BACKGROUND/AIMS: The metabolic syndrome (MS) has become an epidemiological problem in Western countries. We developed a diet-induced obese rat model that mimics all the symptoms of MS in humans, but whose insulin resistance, hyperphagia and hyperleptinemia are caused by nutrition rather than genetic modifications. METHODS: Spontaneously hypertensive rats (SHR) were allowed for 12 weeks to choose between a cafeteria diet (CD, 20.3 kJ/g) and standard rat chow (11.7 kJ/g). Controls received rat chow. RESULTS: Body weight (BW) exceeded control levels when SHR were fed with CD. The increase in BW was attributed to enhanced energy intake. The abundance of abdominal fat as well as the plasma levels of leptin and triglycerides increased concomitant with glucose, insulin and C-peptide. This prediabetic condition was further confirmed by a markedly increased insulin response following glucose challenge and by impaired glucose utilization after insulin tolerance tests. CONCLUSION: Increases in food intake and BW despite hyperleptinemia indicate leptin resistance following CD feeding. CD-fed SHR feature leptin and insulin resistance, hypertension and obesity, thus mimicking the situation of MS patients. As such, our model is more suitable than the genetically modified rat models used to study human MS. Copyright 2010 S. Karger AG, Basel.
BACKGROUND/AIMS: The metabolic syndrome (MS) has become an epidemiological problem in Western countries. We developed a diet-induced obeserat model that mimics all the symptoms of MS in humans, but whose insulin resistance, hyperphagia and hyperleptinemia are caused by nutrition rather than genetic modifications. METHODS: Spontaneously hypertensiverats (SHR) were allowed for 12 weeks to choose between a cafeteria diet (CD, 20.3 kJ/g) and standard rat chow (11.7 kJ/g). Controls received rat chow. RESULTS: Body weight (BW) exceeded control levels when SHR were fed with CD. The increase in BW was attributed to enhanced energy intake. The abundance of abdominal fat as well as the plasma levels of leptin and triglycerides increased concomitant with glucose, insulin and C-peptide. This prediabetic condition was further confirmed by a markedly increased insulin response following glucose challenge and by impaired glucose utilization after insulin tolerance tests. CONCLUSION: Increases in food intake and BW despite hyperleptinemia indicate leptin resistance following CD feeding. CD-fed SHR feature leptin and insulin resistance, hypertension and obesity, thus mimicking the situation of MSpatients. As such, our model is more suitable than the genetically modified rat models used to study humanMS. Copyright 2010 S. Karger AG, Basel.
Authors: Johanna Schuchard; Martina Winkler; Ines Stölting; Franziska Schuster; Florian M Vogt; Jörg Barkhausen; Christoph Thorns; Robson A Santos; Michael Bader; Walter Raasch Journal: Br J Pharmacol Date: 2015-06-12 Impact factor: 8.739
Authors: Martina Winkler; Johanna Schuchard; Ines Stölting; Florian M Vogt; Jörg Barkhausen; Christoph Thorns; Michael Bader; Walter Raasch Journal: Br J Pharmacol Date: 2016-03-27 Impact factor: 8.739