Intestinal
Inflammation Caused By Magnesium Deficiency Alters Basal and
Oxidative
Stress-Induced Intestinal Function
Scanian Bj, et al.
Mol Cell Biochem, 2007 Dec; 306(1-2):59-69.
The aim of this study was to determine tile effect of
magnesium deficiency on small intestinal morphology and
function.
Rats were assigned to 4 groups and placed on magnesium
sufficient or deficient diet for 1 or 3 weeks. Infiltration
of
neutrophils and mucosal injury were assessed in stained
sections of small intestine. Magnesium deficiency alone
induced a significant increase in neutrophil infiltration
and increased vascular ICAM-1 expression, in the absence of
changes in mucosal injury or expression of proinflammatory
mediators. Magnesium deficiency was associated with
hyposecretory epithelial cell responses and vascular
macromolecular leak in the small intestine and lung, which
was attributed partly to reduced expression of NOS-3. To
determine the effect of hypomagnesmia on the intestinal
responses to a known oxidative stress, groups of rats were
randomized to either sham operation or superior mesenteric
artery occlusion for 10 (non-injurious) or 30 (injurious)
minutes followed by a 1- or 4-hour reperfusion period. In
response to mesenteric ischemia/reperfusion, deficient rats
showed exaggerated PMN influx, but similar mucosal injury.
Intestinal ischemia in sufficient animals induced vascular
macromolecular leak in the small intestine and lung at 4
hours of reperfusion, with levels similar to those observed
in untreated deficient rats. Acute magnesium repletion of
deficient rats 24 hours before surgery attenuated the
exaggerated inflammation in deficient rats. These data show
that magnesium deficiency induced a subclinical inflammation
in the small intestine in the absence of mucosal injury, but
with significant functional changes in local and remote
organs and increased sensitivity to oxidative stress.
Long-Term Effect of
Magnesium Consumption on the Risk of Symptomatic Gallstone
Disease Among Men
Tsai CJ, et al.
Am J Gastroenterol, 2007 Dec 12.
Magnesium deficiency can cause dyslipidemia and insulin
hypersecreation, which may facilitate gallstone formation.
However, the effect of long-term consumption of magnesium on
the risk of gallstone disease is unknown. We
prospectively studied magnesium consumption and risk of
gallstone disease in a cohort of 42,705 U.S. men from 1986
to 2002. Magnesium consumption was assessed using a
validated semiquantitative food frequency questionnaire.
Newly diagnosed gallstone disease was ascertained
biennially. We documented 2,195 incident cases of
symptomatic gallstones during 560,810 person-years of
follow-up. The age-adjusted relative risks (RRs) for men
with total magnesium intake and dietary magnesium, when the
highest and lowest quintiles were compared, were 0.67 and
0.67 respectively. After adjusting for multiple potential
confounding variables, when extreme quintiles were compared,
the multivariate RR of total magnesium intake and dietary
magnesium remained significant with a dose-response
relationship. Our findings suggest a protective role of
magnesium consumption in the prevention of symptomatic
gallstone disease among men.
Role of dietary magnesium in
cardiovascular disease prevention, insulin
sensitivity and diabetes.
Bo S, Pisu E.
Curr Opin Lipidol, 208 Feb ; 19(1) :50-6.
This review summarizes the evidence for benefits of
magnesium on metabolic abnormalities, inflammatory
parameters,
and cardiovascular risk factors and related-potential
mechanisms. Controversy due to contrasting results in the
literature is also discussed. Increased dietary magnesium
intake confers protection against the incidence of diabetes,
metabolic syndrome, hypertension, and cardiovascular
disease. It ameliorates insulin resistance, serum lipid
profiles,
and lowers inflammation, endothelial dysfunction, oxidative
stress, and platelet aggregability. Magnesium acts as a mild
calcium antagonist on vascular smooth muscle tone, and on
postreceptor insulin signaling; it is critically involved in
energy metabolism, fatty acid synthesis, glucose
utilization, ATPase functions, release of neurotransmitters,
and
endothelial cell function and secretion. Prospective
studies, however, have found only a modest effect for
dietary
magnesium on incident pathologies. Furthermore, magnesium
supplementation on glucose metabolism, blood lipid
levels, and ischemic heart disease has given inconsistent
results. There is strong biological plausibility for the
direct
impact of magnesium intake on metabolic and cardiovascular
risk factors, but in-vivo magnesium deficiency might play
only a modest role. Reverse causality, the strong
association between magnesium and other beneficial
nutrients, or the possibility that people who choose
magnesium-rich foods are more health conscious may be
confounding factors.
A Deleterious Interaction Between Copper
Deficiency and Sugar Ingestion May Be
the Missing Link in Heart Disease
Aliabadi H.
Med Hypotheses, 2008 Jan 3.
Copper deficiency plays a vital role in atherogenesis. To
the long list of risk factors for atherosclerotic
cardiovascular
disease should be added the deleterious interaction between
copper deficiency and carbohydrate consumption. Here we
critically evaluate the role of copper in the diet and its
role as a possible etiological factor in the development of
cardiovascular disease. A possible mechanism for the
development of heart disease due to copper deficiency is
proposed. There are many known risk factors for the
development of heart disease, including hyperlipidemia and
hypertension; however, little emphasis has been placed on
the role of copper on heart disease. Over the last couple of
decades, dietary copper deficiency has been shown to cause a
variety of metabolic changes, including
hypercholesterolemia, hypertriglyceridemia, hypertension,
and glucose intolerance. Interestingly, these changes are
common in the United States population and they are known
risk factors for heart disease. Further research in this
field is warranted considering the profound implications to
people in the United States and around the world who consume
processed foods marginally deficient in copper and replete
with sugar. The only nutritional condition with signs and
symptoms of atherosclerotic cardiovascular disease may be
copper deficiency. Improving levels of copper in the diet,
by appropriate food selection or by addition of a daily
multi-vitamin, is recommended.
Copper,
Chromium, Manganese, Iron, Nickel, and Zinc Levels in
Biological
Samples of Diabetes Mellitus Patients
Kazi TG, et al .
Biol Trace Elem Res, 2008 Jan 11.
There is accumulating evidence that the metabolism of
several trace elements is altered in diabetes mellitus
and that
these nutrients might have specific roles in the
pathogenesis and progress of this disease. The aim of
present study was to compare the level of essential
trace elements, chromium (Cr), copper (Cu), iron (Fe),
manganese (Mn), nickel (Ni), and zinc (Zn) in biological
samples (whole blood, urine, and scalp hair) of patients
who have diabetes mellitus type 2 (n = 257), with those
of nondiabetic control subjects (n = 166), age ranged
(45-75) of both genders. The element concentrations were
measured by means of an atomic absorption
spectrophotometer after microwave-induced acid
digestion. The validity and accuracy was checked by
conventional wet-acid-digestion method and using
certified
reference materials. The overall recoveries of all
elements were found in the range of (97.60-99.49%) of
certified
values. The results of this study showed that the mean
values of Zn, Mn, and Cr were significantly reduced in
blood and scalp-hair samples of diabetic patients as
compared to control subjects of both genders (p <
0.001). The urinary levels of these elements were found
to be higher in the diabetic patients than in the
age-matched healthy controls. In contrast, high mean
values of Cu and Fe were detected in scalp hair and
blood from patients versus the nondiabetic subjects, but
the differences found in blood samples was not
significant (p < 0.05). These results are consistent
with those obtained in other studies, confirming that
deficiency and efficiency of some essential trace metals
may play a role in the development of diabetes mellitus
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