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Microbiome analyses have shown that genes of the carbohydrate metabolism are overrepresented in the human gut microbiome. Accordingly, gut bacteria contain a wide spectrum of enzymes that enable the breakdown of dietary fibres. The main substrates for the gut bacteria are resistant starches, followed by non-starch polysaccharides such as cellulose, hemicellulose, and pectin. During fermentation, short-chain fatty acids develop, such as acetate, propionate, and butyrate, among others. According to data from epidemiological studies, a diet rich in fibres lowers the risk of bowel cancer. In vitro studies have shown that bacterially produced butyrate may have a role in this, as it inhibits the proliferation of cancer cells and induces cell differentiation. Furthermore, the effects of short-chain fatty acids are associated with the prevention of the metabolic syndrome. Diets rich in fibre correlate with higher concentrations of the appetite-lowering hormone peptide YY (PYY) and GLP-1 (glucagon-like peptide), which has a positive effect on insulin secretion in the pancreatic cells and insulin sensitivity in the target tissues.©Georg Thieme Verlag KG Stuttgart. Source

Schmid H.A.,Novartis | Lambertini C.,Novartis | Van Vugt H.H.,Novartis | Barzaghi-Rinaudo P.,Novartis | And 5 more authors.
Neuroendocrinology | Year: 2012

Background: Activation of somatostatin receptors (sstr1-5) by somatostatin and its analogues exerts an inhibitory effect on hormone secretion and provides the basis for the treatment of a range of endocrine diseases such as acromegaly, Cushing's disease and neuroendocrine tumors (NET). The lack of well-characterized commercially available sstr subtype-specific antibodies prevents routine identification of the sstr expression profile in patients. Methods: We generated and characterized new mouse monoclonal antibodies (mAbs) targeting the five human sstr subtypes using ELISA and immunohistochemistry, and tested their suitability in formalin-fixed and paraffin-embedded (FFPE) human tissues and archival samples of normal pancreatic tissue and NET. Results: All mAbs were highly specific with no cross-reactivity. The sstr1-5 immunoreactivity in gastrointestinal NET (n = 67) was correlated with clinicopathologic data. With the exception of sstr3, NET were highly positive for all receptor subtypes (42, 63, 6, 32 and 65% of tumors were positive for sstr1, sstr2a, sstr3, sstr4 and sstr5, respectively). sstr1, sstr2a and sstr5 were present at the plasma membrane and in the cytoplasm of tumor cells, whereas sstr3 and sstr4 were almost exclusively cytoplasmic. Immunoreactivity of sstr1, sstr2a and sstr4 tended to decrease as tumor aggressiveness increased. sstr5 showed an opposite pattern, with higher staining in well-differentiated carcinomas compared with well-differentiated tumors. sstr5 immunoreactivity was correlated with the presence of metastases and angioinvasion, suggesting a possible association with more aggressive behavior. Conclusion: Determination of the sstr1-5 by immunohistochemistry using subtype-specific mAbs is feasible in FFPE tissue and may provide a tool for routine clinical practice. Copyright © 2011 S. Karger AG, Basel. Source

The biological effect of many polyphenols, such as flavonoids and lignans, is influenced by the way in which they are metabolised in the gut. Compounds that are not resorbed in the small intestine can be metabolised by bacteria in the large intestine. The bacterial transformation of bioactive polyphenols can increase or attenuate their effect. Studies have shown that isoflavonoids and phytolignans develop their full biological activity only once they have been activated by intestinal bacteria. By isolating the gut bacteria involved, researchers have successfully explained the transformation of the lignan secoisolariciresinol diglucoside (SDG) into the notably more bioactive enterolactone. A human study showed that the metabolisation of SDG depends on the individually different composition of the gut microbiota. Gut bacteria therefore influence the bioavailability and chemopreventive effectiveness of polyphenols. © Georg Thieme Verlag KG Stuttgart · New York. Source

Schurmann A.,Deutsches Institute For Ernahrungsforschung
Diabetologie und Stoffwechsel | Year: 2016

Prof. Dr. Annette Schürmann received the Werner-Creutzfeld Award from the German Diabetes Assoziation in May 2016 for her outstanding contributions to improve the knowledge on the pathomechansims of type 2 diabetes. Her research focus is on the genetics and pathpyhsiology of obesity and type 2 diabetes. In this field she participated in the clarification of (1) the genetic contribution on the development of obesity and diabetes, the (2) role of ARF-GTPases on lipid storage and (3) the molecular structure and function of glucose transporters. In this article Dr. Schürmann summarizes the most important findings of her research group. Copyright © 2016, Georg Thieme Verlag KG. All rights reserved. Source

Becker M.,Leibniz Institute for Molecular Pharmacology | Siems W.-E.,Leibniz Institute for Molecular Pharmacology | Kluge R.,Deutsches Institute For Ernahrungsforschung | Gembardt F.,University of Hull | And 5 more authors.
PLoS ONE | Year: 2010

Background: According to the World Health Organization (WHO) there is a pandemic of obesity with approximately 300 million people being obese. Typically, human obesity has a polygenetic causation. Neutral endopeptidase (NEP), also known as neprilysin, is considered to be one of the key enzymes in the metabolism of many active peptide hormones. Methodology/Principal Findings: An incidental observation in NEP-deficient mice was a late-onset excessive gain in body weight exclusively from a ubiquitous accumulation of fat tissue. In accord with polygenetic human obesity, mice were characterized by deregulation of lipid metabolism, higher blood glucose levels, with impaired glucose tolerance. The key role of NEP in determining body mass was confirmed by the use of the NEP inhibitor candoxatril in wild-type mice that increased body weight due to increased food intake. This is a peripheral and not a central NEP action on the switch for appetite control, since candoxatril cannot cross the blood-brain barrier. Furthermore, we demonstrated that inhibition of NEP in mice with cachexia delayed rapid body weight loss. Thus, lack in NEP activity, genetically or pharmacologically, leads to a gain in body fat. Conclusions/Significance: In the present study, we have identified NEP to be a crucial player in the development of obesity. NEP-deficient mice start to become obese under a normocaloric diet in an age of 6-7 months and thus are an ideal model for the typical human late-onset obesity. Therefore, the described obesity model is an ideal tool for research on development, molecular mechanisms, diagnosis, and therapy of the pandemic obesity. © 2010 Becker et al. Source

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