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MAGNESIUM DEFICIENCY IS ASSOCIATED WITH INSULIN RESISTANCE
IN OBESE CHILDREN
Diabetes Care 2005 May;28(5): 1175-81
Huerta MG, et al.
Type 2 diabetes and insulin resistance has been
associated with magnesium deficiency. This study looks at
obese children with the intent on determining if they
exhibit serum or dietary magnesium deficiency and
potentially insulin resistance. Two groups of 24 were put
into this study. One group was composed of obese
non-diabetic children, while the other group was made up of
sex and puberty matched lean controls.
Measured were: serum magnesium, indices of insulin
sensitivity; dietary magnesium intake, and body
composition. The serum magnesium was significantly lower in
the obese children, and it was inversely
correlated with fasting insulin and positively correlated
with quantitative insulin sensitivity check index
(QUICK). The magnesium intake was significantly lower in the
obese children, ands intake was inversely
associated with fasting insulin and directly correlated to
QUICK. The research found that there is an
association between magnesium deficiency and insulin
resistance in childhood. Magnesium deficiency
could be secondary to lower magnesium intake. The use of
magnesium supplementation or increased intake
of magnesium-rich foods could be a recommendation for
preventing type 2 diabetes in obese children.
OXIDATIVE STRESS AND MAGNESIUM
Clin Calcium 2005 Feb;15(2):194-202
Hasebe N.
Normal metabolism will generate
a variety of free radicals that would ideally be handled by
the body's
elaborate antioxidant system. A variety of factors,
including lifestyle, environment, and pathologies can
cause oxidative stress due to the presence of excessive free
radicals. Cardiovascular diseases, cancer, and
other chronic degenerative conditions have been related to
oxidative stress. The antioxidants can delay or
prevent oxidative stress. Magnesium is one of the most
efficient antioxidants, playing a role in more than
300 enzymatic reactions and is critically involved in energy
metabolism, glucose utilization, protein
synthesis, fatty acid synthesis and breakdown, ATPase
functions and virtually all hormonal reactions. This
review summarizes the process of oxidative stress and all of
the pathways through which magnesium is
involved in fighting this stress.
MAGNESIUM AND MICROVASCULAR ENDOTHELIAL CELLS: A ROLE IN
INFLAMMATION AND
ANGIOGENESIS
Front Biosci 2005 May 1;10:1177-82
Bernardin D, et al.
Microvascular endothelial
cells are protagonists to inflammation and angiogenesis.
In vivo studies have
demonstrated that magnesium deficiency promotes
inflammation and impairs angiogenesis. In this study,
the effect of magnesium levels on microvascular 1G11
cells is looked at. The study found that low
magnesium inhibits endothelial growth and migration, but
leads to an increase in some inflammatory
markers. The study clearly showed that low magnesium
increases the formation of interleukin 1a and 6,
nitric oxide (a mediator of inflammatory responses), and
of VCAM - which mediates monocyte/endothelial
interactions. High magnesium induces critical events in
angiogenesis. The study results demonstrate a direct
role for magnesium in regulating microvascular functions
and gives a molecular explanation to the link
among magnesium, angiogenesis, and inflammation seen in
the in vivo studies.
CALCIUM FORTIFICATION SYSTEMS DIFFER
IN BIOAVAILABILITY
J Am Diet Assoc 2005 May;105(5):807-809
Heaney RP, et al.
This study compares
the bioavailability of calcium from two fortification
systems in orange juice. Study
design was randomized, crossover, within-subject on 25
healthy premenopausal women in an academic
health science center. The study looked at two commercially
available calcium fortified orange juices. The
subjects ingested an amount of orange juice to deliver 500mg
of calcium at breakfast after fasting overnight.
The studied compared calcium citrate malate versus a mix of
tricalcium phosphate and calcium lactate. The
measure of importance was the AUC (area under the curve) for
increases in serum calcium at 0 to 9 hours
after ingestion of the orange juice. The calcium citrate
malate had a 48% greater absorption than the calcium
phosphate/lactate combination. The researchers concluded
that equivalent calcium contents on the
nutritional label do not guarantee equivalent nutritional
value. The manufacturers need to provide the
consumer real absorption data.
EFFECTS OF POTASSIUM ALKALI AND CALCIUM SUPPLEMENTATION ON
BONE TURNOVER IN
POSTMENOPAUSAL WOMEN
J Clin Endocrinol Metab 2005 Jun;90(6):3528-33
Sakhaee K, et al.
Potassium citrate increases alkali load, which may
improve calcium balance. Calcium supplementation
inhibits PTH secretion which slows postmenopausal bone loss.
This study looks at the use of potassium
citrate and calcium citrate (alone or in combination) to
inhibit bone loss. The following treatments were
evaluated in a crossover study on 18 postmenopausal women:
potassium citrate (40 mmol/d), calcium citrate
(20 mmol/d), the combination, and placebo. Serum and 24-hour
urine were assessed for calcium
metabolism, alkali load, and bone turnover markers.
Potassium citrate, as compared to placebo, increased
alkali load, decreased urinary calcium, and did not change
serum PTH or bone turnover markers. Calcium
citrate, alone, increased absorbed calcium, decreased serum
PTH, and decreased bone resorption markers.
The combination of potassium and calcium citrate delivered
the greatest alkali load, the same absorbed
calcium (as the calcium alone). Compared to the placebo, the
combo therapy increased urinary calcium,
reduced serum PTH, gave a clear alkali load, and reduced
bone resorption markers. Bone resorption markers
decreased as treatment changed from placebo to potassium, to
calcium, and then to the combination
treatment. Conclusion: In postmenopausal women, the
combination treatment with potassium and calcium
citrate inhibited bone resorption by providing an alkali
load and increased absorbed calcium.
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