Hyperinsulinemia and Sympathoadrenal System Activity in the Rat<sup>a</sup>

Květňanský, Richard; Rusnak, Milan; Gašperíková, Daniela; Jeloková, Jana; Zórad, Štefan; Vietor, Ilja; Pacák, Karel; Seböková, E; Macho, L; Sabban, Esther L.; Klimeš, I

doi:10.1111/j.1749-6632.1997.tb51827.x

Cited by 11 publications

(4 citation statements)

References 60 publications

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“…This model of essential hypertension was derived from selectively bred Wistar Kyoto rats with high blood pressure (Okamoto and Aoki, 1963) and has been considered to be a model for abdominal obesity and metabolic syndrome (Kvetnansky et al, 1997; Reaven et al, 1989). These rats have insulin resistance, hypertriacylglycerolaemia and hypertension like most obese humans.…”

Section: Rodent Models Of Obesity and Obesity Resistance: Sleep/wamentioning

confidence: 99%

Sleep and obesity: A focus on animal models

Mavanji

Billington

Kotz

et al. 2012

Neuroscience & Biobehavioral Reviews

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The rapid rise in obesity prevalence in the modern world parallels a significant reduction in restorative sleep (Agras et al., 2004; Dixon et al., 2007; Dixon et al., 2001; Gangwisch and Heymsfield, 2004; Gupta et al., 2002; Sekine et al., 2002; Vioque et al., 2000; Wolk et al., 2003). Reduced sleep time and quality increases the risk for obesity, but the underlying mechanisms remain unclear (Gangwisch et al., 2005; Hicks et al., 1986; Imaki et al., 2002; Jennings et al., 2007; Moreno et al., 2006). A majority of the theories linking human sleep disturbances and obesity rely on self-reported sleep. However, studies with objective measurements of sleep/wake parameters suggest a U-shaped relationship between sleep and obesity. Studies in animal models are needed to improve our understanding of the association between sleep disturbances and obesity. Genetic and experimenter-induced models mimicking characteristics of human obesity are now available and these animal models will be useful in understanding whether sleep disturbances determine propensity for obesity, or result from obesity. These models exhibit weight gain profiles consistently different from control animals. Thus a careful evaluation of animal models will provide insight into the relationship between sleep disturbances and obesity in humans. In this review we first briefly consider the fundamentals of sleep and key sleep disturbances, such as sleep fragmentation and excessive daytime sleepiness (EDS), observed in obese individuals. Then we consider sleep deprivation studies and the role of circadian alterations in obesity. We describe sleep/wake changes in various rodent models of obesity and obesity resistance. Finally, we discuss possible mechanisms linking sleep disturbances with obesity.

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Section: Rodent Models Of Obesity and Obesity Resistance: Sleep/wamentioning

confidence: 99%

Sleep and obesity: A focus on animal models

Mavanji

Billington

Kotz

et al. 2012

Neuroscience & Biobehavioral Reviews

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“…The SHR, a well-known experimental model to study hypertension, have been also proposed as a model of insulin resistance. These rats show hypertriacylglycerolaemia, abdominal obesity and hypertension ( 79 , 83 ) . In the background of SHR, different strains of corpulent SHR, such as obese SHR named, Koletsky rats, SHR/N-corpulent rats and SHR/NDmc-corpulent rats, seem to be even more adequate to study the metabolic syndrome than the SHR.…”

Section: Obese Spontaneously Hypertensive Ratsmentioning

confidence: 99%

Experimental rat models to study the metabolic syndrome

2009

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Being the metabolic syndrome a multifactorial condition, it is difficult to find adequate experimental models to study this pathology. The obese Zucker rats, which are homozygous for the fa allele, present abnormalities similar to those seen in human metabolic syndrome and are a widely extended model of insulin resistance. The usefulness of these rats as a model of non-insulin-dependent diabetes mellitus is nevertheless questionable, and they neither can be considered a clear experimental model of hypertension. Some experimental models different from the obese Zucker rats have also been used to study the metabolic syndrome. Some derive from the spontaneously hypertensive rats (SHR). In this context, the most important are the obese SHR, usually named Koletsky rats. Hyperinsulinism, associated with either normal or slightly elevated levels of blood glucose, is present in these animals, but SHR/N-corpulent rats are a more appropriated model of non-insulin-dependent diabetes mellitus. The SHR/NDmc corpulent rats, a subline of SHR/N-corpulent rats, also exhibit metabolic and histopathologic characteristics associated with human metabolic disorders. A new animal model of the metabolic syndrome, stroke-prone -SHR (SHRSP) fatty rats, was obtained by introducing a segment of the mutant leptin receptor gene from the Zucker line heterozygous for the fa gene mutation into the genetic background of the SHRSP. Very recently, it has been developed as a non-obese rat model with hypertension, fatty liver and characteristics of the metabolic syndrome by transgenic overexpression of a sterol-regulatory element-binding protein in the SHR rats. The Wistar Ottawa Karlsburg W rats are also a new strain that develops a nearly complete metabolic syndrome. Moreover, a new experimental model of low-capacity runner rats has also been developed with elevated blood pressure levels together with the other hallmarks of the metabolic syndrome.Zucker rats: Obesity: Metabolic syndrome: Insulin resistanceThe metabolic syndrome has been recognised in the medical literature for more than 80 years. The syndrome does not constitute one single illness. Instead, it can be defined as a group of health problems, caused by genetic and environmental factors, whose common fundamental pathogenic component is resistance to insulin. These problems may occur in one individual simultaneously or one by one, but their appearance together in one person is significant as these patients are more prone to CVD in general and to coronary disease in particular.In its Third Panel of Adult Treatment, part of the National Program for Cholesterol Education, the U.S. National Health Institute gave a definition of the metabolic syndrome based on risk factors, which is straightforward to apply in epidemiological studies and daily clinical practice (1) . This definition does not require direct demonstration of resistance to insulin, which in clinical practice may be difficult to establish. The metabolic syndrome is assumed to exist when three or more of the following risk factor...

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“…In addition, these animals have been shown to have other components of MetS, such as insulin resistance, hyper-triacylglycerolaemia and abdominal obesity. 19 The administration of MSG, a neuroexcitatory amino acid during the neonatal period of SHR, can injure the central nervous system which results in acute degeneration of the arcuate nucleus of the hypothalamus. As a consequence, these animals develop or have an increased insulin resistance, progressively increased central body adiposity, triglyceride levels and inflammatory state.…”

Section: Introductionmentioning

confidence: 99%

Kefir reduces insulin resistance and inflammatory cytokine expression in an animal model of metabolic syndrome

et al. 2016

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There is growing evidence that kefir can be a promising tool in decreasing the risk of many diseases, including metabolic syndrome (MetS). The aim of the present study was to evaluate the effect of kefir supplementation in the diet of Spontaneously Hypertensive Rats (SHR) in which MetS was induced with monosodium glutamate (MSG), and to determine its effect on metabolic parameters, inflammatory and oxidation marker expression and glycemic index control. Thirty animals were used in this experiment. For the induction of MetS, twenty two-day-old male SHR received five consecutive intradermal injections of MSG. For the Negative Control, ten newborn male SHR received intradermal injections of saline solution (0.9% saline solution). After weaning, animals received standard diet and water ad libitum until reaching 3 months old, for the development of MetS. They were then divided into three groups (n = 10): negative control (NC, 1 mL saline solution per day), positive control (PC, 1 mL saline solution per day) and the Kefir group (1 mL kefir per day). Feeding was carried out by gavage for 10 weeks and the animals received standard food and water ad libitum. Obesity, insulin resistance, pro- and anti-inflammatory markers, and the histology of pancreatic and adipose tissues were among the main variables evaluated. Compared to the PC group, kefir supplementation reduced plasma triglycerides, liver lipids, liver triglycerides, insulin resistance, fasting glucose, fasting insulin, thoracic circumference, abdominal circumference, products of lipid oxidation, pro-inflammatory cytokine expression (IL-1β) and increased anti-inflammatory cytokine expression (IL-10). The present findings indicate that kefir has the potential to benefit the management of MetS.

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Hyperinsulinemia and Sympathoadrenal System Activity in the Rat^a

Cited by 11 publications

References 60 publications

Sleep and obesity: A focus on animal models

Sleep and obesity: A focus on animal models

Experimental rat models to study the metabolic syndrome

Kefir reduces insulin resistance and inflammatory cytokine expression in an animal model of metabolic syndrome

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Hyperinsulinemia and Sympathoadrenal System Activity in the Rata

Cited by 11 publications

References 60 publications

Sleep and obesity: A focus on animal models

Sleep and obesity: A focus on animal models

Experimental rat models to study the metabolic syndrome

Kefir reduces insulin resistance and inflammatory cytokine expression in an animal model of metabolic syndrome

Contact Info

Product

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Hyperinsulinemia and Sympathoadrenal System Activity in the Rat^a