Peptide YY containing enteroendocrine cells and peripheral tissue sensitivity to PYY and PYY(3-36) are maintained in diet-induced obese and diet-resistant rats
ABSTRACT Peptide YY (PYY) is a gastrointestinal hormone, localized in enteroendocrine L-cells. Its hydrolyzed form PYY(3-36) is a satiety factor. The aim of this study was to identify if intestinal PYY enteroendocrine cells or content correlate with the diet-induced obese (DIO) or diet-resistant (DR) phenotypes. We also examined intestinal sensitivity to PYY and PYY(3-36) in DIO and DR rats. Animals were maintained on a medium-high fat diet and split into DIO and DR groups based on weight gain. PYY immunoreactive cells were unaltered in DIO intestine and stomach compared to DR rats. PYY content and circulating levels were also unchanged in DIO rats. Intestinal PYY and PYY(3-36) responses were enhanced in fasted rats, and equipotent in both DIO and DR jejunum. We conclude that PYY cell number, tissue content and peripheral sensitivity are maintained in DIO rats. Our data suggests that neither PYY nor PYY(3-36) contribute to the maintenance of either the DIO or DR phenotype, and that peripheral resistance to PYY and PYY(3-36) does not accompany DIO.
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- "Animals that were of intermediate weights (600–700 g) were eliminated from this study as they could not be reliably classified as DR or DIO rats. The DIO and DR phenotypes were validated in accordance with the DIO model of others (Levin and Dunn-Meynell, 2002; Hyland et al., 2007; Li et al., 2011) and in our own colony (Smith and Ferguson, 2012). "
ABSTRACT: Obesity is a chronic metabolic condition with important public health implications associated with numerous co-morbidities including cardiovascular disease, insulin resistance, and hypertension. The renin angiotensin system (RAS), best known for its involvement in cardiovascular control and body fluid homeostasis has, more recently, been implicated in regulation of energy balance. Interference with the RAS (genetically or pharmacologically) has been shown to influence body weight gain. In this study we investigated the effects of systemic AT1 receptor blockade using losartan on ingestive behaviors and weight gain in diet induced obese (DIO) rats. Prior to losartan administration (30 mg/kg/day) body weight gain remained constant within the DIO animals (3.6 ± 0.3 g/day, n = 8), diet resistant (DR) animals (2.1 ± 0.6 g/day, n = 8) and in the age-matched chow fed control (CHOW) animals (2.8 ± 0.3 g/day, n = 8), Losartan administration abolished body weight gain in animals fed a high fat diet (DIO: -0.4 ± 0.7 g/day, n = 8; and DR: -0.8 ± 0.3 g/day, n = 8) while chow fed animals continued to gain weight (2.2 ± 0.3 g/day, n = 8) as they had previously to oral administration of losartan. This decrease in daily body weight gain was accompanied by a decrease in food intake in the HFD fed animals. Following the removal of losartan, both the DIO and DR animals again showed daily increases in body weight gain and food intake which were similar to control values. Our data demonstrate that oral losartan administration attenuates body weight gain in animals fed a HFD whether the animal is obese (DIO) or not DR while having no effect on body weight gain in age-matched chow fed animals suggesting a protective effect of losartan against body weight gain while on a HFD.Frontiers in Psychology 07/2014; 5:832. DOI:10.3389/fpsyg.2014.00832 · 2.80 Impact Factor
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ABSTRACT: The global population is getting obese. From developed to developing countries the pandemic is now irrefutable. Research focusing on obesity has increased exponentially over the past few decades but yet no solution has been found. Dietary fat has been blamed for this epidemic because people adapted to a high-fat diet develop hyperphagic behavior and therefore become obese. The aim of this work was to understand the mechanisms by which a high-fat diet can induce hyperphagia starting from behavorial studies to the molecular biology behind it. These studies have been conducted in two animal models: Rattus norvegicus and Mus musculus. The results of these studies have shown that rats subjected to a chronic high-fat diet become hyperphagic upon vagal insensitivity to dietary fat compared to rats fed a low-fat diet. Also, we demonstrated that the cholecystokinin receptor 1 plays an important role in the detection of dietary fat. Finally, we proposed a molecular model of the adaptation of the nodose ganglia by which a decreased expression of the leptin receptor (anorexigenic) was associated with an increased expression of the cannabinoid receptor (orexigenic). This suggests one of the many mechanisms underlying hyperphagic behavior in rats fed a chronic high-fat diet. In conclusion, we have shown that diet is able to interact with genes involved in short-term regulation of food intake. These findings are critical in understanding the potential causes of obesity. The human genome has evolved from the direct interaction between environment and diet; it is not counterintuitive to think that diet can influence gene expression. Why does a high-fat diet induce a hyperphagic response in the organism? Can we find answers by looking back in time and observe how people, diet and environment evolved together? Does the thrifty gene theory make sense in this context? These are questions that need to be answered in order to find a solution to obesity.
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ABSTRACT: Laparoscopic sleeve gastrectomy is known to be a safe and effective procedure for treating morbid obesity and is performed with increasing frequency both in Europe and the USA. Despite its broad use, many questions about the remaining gastric tube diameter, its long-term efficacy, its effects on gastric emptying, and the hormones involved still remain to be answered. In order to use such a relatively new surgical procedure wisely, it is essential for every surgeon and physician to understand how sleeve gastrectomy acts in obesity and what its potential benefits on the patients' metabolism are. This review focuses on the most important pathophysiologic questions referred to sleeve gastrectomy on the literature so far, in an attempt to evaluate the different issues still pending on the subject.Obesity Surgery 04/2010; 20(10):1448-55. DOI:10.1007/s11695-010-0148-5 · 3.74 Impact Factor