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Background Diabetes 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. Methods Experimental 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. 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. Conclusion This 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.

Acrylamide maybe formed in food cooked at very high temperature. Its role on gastric mucosa defenseis not fully elucidated. Hence the role of acrylamide consumption on gastric mucosal integrity was investigated. Fifty‐four animals (150–200g) were divided into 3 groups of 18 rats: Group 1 ‐ control (distilled water 0.2ml), Groups 2 (7.5mg/kg acrylamide) and 3 (15mg/kg acrylamide). All treatments were done orally for 28 days. Post‐treatment, gastric juice (modified pylorus ligation method) was obtained per group (n=5) and analysed for gastric acidity. Gastric antioxidants status (superoxide dismutase, glutathione, catalase, lipid peroxidation), tissue bicarbonate and prostaglandins‐E2 were assayed per group (n=5). Blood was collected via cardiac puncture for haematological indices and gastric mucus content was evaluated per group (n=5). Cell counts (parietal and mucous) and gastric histology was evaluated per group (n=3) using haematoxylin and eosin (H&E) and Periodic acid Schiff (PAS) stains. Mucus content, bicarbonate, prostaglandins‐E2, superoxide dismutase, glutathione, catalase, mucous cell count were reduced (p<0.05) in the acrylamide groups compared to control. Gastric acidity, nitric oxide, parietal cell count and lipid peroxidation were increased (p<0.05) in the acrylamide groups compared to control. White blood cell count in group 2 was increased but decreased in group 3 compared to control (p<0.05). Acrylamide treatment groups had gastric epithelial cells with poor architecture, lamina propria and submucosa inflammatory cell infiltration. Vascular congestion and limited production of mucus was observed. This study suggests that acrylamide consumption causes a dose‐dependent degeneration of gastric mucosa integrity via reductions in gastric protective factors which thus predisposes the gastric mucosa to erosions and lesions.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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Introduction: Acrylamide, a byproduct of the cooking process, has been reported to be a toxicant with likely carcinogenic properties. Its impairment of gastric function has been previously reported. In this study its effects on gastrointestinal motility and intestinal structure was investigated in male Wistar rats.Methods: Forty-five rats (120-180g) were divided into 3 equal groups (n=15) and treated p.o with either 0.2ml distilled-water, or acrylamide (7.5mg/kg and 15mg/kg respectively) for 28days. Thereafter, gastric emptying and intestinal motility was assessed. Intestinal structure (duodenum, jejunum and ileum), mucosal and intestinal cell counts were evaluated using histological techniques.Results: Gastric emptying and intestinal transit time increased (p<0.05) in the experimental (acrylamidetreated; 7.5mg/kg and 15mg/kg) groups compared to control. Mucosal cell counts (duodenum, jejunum and ileum) and ileum intestinal cell counts (p<0.05) were reduced in the experimental groups compared to control. Compared to control, duodenal samples of the experimental groups showed severe coagulative necrosis and sloughing off of the villi, luminal filling with necrotic debris, disruption and necrosis of the crypts of Lieberkühn, moderate polymorphonuclear cell infiltration and vascular congestion. These pathologies albeit with less severity were also observed in the jejunum and ileum of acrylamide treated groups.Conclusion: Increased oral exposure to acrylamide impairs gastric emptying, intestinal motility, mucus secretion and compromises digestive and absorptive functions of the small intestines, especially the duodenum. These observations may be ascribed to acrylamide-induced impaired neuronal signaling, autonomic neuropathy, oxidative stress, inflammation and cell necrosis. Keywords: Acrylamide, gastrointestinal tract, gastric emptying, intestinal motility, small intestines