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CELLULAR CHROMIUM ENHANCES ACTIVATION
OF INSULIN RECEPTOR KINASE
Biochemistry 2005 Jun 7;44(22):8167-75.
Wang H; Kruszewski A; Brautigan DL.
Chromium has been touted for decades as a factor that
improves glucose tolerance by enhancing insulin action.
However, the mechanism for this is not known. In this study
the pretreatment of CHO-IR cells with chromium
enhanced tyrosine phosphorylation of the insulin receptor.
Several chromium (III) compounds were effective at
enhancing insulin receptor phosphorylation, but did not
directly activate insulin receptor kinase. Chromium did not
inhibit protein tyrosine phosphatase (PTP1B). Chromium did
not effect reversible redox regulation of PTP1B.
Chromium treated cells had higher specific activity of
insulin dependent kinase relative to controls. Researchers
conclude that cellular chromium potentiates insulin
signaling by increasing insulin receptor kinase activity,
separate
from inhibition of PTPase. This suggests that nutritional
and pharmacological therapies may complement one another
in combating insulin resistance, the hallmark of type 2
diabetes.
MATERNAL AND PERINATAL MAGNESIUM
RESTRICTION PREDISPOSES RAT PUPS TO
INSULIN RESISTANCE AND GLUCOSE INTOLERANCE
J Nutr 2005
Jun;135(6):1353-8.
Venu L; Kishore YD; Raghunath M.
Impaired intrauterine
development leads to insulin resistance and its associated
metabolic disturbances. These
researchers had reported that increased body fat (a
forerunner of insulin resistance) was seen in mineral
restricted rat
dams. In an attempt to find the causative mineral(s), the
researchers looked at magnesium dietary restriction. In the
study, the rat dams were in groups that 1) received a 70%
magnesium restricted diet, and 2) a pair-fed control diet.
After 9 weeks, they were mated with control males. The
control dams and pups were fed the control diet throughout,
while part of the magnesium restricted dams switched to a
control diet at parturition (RP), and the offspring weaned
onto the control diet. The offspring of the remaining
restricted dams were weaned onto the control diet (RW) or
the
magnesium restricted diet. The offspring were studied on
postnatal days 90 and 180. On postnatal day 180, R, RP,
and RW offspring were insulin resistant and had a lower
insulin response to glucose challenge than group C, and
glucose tolerance was impaired only in the RW group.
Maternal magnesium restriction was seen to irreversibly
increase body fat and induce insulin resistance in the
offspring by 6 months of age, and additional perinatal
deficiency
impairs glucose tolerance.
ZINC AND SKIN HEALTH: OVERVIEW OF
PHYSIOLOGY AND PHARMACOLOGY
Dermatol Surg 2005
Jul;31(7Pt 2):837-47: discussion 847.
Schwartz JR; Marsh RG; Draelos ZD.
Zinc is known to play a
critical role in human physiology, which explains the
reason for its many therapeutic
applications. The specific roles for zinc in maintaining
skin health and function are not well understood, and
have
been based on manifestations seen in zinc deprivation,
including moderate to severe dermatitis. This provides a
critical
review of published science on the physiologic
importance of zinc to skin, biochemical basis, and
pharmacological
aspects of zinc therapeutics. The skin is continually
being reformed, which places a high demand on zinc based
systems that are in charge of the processes. Zinc’s
physiological importance is clearly seen in studies on
wound
healing and inflammation reduction. Administering zinc
externally during these situations has increased the
rates of
the natural processes. The topical application of zinc
grants a pharmacologic optimization of zinc delivery,
mediated
by the solubility of the zinc material and product
matrix.
CETUXIMAB THERAPY AND SYMPTOMATIC
HYPOMAGNESEMIA
J Natl Cancer Inst 2005 Aug 17;97(16):1221-4.
Schrag D; et al.
This group had observed and
reported that people receiving cetuximab, a monoclonal
antibody against epithelial
growth factor receptor (EGFR) occasionally developed a
magnesium wasting syndrome with inappropriate urinary
excretion. This was initially observed in a 34 year old male
with metastatic colorectal cancer, who had developed
profound fatigue along with symptomatic hypocalcemia and
hypomagnesemia on cetuximab, but no other medication
with potential for magnesium wasting. The use of intravenous
magnesium supplementation was needed for the rest of
the cetuximab treatment, and this electrolyte abnormality
resolved with discontinuation of cetuximab treatment. This
case lead to review of 154 colorectal cancer patients’ data
who had been on cetuximab. Only 22% of these had serum
magnesium measured during the treatment, and 8 of these had
substantially graded cases of hypomagnesemia. It is
known that EGFR is strongly expressed in the kidney, and
especially in the ascending loops of Henle, where 70% of
filtered magnesium is reabsorbed, EDFR blockade could
interfere with magnesium transport. These symptoms can
readily be helped with supplementation, there suggest that
when fatigue or hypocalcemia is seen in cetuximab therapy,
that magnesium levels be measured and repleted with
magnesium supplementation when indicated.
EFFECTS OF POTASSIUM ALKALI AND
CALCIUM SUPPLEMENATION ON BONE TURNOVER
IN POSTMENOPAUSAL WOMEN
J Clin Endocrinol Metab 2005 Jun;90(6):3528-33.
Sakhaee K; Maalouf NM; Abrams SA; Pak CY.
Potassium citrate may improve calcium balance by
conferring an alkali load. Calcium supplementation slows
postmenopausal bone loss by inhibiting PTH secretion. This
study explores whether combined treatment with
potassium citrate and calcium citrate is more effective than
either agent alone in inhibiting bone loss. In a crossover
study involving 18 postmenopausal women, the following
treatments were compared: potassium citrate (4.5 g or 40
mmol/d), calcium citrate (800 mg or 20 mmol/d), combined
treatment, and placebo. During the last 2 days of each 2-
week phase, serum and 25 hour urine were collected for
assessment of calcium metabolism, alkali load, and bone
turnover markers. Compared with placebo, potassium citrate
provided an alkali load and significantly decreased
urinary calcium without changing serum PTH (sPTH) or bone
turnover markers. Calcium citrate significantly
increased absorbed calcium, marginally decreased sPTH, and
significantly reduced bone resportion markers.
Combined treatment retained key features of potassium
citrate and calcium citrate. However, more alkali was
delivered than with potassium citrate alone, and absorbed
calcium did not differ from calcium citrate alone. Compared
with placebo, combined treatment increased urinary calcium,
marginally reduced sPTH, provided a clear alkali load,
and reduced the bone resorption markers serum type I
collagen C-telopeptide and urinary N-telopeptide by 20.4%
(P<0.0001) and 18.2% (P= 0.005), respectively. A significant
trend was noted for the decrease in bone resorption
markers as treatment changed from placebo to potassium
citrate to calcium citrate to combined treatment. In
postmenopausal women, combined treatment with potassium
citrate and calcium citrate inhibits bone resorption by
providing an alkali load and increasing absorbed calcium.
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