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Accepted Preprint first posted online on 1 May 2008

Journal of Endocrinology 2008;198:51.

Journal of Endocrinology (2008) In press  DOI: 10.1677/JOE-08-0072
© 2008 Society for Endocrinology
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RESEARCH-ARTICLE

Metabolic recovery of adipose tissue is associated with improvement in insulin resistance and in glycemic control in a model of experimental diabetes.

 Julie Takada, Miriam Fonseca-Alaniz, Tarcila Ferraz de Campos, Sandra Andreotti, Amanda Campana, Maristela Okamoto, Cristina Borges-Silva, Ubiratan Machado and Fabio Lima

J Takada, Physiology and Biophysics, University of Sao Paulo, Sao Paulo, 05508-900, Brazil
M Fonseca-Alaniz, Physiology and Biophysics, University of Sao Paulo, Sao Paulo, Brazil
T Ferraz de Campos, Physiology and Biophysics, University of Sao Paulo, Sao Paulo, Brazil
S Andreotti, Physiology and Biophysics, University of Sao Paulo, Sao Paulo, Brazil
A Campana, Physiology and Biophysics, University of Sao Paulo, Sao Paulo, Brazil
M Okamoto, Physiology and Biophysics, University of Sao Paulo, Sao Paulo, Brazil
C Borges-Silva, Physiology and Biophysics, University of Sao Paulo, Sao Paulo, Brazil
U Machado, Physiology and Biophysics, University of Sao Paulo, Sao Paulo, Brazil
F Lima, Physiology and Biophysics, University of Sao Paulo, Sao Paulo, Brazil

Correspondence: Julie Takada, Email: jjtakada{at}yahoo.com

Abstract

Obesity and insulin resistance are highly correlated with metabolic disturbances. Both the excess and the lack of adipose tissue can lead to severe insulin resistance and diabetes. Adipose tissue plays an active role in energy homeostasis, in hormone secretion and other proteins that affect insulin sensitivity, appetite, energy balance and lipid metabolism. Rats with streptozotocin-induced diabetes during the neonatal period develop the classic diabetic picture of hyperglycemia, hypoinsulinemia and insulin resistance in adulthood. Low body weight and reduced epididymal fat mass were also seen in this model. The aim of this study was to investigate the metabolic repercussions on the adipose tissue of chronic treatment with antidiabetic drugs in these animals. In the 4th week post birth, diabetic animals started an 8-week treatment with pioglitazone, metformin or insulin. Animals were then sacrificed, epididymal fat pads were excised and blood samples were collected for biological and biochemical assays. Pioglitazone and insulin treatments, but not metformin, reduced hyperglycemia, polydipsia and polyphagia. Although all antidiabetic therapies improved insulin sensitivity, this was particularly noteworthy in the pioglitazone-treated rats. Furthermore, a recovery of adipose mass and insulin levels were observed in pioglitazone and insulin, but not metformin-treated animals. Treatments with insulin or pioglitazone were able to correct significantly, but not completely, the metabolic abnormalities, parallel to full recovery of adipose mass, indicating that not only the low insulin levels, but the lack of adipose tissue, might play a significant role on pathophysiology of this particular diabetes model.






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