Today's and yesterday's of pathophysiology: Biochemistry of metabolic syndrome and animal models

Aydın, Süleyman; Aksoy, Aziz; Kalaycı, Mehmet; Yılmaz, Musa; Kuloğlu, Tuncay; Citil, Cihan; Çatak, Zekiye

doi:10.1016/j.nut.2013.05.013

Cited by 98 publications

(70 citation statements)

References 83 publications

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“…Obesity in many currently used pre-clinical animal models, is mediated by a monogenic disruption in leptin signaling [29–34] or is initiated by high fat feeding (DIO models) [32,35,36]. A monogenic cause for obesity is rare in humans [37].…”

Section: Introductionmentioning

confidence: 99%

Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse

Droz¹,

Sneed²,

Jackson³

et al. 2017

PLoS ONE

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Obesity in many current pre-clinical animal models of obesity and diabetes is mediated by monogenic mutations; these are rarely associated with the development of human obesity. A new mouse model, the FATZO mouse, has been developed to provide polygenic obesity and a metabolic pattern of hyperglycemia and hyperinsulinemia, that support the presence of insulin resistance similar to metabolic disease in patients with insulin resistance/type 2 diabetes. The FATZO mouse resulted from a cross of C57BL/6J and AKR/J mice followed by selective inbreeding for obesity, increased insulin and hyperglycemia. Since many clinical studies have established a close link between higher body weight and the development of type 2 diabetes, we investigated whether time to progression to type 2 diabetes or disease severity in FATZO mice was dependent on weight gain in young animals. Our results indicate that lighter animals developed metabolic disturbances much slower and to a lesser magnitude than their heavier counterparts. Consumption of a diet containing high fat, accelerated weight gain in parallel with disease progression. A naturally occurring and significant variation in the body weight of FATZO offspring enables these mice to be identified as low, mid and high body weight groups at a young age. These weight groups remain into adulthood and correspond to slow, medium and accelerated development of type 2 diabetes. Thus, body weight inclusion criteria can optimize the FATZO model for studies of prevention, stabilization or treatment of type 2 diabetes.

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Section: Introductionmentioning

confidence: 99%

Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse

Droz¹,

Sneed²,

Jackson³

et al. 2017

PLoS ONE

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“…Metabolic syndrome (MS) combines several metabolic alterations including glucose intolerance, insulin resistance, hyperinsulinemia, central adiposity, dyslipidemia, arterial hypertension, atherosclerosis, proinflammatory status, microalbuminuria, and obesity [1]. Its pathogenesis is not clearly understood and very complex.…”

Section: Background and Aimsmentioning

confidence: 99%

Specificity of Metabolic Syndrome Model Reproduction at Pubertal and Adult Male Rats

Bondarenko

Karatzuba

Shayakhmetova

et al. 2015

Romanian Journal of Diabetes Nutrition and Metabolic Diseases

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Background and Aims: Comparative estimation of metabolic syndrome (MS) mediated changes of blood, cardio-vascular system, liver, pancreas and kidneys morphologic structure in adult and pubertal rats. Materials and Methods: Wistar albino male rats of two age categories (young animals of 21 days age (50-70g) and adults (160-180g)) were divided into 4 groups (8 animals in each): 1 -Control 1 (intact young rats); 2 -Control 2 (intact adult rats); 3 -MS3 (young rats with MS) and 4 -MS4 (adult rats with MS

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“…Recently, MetS has been associated with peptide hormones that are synthesized in a multitude of tissues [1]. For instance, it was reported that ghrelin levels fell [2] while leptin levels increased [3], and the synthesis of other adipokine hormones either decreased or increased in MetS [2]. Two new neuropeptide hormones synthesized from preprosalusin, the 28-amino acid Salusin-α (Sal-α) and the 20 amino-acid Salusin-β (Sal-β), were discovered about 10 years ago; they affect the cardiovascular system [4,5].…”

Section: Introductionmentioning

confidence: 99%

“…The functional impairment of the brain, caused by excessive feeding, produces an abnormal physiological and homeostatic response and increases the amount of fatty tissue. Abnormal values resulting from dysfunctions in several organs, including the liver and brain, due to MetS disturb homeostasis [2]. The excess glucose taken up as a result of liver dysfunction is converted to fatty acids and lipids, and this conversion brings about NAFL [2].…”

Section: Introductionmentioning

confidence: 99%

“…Abnormal values resulting from dysfunctions in several organs, including the liver and brain, due to MetS disturb homeostasis [2]. The excess glucose taken up as a result of liver dysfunction is converted to fatty acids and lipids, and this conversion brings about NAFL [2]. Elevated transformation of fatty acids to triglycerides (TG) and very low-density lipoprotein cholesterol (VLDL-C) in the liver causes heart disease and chronic diabetes.…”

Section: Introductionmentioning

confidence: 99%

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Brain, Liver, and Serum Salusin-Alpha and -Beta Alterations in Sprague-Dawley Rats with or Without Metabolic Syndrome

et al. 2014

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BackgroundThis metabolic syndrome (MetS) study was designed to investigate changes in expression of the neuropeptides salusin-α (Sal-α) and salusin-β (Sal-β) in brain and liver tissue in response to obesity and related changes induced by high-fructose diet and explored how these changes were reflected in the circulating levels of Sal-α and Sal-β, as well as revealing how the lipid profile and concentrations of glucose and uric acid were altered.Material/MethodsThe study included 14 Sprague-Dawley rats. The control group was fed ad libitum on standard rat pellets, while the intervention group was given water with 10% fructose in addition to the standard rat pellet for 3 months. Sal-α and Sal-β concentrations in the serum and tissue supernatants were measured by ELISA, and immunohistochemical staining was used to demonstrate expression of the hormones in brain and liver.ResultsSal-α and Sal-β levels in both the serum and the brain and liver tissue supernatants were lower in the MetS group than the control group. Sal-α and Sal-β were shown by immunohistochemistry to be produced in the brain epithelium, the supraoptic nucleus of the hypothalamus, and the liver hepatocytes.ConclusionsThe decrease in Sal-α and Sal-β might be involved in the etiopathology of the metabolic syndrome induced by fructose.

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Today's and yesterday's of pathophysiology: Biochemistry of metabolic syndrome and animal models

Cited by 98 publications

References 83 publications

Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse

Correlation of disease severity with body weight and high fat diet in the FATZO/Pco mouse

Specificity of Metabolic Syndrome Model Reproduction at Pubertal and Adult Male Rats

Brain, Liver, and Serum Salusin-Alpha and -Beta Alterations in Sprague-Dawley Rats with or Without Metabolic Syndrome

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