Abstract

BackgroundDiabetes mellitus has been reported to cause thyroid dysfunction, which may also impair renal function. Magnesium has been reported to exert ameliorative effects in diabetes mellitus. This study investigated thyroid and renal functions in experimental type-2-diabetic Wistar rats. MethodsExperimental type-2-diabetes was induced using short duration high-fat (30%) diet feeding followed by single-dose streptozotocin (35 mg/kg i.p.). Fifty rats were randomly divided into five equal groups consisting of control, diabetes untreated, diabetes treated with either magnesium (250 mg/kg) or metformin (250 mg/kg) and diabetes treated with both metformin and magnesium simultaneously.All treatments were carried out orally for 14days post-diabetes induction. Body weight and blood glucose was monitored using the tail tipping method before diabetes induction and thereafter on days 1,7,14 post-treatment respectively. Thereafter, blood samples were collected by cardiac puncture after light anesthesia into plain and EDTA sample bottles. Total protein, albumin, globulin (plasma) and insulin (serum) were assayed in all samples obtained. Thyroid stimulating hormone (TSH), triiodothyronine, thyroxine was also evaluated (n = 5/group) in serum while blood urea nitrogen (BUN), creatinine was assessed (n = 5/group) in plasma. Kidney homogenates were obtained per group and analyzed for renal superoxide dismutase (SOD), reduced glutathione (GSH) and lipid peroxidation (MDA). Kidney histology was also evaluated per group using both Haematoxylin and Eosin and periodic acid Schiff stains. ResultsBody weight, blood glucose, insulin, renal MDA was increased in diabetic untreated compared to other groups. Reductions (P < 0.05) in TSH, triiodothynine, Renal SOD and GSH levels where observed in diabetic untreated compared to other groups. Renal histology in diabetic untreated showed glomerula sclerosis, fused messengial cells and either collapsed tubular lumen or lumen with eosinophilic renal cast. These pathologies where partially reversed in the other experimental groups. ConclusionThis study suggests that thyroid and renal impairment may be present in experimental type-2-diabetes. Treatment with oral magnesium may cause a partial restoration of thyroid function that may impede the development of renal dysfunction.

Highlights

  • Diabetes and thyroid disorders are common endocrine disorders that have been shown to mutually influence each other [1]

  • Values obtained in the diabetic untreated group, magnesium treated diabetic, metformin treated diabetic as well as the magnesium and metformin co-treatment diabetic groups had 35.28%, 26.11%, 35.07% and 37.37% increase in body weight compared to their respective day 0 values (Table 1)

  • The increased morbidity and mortality associated with diabetes mellitus may be as a result of the multifaceted pathology of the syndrome, which results in it exerting its effects on various organ systems in the body [20]

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Summary

Introduction

Diabetes and thyroid disorders are common endocrine disorders that have been shown to mutually influence each other [1]. Altered thyroid states have been reported to occur in diabetes mellitus resulting in reductions in thyroid stimulating hormone in triiodothyronine levels [6]. Diabetes mellitus has been reported to cause thyroid dysfunction, which may impair renal function. This study investigated thyroid and renal functions in experimental type-2-diabetic Wistar rats. Results: Body weight, blood glucose, insulin, renal MDA was increased in diabetic untreated compared to other groups. Reductions (P < 0.05) in TSH, triiodothynine, Renal SOD and GSH levels where observed in diabetic untreated compared to other groups. Renal histology in diabetic untreated showed glomerula sclerosis, fused messengial cells and either collapsed tubular lumen or lumen with eosinophilic renal cast These pathologies where partially reversed in the other experimental groups. Treatment with oral magnesium may cause a partial restoration of thyroid function that may impede the development of renal dysfunction

Methods
Results
Conclusion
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