title: Metabolic recovery of adipose tissue is associated with improvement in insulin resistance in a model of experimental diabetes.
abstract: Obesity and insulin resistance are highly correlated with metabolic disturbances. Both the excess and lack of adipose tissue can lead to severe insulin resistance and diabetes. Adipose tissue plays an active role in energy homeostasis, 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 (EP) fat mass were also seen in this model. The aim of this study was to investigate the glucose homeostasis and metabolic repercussions on the adipose tissue following 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 killed, EP 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 also the lack of adipose tissue might play a significant role on the pathophysiology of this particular diabetes model.
authors.affiliation: Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, 1524 Prof Lineu Prestes Avenue, 05508-900, Sao Paulo, Brazil.
authors.forename: Julie
authors.initials: J
authors.lastname: Takada
authors.forename: Miriam Helena
authors.initials: MH
authors.lastname: Fonseca-Alaniz
authors.forename: Tarcila Beatriz Ferraz
authors.initials: TB
authors.lastname: de Campos
authors.forename: Sandra
authors.initials: S
authors.lastname: Andreotti
authors.forename: Amanda Baron
authors.initials: AB
authors.lastname: Campana
authors.forename: Maristela
authors.initials: M
authors.lastname: Okamoto
authors.forename: Cristina das Neves
authors.initials: Cd
authors.lastname: Borges-Silva
authors.forename: Ubiratan Fabres
authors.initials: UF
authors.lastname: Machado
authors.forename: Fabio Bessa
authors.initials: FB
authors.lastname: Lima
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D002096:C-Peptide / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005947:Glucose / Q000378:metabolism; D005951:Glucose Tolerance Test; D051275:Glucose Transporter Type 4 / Q000032:analysis / Q000235:genetics; D005989:Glycerides / Q000097:blood; D007333:Insulin Resistance; D008066:Lipolysis / Q000187:drug effects; D008297:Male; D000077205:Pioglitazone; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin; D045162:Thiazolidinediones / Q000494:pharmacology
chemical_list: D002096:C-Peptide; D005230:Fatty Acids, Nonesterified; D051275:Glucose Transporter Type 4; D005989:Glycerides; D012333:RNA, Messenger; C495694:Slc2a4 protein, rat; D045162:Thiazolidinediones; D013311:Streptozocin; D005947:Glucose; D000077205:Pioglitazone