Article

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.

Institute of Infection, Immunity and Inflammation and Hotchkiss Brain Institute, Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Calgary, Alta., Canada.
Peptides (Impact Factor: 2.52). 07/2007; 28(6):1185-90. DOI: 10.1016/j.peptides.2007.03.011
Source: PubMed

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.

0 Bookmarks
 · 
66 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: The gastrointestinal (GI) tract is a specialized sensory system that detects and responds to constant changes in nutrient- and bacterial-derived intestinal signals, thus contributing to controls of food intake. Chronic exposure to dietary fat causes morphological, physiological and metabolic changes leading to disruptions in the regulatory feeding pathways promoting more efficient fat absorption and utilization, blunted satiation signals and excess adiposity. Accumulating evidence demonstrates that impaired gastrointestinal signals following long-term high fat consumption are, at least partially, responsible for increased caloric intake. This review focuses on the role of dietary fat in modulating oral and post-oral chemosensory signaling elements responsible for lipid detection and responses, including changes in sensitivity to satiation signals, such as GLP-1, PYY and CCK and their impact on food intake and weight gain. Furthermore, the influence of the gut microbiota on mechanisms controlling energy regulation in the face of excessive fat exposure will be explored. The profound influence of dietary fats on altering complex regulatory feeding pathways can result in dysregulation of body weight and development of obesity, while restoration or manipulation of satiation signaling may prove an effective tool in prevention and treatment of obesity.
    The Journal of nutritional biochemistry 10/2013; 24(10):1663-77. · 4.29 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    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 01/2014; 5:832. · 2.80 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background and Objectives:Gut hormones secreted by enteroendocrine cells (EECs) play a major role in energy regulation. Differentiation of EEC is controlled by the expression of basic helix-loop-helix transcription factors (bHLH). High-fat (HF) feeding alters gut hormone levels, however the impact of HF feeding on bHLH transcription factors on mediating EEC differentiation and subsequent gut hormone secretion and expression is not known.Methods:Outbred Sprague-Dawley rat were maintained on chow or HF-diet for 12 weeks. Gene and protein expression of intestinal bHLH transcription factors, combined with immunofluorescence studies, were analyzed for both groups in the small intestine and colon. Gut permeability, intestinal lipid and carbohydrates transporters as well as circulating levels and intestinal protein expression of gut peptides were determined.Results:We showed that HF feeding resulted in hyperphagia and increased adiposity. HF-fed animals exhibited decreased expression of bHLH transcription factors controlling EECs differentiation (MATH1, NGN3, NEUROD1) and increased expression of bHLH factors modulating enterocyte expression. Furthermore, HF-fed animals had decreased number of total EECs and L-cells. This was accompanied by increased gut permeability and expression of lipid and carbohydrates transporters, and a decrease in circulating and intestinal gut hormone levels.Conclusions:Taken together, our results demonstrate that HF feeding caused decreased secretory lineage (i.e EECs) differentiation through downregulation of bHLH transcription factors resulting in reduced EEC number and gut hormone levels. Thus, impaired EECs differentiation pathways by HF feeding may promote hyperphagia and subsequent obesity.International Journal of Obesity accepted article preview online, 31 January 2014. doi:10.1038/ijo.2014.20.
    International journal of obesity (2005) 01/2014; · 5.22 Impact Factor