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Hiroshi Watanabe, Hiroshi Kosano, Hideo Nishigori; Steroid-Induced Short Term Diabetes in Chick Embryo: Reversible Effects of Insulin on Metabolic Changes and Cataract Formation. Invest. Ophthalmol. Vis. Sci. 2000;41(7):1846-1852.
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purpose. To determine the reversible effect of insulin on glucocorticoid
(GC)-induced cataract formation in relation to systemic metabolic
changes in the developing chick embryo.
methods. Hydrocortisone sodium succinate (HC; 0.25 micromoles) was administered
to 15-day-old embryos followed by administration of long-acting
recombinant human insulin, 4 and 28 hours later. At the indicated time
after HC administration, the incidence of cataractous lenses and any
changes in the components of the lenses, liver, and blood were
results. At 48 hours after HC administration, the following observations were
made: opacification of lenses; an elevation of glucose and lipids in
the blood and lenses; an increase in lipid peroxide (LPO) in the blood,
liver, and lenses; a decrease in glutathione (GSH) in the lens and
liver (at 24 hours after HC administration); and a depletion of
adenosine triphosphate (ATP) in the liver. These changes in response to
HC administration were reversed by a double application of insulin.
conclusions. Insulin antagonizes GC-induced gluconeogenesis, stimulates glycolysis,
and ultimately leads to recovery of decreased activity in the citric
acid cycle. The restoration of ATP by the recovered citric acid cycle
may facilitate de novo synthesis of GSH, which in turn may diminish
GC-induced elevation of LPO in the liver. Thus, the metabolic changes
in response to HC-accelerated gluconeogenesis in the liver, which can
be reversed by insulin, are likely to produce oxidative stress that
leads to cataract formation. GC-induced metabolic changes in the liver,
which are antagonized by insulin, may relate to production of one of
the risk factors for cataract formation.
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