Abstract
The use of experimental models of diabetes mellitus (DM) has been useful in understanding
the complex pathogenesis of DM. Streptozotocin (STZ) injected in rats during the neonatal
period has usually led to the major features described in diabetic patients (hyperglycemia,
polyphagia, polydipsia, polyuria, and abnormal glucose tolerance) in a short period.
Diabetes mellitus is a product of low insulin sensibility and pancreatic beta-cell
dysfunction. Its process is characterized by a symptomless prediabetic phase before
the development of the disease. In this study, we investigated the long-term effects
of diabetes induction regarding the cellular metabolic aspects of this model and its
similarities with diabetes found in humans. Male Wistar rats (5-day old) were intraperitoneally
injected with STZ (150 mg/kg) and followed up for 12 weeks. On the 12th week, animals
were decapitated and peri-epididymal fat pads were excised for adipocyte isolation.
The following studies were performed: insulin-stimulated 2-deoxy-d-[3H]glucose uptake; incorporation of d-[U-14C]-glucose into lipids and conversion into 14CO2; and insulin binding. The weight gain rate of the STZ-treated group became significantly
lower by the eighth week. These rats developed polyphagia, polydipsia, polyuria, and
glycosuria, and impaired glucose tolerance. Biological tests with isolated adipocytes
revealed a reduction in the insulin receptor number and an impairment in their ability
to oxidize glucose as well as to incorporate it into lipids. Interestingly, parallel
to reduced body weight, the adipocyte size of STZ rats was significantly small. We
concluded that apart of a decrease in pancreatic insulin content, this experimental
model of DM promotes a remarkable and sustained picture of insulin resistance in adulthood
that is strongly related to a loss in adipose mass.
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Article info
Publication history
Accepted:
May 17,
2006
Received:
April 24,
2006
Identification
Copyright
© 2007 Published by Elsevier Inc.