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- December 1, 2008 |
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"Preventing Microvascular and Macrovascular Complications of Type 2 Diabetes"Dr. Ehud Ur (biography)
English - 2002-07-19 - 35 minutes
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Summary :
By planning ahead, Dr Ur shows how it may be possible to prevent Type 2 Diabetes complications such as stroke, retinopathy, heart disease, hypertension, renal disease, peripheral vascular disease , neuropathy and foot problems. Uncontrolled hyperglycemia is a major risk factor for complications. Complications sometimes present shortly after time of diagnosis, eg, retinopathy is present in 21% of patients soon after diagnosis of diabetes, and neuropathy is present in 40-50% of patients within 10 years of diabetes onset. Earlier screening and diabetes management prevents complications.
Learning objectives :
To formulate practical approaches in helping to prevent complications of Type 2 Diabetes in patients who are at risk. These complications include stroke, retinopathy, heart disease, hypertension, renal disease, peripheral vascular disease , neuropathy and foot problems.
Bibliographic references :
Resistin expression and regulation in mouse pituitary.
Morash B, Willkinson D, Ur E, Wilkinson M.
Department of Obstetrics and Gynaecology, Faculty of Medicine, Dalhousie
University, 5980 University Avenue, B3J 3G9, Halifax, NS, Canada
Resistin, a new adipocytokine, is expressed in human, rat and mouse
adipose tissue. Its putative role as a mediator of insulin resistance is
controversial. We hypothesized that resistin, in common with leptin, has
multiple roles in non-adipose tissues. Using reverse transcription
polymerase chain reaction (RT-PCR) we show that the resistin gene (Retn)
is expressed in mouse brain (hypothalamus and cortex) and pituitary gland.
Immunohistochemistry revealed resistin protein in the arcuate nucleus and
pituitary gland. Semi-quantitative RT-PCR analysis indicated that Retn
mRNA is developmentally regulated in the pituitary. Expression was lowest
at birth, increased abruptly between postnatal days 14 and 25 (four-fold;
P<0.001), and declined thereafter. This peak in pituitary Retn mRNA was
unaffected by early weaning but was abolished by neonatal treatment with
monosodium glutamate, suggesting that the basal hypothalamus regulates
pituitary Retn. Although the role(s) of endogenous resistin in mouse brain
and pituitary remains to be determined, it may be distinct from its
controversial involvement in insulin resistance. Our data suggest that
local resistin expression could have functional implications during
prepubertal maturation of the hypothalamic-pituitary system.
FEBS Lett 2002 Aug 28;526(1-3):26
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