200 microgram/ day.
2. Increase Urinary Chromium excretion : Acute rise and blood glucose is associated with
rapid urinary loss of chromium.
3. Aging : It is seen that infants have highest levels of chromium in their blood. As age
advances their chromium level decreases gradually. So older people who are also
diabetic (NIDDM) are more prone to develop chromium deficiency.
Role in Diabetes
1. Improvement in glucose metabolism
2. Decrease insulin requirement, thus preventing emergence of insulin resistance.
3. Improved lipid metabolism, thus reducing incidence of atherosclerotic cardio vascular
events. Chromium is shown to increase serum HDL level and slight reduction in LDL.
4. Chromium causes loss of body fat probably through insulin mediated sympathetic out
flow to cause increased thermogenesis, this helps to maintain their weight and attending
risk of obesity.
5. Synodrome X : It's a combination of obesity, hypertension, and diabetes which devlops
in patients with insulin resistance. Chromium by virtus of its insulin sensitizing action and
better lipid metabolism can prevent the development of this complication.
6. Wound healing may be improved by increased FGF, IGF expression particularly useful
in diabetic wounds.
7. As an Immuno-modulator : As many immune cells express insulin receptors and
impairment in their function is seen in diabetes so chromium supplementaion can be of
some benefit.
8. As chromium is closely complexed to nicotine acid and tryptophen it can affect
neurotransmitter function in brain
9. Control of BP by better insulin action.
10. Chromium may play a role in the body's antioxidant agent by preventing lipid
peroxidation thus limiting the progress of chronic disease and aging.
Complications of Chromium therapy.
Recent studies have shown that therapeutic chromium picotinate supplements for a long
period can lead to damage of chromosome in metaphase stage of replecations cycle.
REFERENCES
1. Ripas, Ripar Zinc and Diabetes Mellites-Mineral Med 1995, 86 (10) 415.21
2. Morris B.W. Griffiths H, Kemp G.J. Comlahan between abnormalties in chromium &
glucose metabolism in a group of diabetics clin. Chem 1988; 34; 1525-26.
3. Hypomagenisemia and Diabetes Mellites Tosiello L. Arch Intern Med. 1996 June
10,156 (11) 1143.
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