Type-1 Diabetes Induces Depot-Specific Alterations in Adipocyte Diameter and Mass of Adipose Tissues in the Rat

Abstract

Type-1 diabetes (T1D) is a metabolic disorder associated with massive reduction in mass of adipose tissue. Measuring cell diameter, an index of fat metabolism, we determined depot-specific alterations in weight of adipose tissue, fat cell diameter and size heterogeneity and distribution at 5 depots in streptozotocin (STZ)-induced diabetic rats. T1D was induced by a single injection of STZ. Seven days after the injection, fat depots were isolated, weighted, washed and maintained in tissue culture medium. Using a microscope equipped with calibrated micrometer, cell diameter as well as size distribution pattern and heterogeneity of adipocytes were determined in fresh tissue slices of subcutaneous (SC), proximal epididymal (PE), distal epididymal (DE), perirenal (PR) and retroperitoneal (RP) fat depots. The T1D induced marked reductions in fat mass and mean of fat cell diameter at all depots. The most affected depot was the SC. With the exception of PE, adipocytes at all depots showed significant increases in size heterogeneity. The effect of the diabetes on mean fat cell diameter and size heterogeneity was minimal at PE depot. Depots with similar cell size distribution pattern exhibited similar fat mass reduction. However, the DE depot with a unique cell size distribution pattern showed a fat mass reduction similar to that of PE and PR depots. These data indicate that T1D induces a massive fat mass reduction in a reasonably depot-specific manner and that the fat depots close to survival organs are less vulnerable to fat mobilization. Moreover, peculiar disagreement between cell size distribution and heterogeneity as well as the level of fat mass reduction at DE and PE depots suggests that not only cell size and heterogeneity but also local factors may play roles in depot-specific fat mobilization.

Effects of Rat C-peptide-II on Lipolysis and Glucose Consumption in Cultured Rat Adipose Tissue

“…This has been attributed to the cell binding characteristics of CP; yet to be determined for adipocytes. Previously we have reported that adipose tissues at diff erent anatomical site may not response equally to the same signal [28] and, therefore, the present data may not be applicable to other fat depots. Regarding the experimental model, cell-cell and cell-matrix interactions which have profound eff ects on cell behavior [29] have been absent in the isolated adipocytes used in the Kitabchi et al experiments.…”

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“…Streptozotocin (STZ) or alloxan-induced diabetic rat or mouse is the most currently used animal model for diabetes. A single intraperitoneal or intravenous injection of STZ is well reported to induce insulin-dependent diabetes in rats (Ghorbani et al, 2010;Ghorbani et al, 2013;Shafiee-Nick et al, 2012b). The histologic feature of islets from the pancreas of diabetic animals is characterized by a severe decrease in the number of islets, inflammation, vacuolation of the islets, and degranulation of the beta cells (Adeyemi et al, 2008;Aralelimath, Bhise, 2012).…”

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“…Generally, diabetes is classified to two main types: type-1 diabetes (T1D), previously known as insulin-dependent diabetes mellitus, and type-2 diabetes (T2D), formerly called non-insulin-dependent diabetes mellitus. Patients with T1D show a state of insulin deficiency because of severe defect in islet β-cell function while T2D is characterized by a combination of resistance to action of insulin and insufficiency in insulin secretion (Deshpande et al, 2008).Over time, both types of diabetes lead to serious complications in the body, which include nephropathy, retinopathy, neuropathy, dyslipidemia and cardiovascular diseases (Deshpande et al, 2008;Ghorbani et al, 2010). Currently, beside insulin, the most widely used medication A. Ghorbani 414 for diabetes are oral hypoglycemic drugs including insulin sensitizers (biguanides, thiazolidinediones), insulin secretagogues (sulfonylureas, meglitinides), α-glucosidase inhibitors, incretin agonists and dipeptidyl peptidase-4 inhibitors (Lorenzati et al, 2010).…”