The retinal pigment epithelium of Cr-deficient rats
Introduction
Previous studies [1], [2], [3], [4], [5], [6], [7], [8], [9], [10] have provided strong evidence of the nutritional importance of trace elements in ocular tissues. Since chromium (Cr) was identified as an essential element in 1959 [11], its interaction with insulin in vitro and in vivo has been established [11], [12], [13], and the site of action has been identified on the insulin-sensitive cell membrane [14]. The known effects of trivalent Cr on lowering blood levels of low density lipoproteins, raising high density lipoproteins [15] and improving glucose tolerance [11] are summarized, and Cr is shown to be involved in the metabolism of glucose and lipid.
There have been no reports on experiments designed to clarify the effect of Cr deficiency on the rat retina. The purpose of this study is to investigate the retinas of Cr-deficient rats.
Section snippets
Animals and diets
We used 21-day-old male Wistar Kyoto rats weighing 35.0 to 45.0 grams divided randomly into a Cr-deficient and a control group. The rats were treated in accordance with the ARVO resolution on the use of animals in research. All animals were fed a low Cr powdered diet made by ourselves. The content of the AIN-93G formula-based diet is shown in Table 1. The low Cr diet is the AIN-93G formula-based diet containing sucrose without added Cr. It contains no Cr and is complete in all other nutrients.
Body Weight
The mean body weight of normal 4-month-old rats was 512.5 ± 17.5 g (n = 10) and that of Cr-deficient rats was 508.5 ± 17.0 g (n = 10). There was no significant difference in body weight between Cr-deficient and normal rats. Cr-deficient rats exhibited normal health with no hair loss.
Whole blood Cr level
Whole blood Cr levels of normal and Cr-deficient rats were less than 0.2 μg/l, the limit of sensitivity for Cr measurement.
Blood sugar level
The blood sugar level of normal 4-month-old rats was 65.6 ± 7.0 mg/dl (n = 7) and that of
Discussion
Trivalent chromium was identified as the biologically active metal component of glucose tolerance factor by Schwarz and Mertz [11]. Patients on total parenteral nutrition (TPN) developed severe diabetic symptoms that were refractory to insulin [16]. After the addition of Cr to TPN fluids, diabetic symptoms were alleviated, and exogenous insulin was no longer required. In rats, severe chromium deficiency produced by strict elimination of dietary chromium and environmental chromium contamination
Acknowledgements
The authors thank Dr. Katsuhiko Yokoi for teaching us how to make a Cr-deficient diet.
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