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Article ; Online: Nutrition and L and K-enteroendocrine cells.

Gutierrez-Aguilar, Ruth / Woods, Stephen C

Current opinion in endocrinology, diabetes, and obesity

2011 Volume 18, Issue 1, Page(s) 35–41

Abstract: ... of several hormones produced by enteroendocrine cells in the gastrointestinal tract that secrete incretin hormones ... by new techniques that allow investigation of individual enteroendocrine cells.: Summary: The better ... These hormones influence glucose homeostasis; food intake; gastric, pancreatic and hepatic secretions; and ...

Abstract	Purpose of review: The review highlights the influence of nutrients over the secretion of several hormones produced by enteroendocrine cells in the gastrointestinal tract that secrete incretin hormones. These hormones influence glucose homeostasis; food intake; gastric, pancreatic and hepatic secretions; and gastric and intestinal motility, and these aspects are summarized in this review. Recent findings: This study provides an overview of recent advances in our understanding of the physiology of the incretins, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), as well as of oxyntomodulin. A better understanding of the secretion and action of these hormones at their receptors was made possible by new techniques that allow investigation of individual enteroendocrine cells. Summary: The better understanding of the function of the gastrointestinal incretin hormones and their implications for improving glucose homeostasis and perhaps influencing food intake and appetite as well, new research in this area will help combat metabolic diseases such as type 2 diabetes and obesity.
MeSH term(s)	Animals ; Drug Design ; Enteroendocrine Cells/classification ; Enteroendocrine Cells/cytology ; Enteroendocrine Cells/metabolism ; Enteroendocrine Cells/physiology ; Gastric Inhibitory Polypeptide/genetics ; Gastric Inhibitory Polypeptide/metabolism ; Gastric Inhibitory Polypeptide/physiology ; Glucagon-Like Peptide 1/genetics ; Glucagon-Like Peptide 1/metabolism ; Glucagon-Like Peptide 1/physiology ; Humans ; Incretins/genetics ; Incretins/metabolism ; Incretins/physiology ; Models, Biological ; Nutritional Physiological Phenomena/genetics
Chemical Substances	Incretins ; Gastric Inhibitory Polypeptide (59392-49-3) ; Glucagon-Like Peptide 1 (89750-14-1)
Language	English
Publishing date	2011-02-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2272017-0
ISSN	1752-2978 ; 1752-296X
ISSN (online)	1752-2978
ISSN	1752-296X
DOI	10.1097/MED.0b013e32834190b5
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Article ; Online: The gastrin-releasing peptide analog bombesin preserves exocrine and endocrine pancreas morphology and function during parenteral nutrition.

Pierre, Joseph F / Neuman, Joshua C / Brill, Allison L / Brar, Harpreet K / Thompson, Mary F / Cadena, Mark T / Connors, Kelsey M / Busch, Rebecca A / Heneghan, Aaron F / Cham, Candace M / Jones, Elaina K / Kibbe, Carly R / Davis, Dawn B / Groblewski, Guy E / Kudsk, Kenneth A / Kimple, Michelle E

American journal of physiology. Gastrointestinal and liver physiology

2015 Volume 309, Issue 6, Page(s) G431–42

Abstract: ... through the enteroendocrine cell-pancreas axis. We confirmed the ability of BBS to directly stimulate intestinal enteroid cells ... through the enteroendocrine cell-pancreas axis. ... Here we examine the role of the enteric peptide bombesin (BBS) in stimulation of the exocrine and ...

Abstract	Stimulation of digestive organs by enteric peptides is lost during total parental nutrition (PN). Here we examine the role of the enteric peptide bombesin (BBS) in stimulation of the exocrine and endocrine pancreas during PN. BBS protects against exocrine pancreas atrophy and dysfunction caused by PN. BBS also augments circulating insulin levels, suggesting an endocrine pancreas phenotype. While no significant changes in gross endocrine pancreas morphology were observed, pancreatic islets isolated from BBS-treated PN mice showed a significantly enhanced insulin secretion response to the glucagon-like peptide-1 (GLP-1) agonist exendin-4, correlating with enhanced GLP-1 receptor expression. BBS itself had no effect on islet function, as reflected in low expression of BBS receptors in islet samples. Intestinal BBS receptor expression was enhanced in PN with BBS, and circulating active GLP-1 levels were significantly enhanced in BBS-treated PN mice. We hypothesized that BBS preserved islet function indirectly, through the enteroendocrine cell-pancreas axis. We confirmed the ability of BBS to directly stimulate intestinal enteroid cells to express the GLP-1 precursor preproglucagon. In conclusion, BBS preserves the exocrine and endocrine pancreas functions during PN; however, the endocrine stimulation is likely indirect, through the enteroendocrine cell-pancreas axis.
MeSH term(s)	Amylases/metabolism ; Animals ; Bombesin/pharmacology ; DNA/metabolism ; Food, Formulated ; Gastrin-Releasing Peptide/analogs & derivatives ; Gene Expression Regulation ; Hyperglycemia/blood ; Islets of Langerhans/anatomy & histology ; Islets of Langerhans/drug effects ; Lipase/metabolism ; Male ; Mice ; Mice, Inbred ICR ; Pancreas, Exocrine/anatomy & histology ; Pancreas, Exocrine/drug effects ; Pancreatic Hormones/metabolism ; Parenteral Nutrition/adverse effects
Chemical Substances	Pancreatic Hormones ; Gastrin-Releasing Peptide (80043-53-4) ; DNA (9007-49-2) ; Lipase (EC 3.1.1.3) ; Amylases (EC 3.2.1.-) ; Bombesin (PX9AZU7QPK)
Language	English
Publishing date	2015-07-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00072.2015
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Article ; Online: Nutrient sensing of gut luminal environment.

Moran, A W / Daly, K / Al-Rammahi, M A / Shirazi-Beechey, S P

The Proceedings of the Nutrition Society

2020 Volume 80, Issue 1, Page(s) 29–36

Abstract: ... those expressed in L-cells, are currently being assessed as potential new pathways for treating diabetes and ... enteroendocrine cells and responsive to dietary sweetener additives, has already been successfully explored and utilised ... of nutrients have been identified. Many are localised to intestinal enteroendocrine (chemosensory) cells ...

Abstract	Sensing of nutrients by chemosensory cells in the gastrointestinal tract plays a key role in transmitting food-related signals, linking information about the composition of ingested foods to digestive processes. In recent years, a number of G protein-coupled receptors (GPCR) responsive to a range of nutrients have been identified. Many are localised to intestinal enteroendocrine (chemosensory) cells, promoting hormonal and neuronal signalling locally, centrally and to the periphery. The field of gut sensory systems is relatively new and still evolving. Despite huge interest in these nutrient-sensing GPCR, both as sensors for nutritional status and targets for preventing the development of metabolic diseases, major challenges remain to be resolved. However, the gut expressed sweet taste receptor, resident in L-enteroendocrine cells and responsive to dietary sweetener additives, has already been successfully explored and utilised as a therapeutic target, treating weaning-related disorders in young animals. In addition to sensing nutrients, many GPCR are targets for drugs used in clinical practice. As such these receptors, in particular those expressed in L-cells, are currently being assessed as potential new pathways for treating diabetes and obesity. Furthermore, growing recognition of gut chemosensing of microbial-produced SCFA acids has led further attention to the association between nutrition and development of chronic disorders focusing on the relationship between nutrients, gut microbiota and health. The central importance of gut nutrient sensing in the control of gastrointestinal physiology, health promotion and gut-brain communication offers promise that further therapeutic successes and nutritional recommendations will arise from research in this area.
MeSH term(s)	Enteroendocrine Cells/metabolism ; Gastrointestinal Hormones/metabolism ; Gastrointestinal Tract/metabolism ; Humans ; Intestinal Mucosa/metabolism ; Nutrients/metabolism ; Nutritional Physiological Phenomena/physiology ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction/physiology
Chemical Substances	Gastrointestinal Hormones ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2020-08-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391142-1
ISSN	1475-2719 ; 0029-6651
ISSN (online)	1475-2719
ISSN	0029-6651
DOI	10.1017/S0029665120007120
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Article ; Online: Development of innovative tools for investigation of nutrient-gut interaction.

Huang, Wei-Kun / Xie, Cong / Young, Richard L / Zhao, Jiang-Bo / Ebendorff-Heidepriem, Heike / Jones, Karen L / Rayner, Christopher K / Wu, Tong-Zhi

World journal of gastroenterology

2020 Volume 26, Issue 25, Page(s) 3562–3576

Abstract: ... of gut hormone secretion from enteroendocrine cells. This review discusses the evolution of ... The gastrointestinal tract is the key interface between the ingesta and the human body. There is ... the secretion of numerous hormones, is critical to the regulation of appetite, body weight and blood glucose ...

Abstract	The gastrointestinal tract is the key interface between the ingesta and the human body. There is wide recognition that the gastrointestinal response to nutrients or bioactive compounds, particularly the secretion of numerous hormones, is critical to the regulation of appetite, body weight and blood glucose. This concept has led to an increasing focus on "gut-based" strategies for the management of metabolic disorders, including type 2 diabetes and obesity. Understanding the underlying mechanisms and downstream effects of nutrient-gut interactions is fundamental to effective translation of this knowledge to clinical practice. To this end, an array of research tools and platforms have been developed to better understand the mechanisms of gut hormone secretion from enteroendocrine cells. This review discusses the evolution of
MeSH term(s)	Diabetes Mellitus, Type 2 ; Enteroendocrine Cells ; Gastrointestinal Hormones ; Gastrointestinal Microbiome ; Gastrointestinal Tract ; Humans ; Nutrients
Chemical Substances	Gastrointestinal Hormones
Language	English
Publishing date	2020-08-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2185929-2
ISSN	2219-2840 ; 1007-9327
ISSN (online)	2219-2840
ISSN	1007-9327
DOI	10.3748/wjg.v26.i25.3562
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Article ; Online: Molecular mechanisms underlying nutrient-stimulated incretin secretion.

Parker, Helen E / Reimann, Frank / Gribble, Fiona M

Expert reviews in molecular medicine

2010 Volume 12, Page(s) e1

Abstract: ... of organ and whole-animal perfusion techniques, cell line models and primary L- and K-cells has led ... responsiveness of L- and K-cells. ... polypeptide (GIP) are released from enteroendocrine cells in the intestinal epithelium in response to nutrient ...

Abstract	The incretin hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are released from enteroendocrine cells in the intestinal epithelium in response to nutrient ingestion. The actions of GLP-1 and GIP - not only on local gut physiology but also on glucose homeostasis, appetite control and fat metabolism - have made these hormones an attractive area for drug discovery programmes. The potential range of strategies to target the secretion of these hormones therapeutically has been limited by an incomplete understanding of the mechanisms underlying their release. The use of organ and whole-animal perfusion techniques, cell line models and primary L- and K-cells has led to the identification of a variety of pathways involved in the sensing of carbohydrate, fat and protein in the gut lumen. This review focuses on our current understanding of these signalling mechanisms that might underlie nutrient responsiveness of L- and K-cells.
MeSH term(s)	Animals ; Enteroendocrine Cells/cytology ; Enteroendocrine Cells/metabolism ; Food ; Humans ; Incretins/metabolism ; Protein Processing, Post-Translational ; Receptors, G-Protein-Coupled
Chemical Substances	Incretins ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2010-01-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1462-3994
ISSN (online)	1462-3994
DOI	10.1017/S146239940900132X
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Article ; Online: Nutrient-mediated modulation of incretin gene expression: a systematic review.

Martínez-Rodríguez, R / Gil, A

Nutricion hospitalaria

2012 Volume 27, Issue 1, Page(s) 46–53

Abstract: ... gene expression in L and K enteroendocrine cells. On the other hand, it has been shown that the hexosamine ... and released by ileum and colon L cells, in contrast to GIP which does it by K cells in duodenum and ... food intake by gut enteroendocrine cells, reaching to pancreas where produce a potentiating effect on insulin ...

Abstract	Incretins are a cluster of hormones which are secreted and released into the bloodstream after food intake by gut enteroendocrine cells, reaching to pancreas where produce a potentiating effect on insulin release. The aim of this study was to perform a systematic review of incretins gene expression mediated by nutrients using specific search equations in the PubMed database. The two most relevant incretins are GLP-1 and GIP, which come from proglucagon and proGIP precursor respectively. GLP-1 is mainly synthesized and released by ileum and colon L cells, in contrast to GIP which does it by K cells in duodenum and proximal jejunum. It has been shown that canonical Wnt signalling pathway is closely related to the production of these hormones, since transcription factor TCF7L2 affects proglucagon and proGIP gene expression in L and K enteroendocrine cells. On the other hand, it has been shown that the hexosamine biosynthetic pathway can produce N-linked glycosylation of -catenin, an essential component of canonical Wnt signalling. This process hinders β-catenin phosphorylation and, thereby prevents proteasome degradation. Increasing glucose concentration enhances the hexosamine pathway and thus β-catenin glycosylation. This causes a β-catenin cytoplasmic accumulation allowing entry into nucleus, where it exerts its action by binding to a clump of molecules and transcription factors, allowing to express the target genes, including the incretin hormones. There is also evidence that glucose, through the hexosamine pathway, can induces autocrine activation of Wnt signalling pathway by stimulating secretion of Wnt proteins.
MeSH term(s)	Animals ; Gene Expression/physiology ; Gene Expression Regulation/physiology ; Hexosamines/metabolism ; Humans ; Incretins/biosynthesis ; Incretins/genetics ; Nutritional Physiological Phenomena ; Wnt Proteins/genetics ; Wnt Proteins/metabolism
Chemical Substances	Hexosamines ; Incretins ; Wnt Proteins
Language	Spanish
Publishing date	2012-01
Publishing country	Spain
Document type	Journal Article ; Meta-Analysis ; Review
ZDB-ID	1481223-x
ISSN	1699-5198 ; 0212-1611
ISSN (online)	1699-5198
ISSN	0212-1611
DOI	10.1590/S0212-16112012000100006
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Article ; Online: Role of nutrient-sensing taste 1 receptor (T1R) family members in gastrointestinal chemosensing.

Shirazi-Beechey, Soraya P / Daly, Kristian / Al-Rammahi, Miran / Moran, Andrew W / Bravo, David

The British journal of nutrition

2014 Volume 111 Suppl 1, Page(s) S8–15

Abstract: ... that T1R2-T1R3, in association with G-protein gustducin, is expressed in intestinal K and L endocrine cells ... on the apical domain of cholecystokinin (CCK) expressing cells is a luminal sensor for a number of L-amino acids ... T1R1, T1R2 and T1R3 in intestinal sweet and L-amino acid sensing. The impact of exploiting T1R2-T1R3 ...

Abstract	Luminal nutrient sensing by G-protein-coupled receptors (GPCR) expressed on the apical domain of enteroendocrine cells activates intracellular pathways leading to secretion of gut hormones that control vital physiological processes such as digestion, absorption, food intake and glucose homeostasis. The taste 1 receptor (T1R) family of GPCR consists of three members: T1R1; T1R2; T1R3. Expression of T1R1, T1R2 and T1R3 at mRNA and protein levels has been demonstrated in the intestinal tissue of various species. It has been shown that T1R2-T1R3, in association with G-protein gustducin, is expressed in intestinal K and L endocrine cells, where it acts as the intestinal glucose (sweet) sensor. A number of studies have demonstrated that activation of T1R2-T1R3 by natural sugars and artificial sweeteners leads to secretion of glucagon-like peptides 1&2 (GLP-1 and GLP-2) and glucose dependent insulinotropic peptide (GIP). GLP-1 and GIP enhance insulin secretion; GLP-2 increases intestinal growth and glucose absorption. T1R1-T1R3 combination co-expressed on the apical domain of cholecystokinin (CCK) expressing cells is a luminal sensor for a number of L-amino acids; with amino acid-activation of the receptor eliciting CCK secretion. This article focuses on the role of the gut-expressed T1R1, T1R2 and T1R3 in intestinal sweet and L-amino acid sensing. The impact of exploiting T1R2-T1R3 as a nutritional target for enhancing intestinal glucose absorption and gut structural maturity in young animals is also highlighted.
MeSH term(s)	Amino Acids/metabolism ; Animals ; Chemoreceptor Cells/metabolism ; Enteroendocrine Cells/metabolism ; Gastrointestinal Hormones/metabolism ; Glucose/metabolism ; Humans ; Intestines/cytology ; Intestines/growth & development ; Intestines/metabolism ; Nutritional Status ; Receptors, G-Protein-Coupled/metabolism ; Sensation ; Signal Transduction ; Sweetening Agents/metabolism ; Taste ; Transducin/metabolism
Chemical Substances	Amino Acids ; Gastrointestinal Hormones ; Receptors, G-Protein-Coupled ; Sweetening Agents ; taste receptors, type 1 ; gustducin (147979-21-3) ; Transducin (EC 3.6.5.1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2014-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	280396-3
ISSN	1475-2662 ; 0007-1145
ISSN (online)	1475-2662
ISSN	0007-1145
DOI	10.1017/S0007114513002286
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Article: Nutrient regulation of enteroendocrine cellular activity linked to cholecystokinin gene expression and secretion.

Nilaweera, K N / Giblin, L / Ross, R P

Journal of physiology and biochemistry

2010 Volume 66, Issue 1, Page(s) 85–92

Abstract: The hormone cholecystokinin is produced by the enteroendocrine I cells in the intestine, and ... it plays an important role in a number of physiological processes including digestion and food intake ... Recent data suggest that cholecystokinin gene expression and protein secretion are regulated ...

Abstract	The hormone cholecystokinin is produced by the enteroendocrine I cells in the intestine, and it plays an important role in a number of physiological processes including digestion and food intake. Recent data suggest that cholecystokinin gene expression and protein secretion are regulated by macronutrients. The mechanism involves a change in intracellular levels of cAMP and Ca(+2), brought about by the activity of a number of nutrient-responsive G protein-coupled receptors, nutrient transporters, ion channels and intracellular enzymes. How these intracellular responses could lead to gene expression and protein secretion are discussed along with new directions for future investigation.
MeSH term(s)	Animals ; Calcium/metabolism ; Cholecystokinin/genetics ; Cholecystokinin/metabolism ; Cyclic AMP/metabolism ; Enteroendocrine Cells/metabolism ; Gene Expression ; Humans ; Intestinal Mucosa/metabolism ; Ion Channels/metabolism ; Nutritional Physiological Phenomena
Chemical Substances	Ion Channels ; Cholecystokinin (9011-97-6) ; Cyclic AMP (E0399OZS9N) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2010-05-04
Publishing country	Spain
Document type	Journal Article ; Review
ZDB-ID	1325104-1
ISSN	1138-7548 ; 0034-9402
ISSN	1138-7548 ; 0034-9402
DOI	10.1007/s13105-010-0012-z
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Article ; Online: Incretins and bone: evolving concepts in nutrient-dependent regulation of bone turnover.

Yavropoulou, Maria P / Yovos, John G

Hormones (Athens, Greece)

2013 Volume 12, Issue 2, Page(s) 214–223

Abstract: ... from K and L cells of the gastrointestinal tract, respectively, and are considered the main mediators ... and nutrient supply has been extensively studied in the past few years, but the underlying ... Postprandial variation of bone turnover markers and the closed relationship between bone remodeling ...

Abstract	Postprandial variation of bone turnover markers and the closed relationship between bone remodeling and nutrient supply has been extensively studied in the past few years, but the underlying pathophysiologic mechanisms remain largely unknown. Recent studies have shown that the acute regulation of bone turnover induced by feeding is probably mediated by gastrointestinal (GI) peptides. The greater response of bone remodeling during oral versus intravenous glucose administration and the inhibition of this response after administration of octreotide, that inhibits the release of GI peptides, further support the existence of a gutbone axis. Glucose-dependent insulinotropic peptide and glucagon-like peptides-1 and -2 are released from K and L cells of the gastrointestinal tract, respectively, and are considered the main mediators of the postprandial response of bone turnover. In this review we outline the most recent evidence that demonstrates the role of incretins in nutrient-dependent regulation of bone metabolism. Further elucidation of the underlying mechanisms can be exploited therapeutically in the future.
MeSH term(s)	Animals ; Bone Development ; Bone Remodeling ; Bone and Bones/metabolism ; Circadian Rhythm ; Diet/adverse effects ; Enteroendocrine Cells/metabolism ; Gastric Inhibitory Polypeptide/metabolism ; Glucagon-Like Peptide 1/metabolism ; Glucagon-Like Peptide 2/metabolism ; Humans ; Incretins/metabolism ; Intestinal Mucosa/metabolism ; Models, Biological
Chemical Substances	Glucagon-Like Peptide 2 ; Incretins ; Gastric Inhibitory Polypeptide (59392-49-3) ; Glucagon-Like Peptide 1 (89750-14-1)
Language	English
Publishing date	2013-07-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2075912-5
ISSN	2520-8721 ; 1109-3099
ISSN (online)	2520-8721
ISSN	1109-3099
DOI	10.14310/horm.2002.1405
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Article: Molecular mechanisms underlying nutrient detection by incretin-secreting cells.

Reimann, Frank

International dairy journal

2010 Volume 20, Issue 4, Page(s) 236–242

Abstract: ... are secreted postprandially from intestinal K- and L-cells, respectively. As incretins, these hormones ... within K- and L-cells. ... in the control of food intake and lipid metabolism. Whilst the enteroendocrine cells producing GIP and GLP-1 are ...

Abstract	The hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are secreted postprandially from intestinal K- and L-cells, respectively. As incretins, these hormones stimulate insulin secretion from the pancreatic beta-cell, and have independently been implicated in the control of food intake and lipid metabolism. Whilst the enteroendocrine cells producing GIP and GLP-1 are therefore attractive targets for the treatment of diabetes and obesity, our understanding of their physiology is fairly limited. The mechanisms employed to sense the arrival of carbohydrate, fat and protein in the gut lumen have been investigated using organ perfusion techniques, primary epithelial cultures and cell line models. The recent development of mice with fluorescently labeled GIP or GLP-1-expressing cells is now enabling the use of single cell techniques to investigate stimulus-secretion coupling mechanisms. This review will focus on the current knowledge of the molecular machinery underlying nutrient sensing within K- and L-cells.
Language	English
Publishing date	2010-01-27
Publishing country	England
Document type	Journal Article
ZDB-ID	1076400-8
ISSN	0958-6946
ISSN	0958-6946
DOI	10.1016/j.idairyj.2009.11.014
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