A rat model of diabetic complications induced by high-fat diet and low-dose streptoxotocin injections

Binh, Doan Viet; Dung, Nguyen Thi Kim; Nhi, Nguyen Bich; Van, Phan

doi:10.15625/0866-7160/v35n3.3396

Cited by 4 publications

(11 citation statements)

References 9 publications

(14 reference statements)

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“…Furthermore, in the induced diabetic models most animals require relatively high dose of streptozotocin (STZ; >50 mg/kg) [17,19,32], which triggers characteristic features of type 1 diabetes more than type 2 diabetes. High fat diet and STZ models are routinely employed for studying diabetes and its associated complications in rats [8,15,20]. In the present study, HFD diet developed insulin resistance and glucose intolerance in the animals.…”

Section: Discussionmentioning

confidence: 62%

“…Srinivasan et al [8] used lard oil and other ingredients in HFD preparation. Binh et al [20] also used complex HFD diet containing lard oil for 24 weeks. Plant-originated fats along with cholesterol have also been used to develop diabetic model for 10 weeks duration [15].…”

Section: Discussionmentioning

confidence: 99%

“…The detrimental effect of continuously elevated serum glucose and lipid levels on various organs including liver, kidney and pancreas is well documented [20,37]. Liver and kidney are the most commonly affected organs [37] exhibiting glycogen deposition, steatosis, fibrosis among other characteristics.…”

Section: Discussionmentioning

confidence: 99%

“…To date, various rat models have been reported for the study of diabetes and its complications [8,15,17,19,20,31]. Similar studies have been also conducted in guinea pigs [3].…”

Section: Discussionmentioning

confidence: 99%

“…Smaller size, ease of handling, omnivorous nature, non-wild tranquil behavior, lower cost, wider availability, easy induction of diabetes, and easier maintenance make rodents a model organism compared to the genetic models with deliberately induced defects in one or more genes [18]. High-fat diets (HFD) are commonly used to develop models for metabolic syndrome and their associated complications [3,19,20]. However, these models require expensive diet and lengthy feeding regimens before any detectable decline of mass of β-cells.…”

Section: Introductionmentioning

confidence: 99%

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High Energy Intake Induced Overexpression of Transcription Factors and Its Regulatory Genes Involved in Acceleration of Hepatic Lipogenesis: A Rat Model for Type 2 Diabetes

et al. 2019

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Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by impaired insulin action and its secretion. The objectives of the present study were to establish an economical and efficient animal model, mimicking pathophysiology of human T2DM to understand probable molecular mechanisms in context with lipid metabolism. In the present study, male Wistar rats were randomly divided into three groups. Animals were fed with high fat diet (HFD) except healthy control (HC) for 12 weeks. After eight weeks, intra peritoneal glucose tolerance test was performed. After confirmation of glucose intolerance, diabetic control (DC) group was injected with streptozotocin (STZ) (35 mg/kg b.w., i.p.). HFD fed rats showed increase (p ≤ 0.001) in glucose tolerance and HOMA-IR as compared to HC. Diabetes rats showed abnormal (p ≤ 0.001) lipid profile as compared to HC. The hepatocyte expression of transcription factors SREBP-1c and NFκβ, and their target genes were found to be upregulated, while PPAR-γ, CPT1A and FABP expressions were downregulated as compared to the HC. A number of animal models have been raised for studying T2DM, but the study has been restricted to only the biochemical level. The model is validated at biochemical, molecular and histopathological levels, which can be used for screening new therapeutics for the effective management of T2DM.

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Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…To date, various rat models have been reported for the study of diabetes and its complications [8,15,17,19,20,31]. Similar studies have been also conducted in guinea pigs [3].…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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High Energy Intake Induced Overexpression of Transcription Factors and Its Regulatory Genes Involved in Acceleration of Hepatic Lipogenesis: A Rat Model for Type 2 Diabetes

et al. 2019

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Amelioration of thyroid dysfunction by magnesium in experimental diabetes may also prevent diabetes-induced renal impairment

Ige

Chidi

Egbeluya

et al. 2019

Heliyon

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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.

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Regional functional and structural abnormalities within the aorta as a potential driver of vascular disease in metabolic syndrome

Ameer

Salman

Alwadi

et al. 2021

Experimental Physiology

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New Findings What is the central question of this study?Is aortic dysfunction, a significant contributor to cardiovascular disease in metabolic syndrome, expressed uniformly across both the thoracic and abdominal aorta? What is the main finding and its importance?Our study shows that, in the setting of metabolic syndrome, functional and structural deficits in the aorta are differentially expressed along its length, with the abdominal portion displaying more extensive vascular abnormalities. It is, therefore, likely that early interventional strategies targeting the abdominal aorta might alleviate cardiovascular pathologies driven by the metabolic syndrome. Abstract The extent of vascular dysfunction associated with metabolic syndrome might vary along the length of the aorta. In this study, we investigated regional functional and structural changes in the thoracic and abdominal aorta of a rat model of metabolic syndrome, namely, high‐fat diet (HFD) streptozotocin‐induced diabetes mellitus (HFD‐D). Four‐week‐old male Wistar albino rats were fed with either HFD or control diet (CD) for 10 weeks. At week 6, 40 mg/kg streptozotocin and its vehicle were injected i.p. into HFD and CD groups, respectively. At the end of the feeding period, rats were euthanised and aortic segments collected for assessment of vascular functional responses and histomorphometry. Tail‐cuff systolic blood pressures (154 ± 6 vs. 110 ± 4 mmHg) and areas under the curve for oral glucose and i.p. insulin tolerance tests were greater in HFD‐D versus CD rats. Abdominal aortic vasoconstriction in response to noradrenaline and KCl was greater in HFD‐D compared with CD rats. Thoracic vasoconstrictor responses to noradrenaline, but not KCl, were greater in the HFD‐D group. Abdominal, but not thoracic, endothelium‐dependent vasorelaxation in response to acetylcholine was blunted in HFD‐D relative to CD rats; however, nitric oxide‐dependent vasorelaxation in HFD‐D rats was impaired in both thoracic and abdominal segments. The abdominal aorta of HFD‐D rats showed deranged interlamellar spacing and increased lipid plaque deposition. In conclusion, vascular dysfunction in metabolic syndrome is expressed differentially along the length of the aorta, with the abdominal aorta exhibiting increased susceptibility to vasoconstrictors and greater deficits in endothelium‐dependent relaxation. These vascular functional abnormalities could potentially underlie the development of hypertensive cardiovascular disease associated with the metabolic syndrome.

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A rat model of diabetic complications induced by high-fat diet and low-dose streptoxotocin injections

Cited by 4 publications

References 9 publications

High Energy Intake Induced Overexpression of Transcription Factors and Its Regulatory Genes Involved in Acceleration of Hepatic Lipogenesis: A Rat Model for Type 2 Diabetes

High Energy Intake Induced Overexpression of Transcription Factors and Its Regulatory Genes Involved in Acceleration of Hepatic Lipogenesis: A Rat Model for Type 2 Diabetes

Amelioration of thyroid dysfunction by magnesium in experimental diabetes may also prevent diabetes-induced renal impairment

Regional functional and structural abnormalities within the aorta as a potential driver of vascular disease in metabolic syndrome

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