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Table of contents
INTRODUCTION
I-Structures and functions of the gastrointestinal tract
I-1 Structures of the intestinal epithelium
I-2 Cell populations of the intestinal epithelium
I-3 Intestinal epithelium renewal
II-Gut microbiota
II-1 General overview of the gut microbiota composition
II-2 The functions of the gut microbiota
II-3 The stability and dietary-dependent alterations of the microbiota composition .
II-4 The microbial metabolites and components
II-4.1 Short-chain fatty acids
II-4.2 Bile acids
II-4.3 Tryptophan metabolites
II-4.4 Lipopolysaccharides
II-5 The role of gut microbiota in metabolic diseases
III- Enteroendocrine functions of the gastrointestinal tract
III-1 The classification of enteroendocrine cells: from the old to a new dogma
III-2 Gut hormonal signaling pathways
III-3 The regulation of enterohormone secretion
III-3.1 The impact of fructose on the secretion of gut enterohormones
III-3.1.1 The intestinal endocrine response to acute fructose exposure
III-3.1.2 The intestinal endocrine response to chronic fructose exposure.
III-3.1.3 The potential sensor of fructose in enteroendocrine cells
III-3.2 The impact of change in the nutrient flow on enterohormone expression
III-3.3 The role of the gut microbiota and its metabolites on the regulation of enteroendocrine cells
III-4 Cholecystokinin: its regulation and main function
III-4.1 Transcript structure and derived molecular forms of cholecystokinin
III-4.2 Stimulation of cholecystokinin secretion
III-4.2.1 The fatty acids
III-4.2.2 Protein hydrolysates and amino acids
III-4.2.3 Sweet and Bitter stimuli
III-4.2.4 Non-nutrient stimuli
III-4.3 Physiological effects of cholecystokinin
III-4.3.1 Food intake
III-4.3.2 Pancreatic secretion, gut motility and gallbladder contraction
III-4.3.3 Pain
III-4.3.4 The central action of cholecystokinin on various behavior processes .
III-5 Regulation of the other gut peptides: Peptide YY, glucagon-like peptide-1, and neurotensin
III-5.1 Peptide YY
III-5.2 Glucagon-like peptide-1
III-5.3 Neurotensin
IV- Gut permeability and its major role in metabolic disorders
IV-1 Gut permeability: definition and main components
IV-1.1 Transcellular permeability
IV-1.2 Paracellular permeability
IV-1.2.1 Tight junction proteins
IV-1.2.1.1 The claudin family
IV-1.2.1.2 Occludin
IV-1.2.1.3 The family of junctional adhesion molecules
IV-1.2.1.4 The family of zonula occludens
IV-1.2.2 The regulation of paracellular permeability
IV-2 The measurement of gut permeability
IV-2.1 In vivo permeability assays
IV-2.2 Ex vivo Ussing chamber system
IV-2.3 In vitro permeability measurements
IV-3 The effect of nutrients on gut permeability
IV-3.1 Lipids and chronic exposure to a high-fat diet
IV-3.2 Sugars
V-Enteric nervous system
V-1 The basic structure and functions of enteric nervous system
V-2 The regulation of enteric nervous system on intestinal barrier function
V-3 The inflammation induced modification in enteric nervous system
V-4 The effects of gut microbiota on enteric nervous system
V-5 The function of enteric nervous system in nutrients sensing
VI- Fructose consumption, transport and metabolism – health consequences of its excessive consumption
VI-1 The pattern of fructose consumption
VI-2 Intestinal transport of fructose
VI-2.1 The main intestinal fructose transporters GLUT5 and GLUT2
VI-2.2 Other potential transporters
VI-2.3 The regulation of GLUT5 in intestinal tissue
VI-2.4 Developmental Regulation of GLUT5
VI-2.5 The regulation of GLUT5 by luminal fructose
VI-3 Ketohexokinase: the key enzyme in fructose metabolism
VI-4 Health outcome of excessive fructose intake
VI-4.1 Liver: the central target
VI-4.2 Fructose intake and functional alteration of other organs
VI-5 Fructose malabsorption
OBJECTIVES
RESULTS
Fructose malabsorption – Ketohexokinase knockout mice model
Article1: Fructose malabsorption modifies the endocrine response of the lower intestine by Modulating microbiota composition and metabolism
Additional Results for Article 1
Article2: Glucose but not fructose alters the intestinal paracellular permeability in association with inflammation in mice and Caco-2 cells
GENERAL DISCUSSION AND PERSPECTIVES
I-The potential physiological consequence of the increase in CCK in the lower intestine
II-The potential link between the increase in intestinal CCK and the symptoms associated with fructose malabsorption
III-Nature of the stimuli able to activate CCK in the lower intestine
IV-The role of the fructose-induced changes in the microbiota composition in the alteration of gastrointestinal endocrine and barrier functions
V-Impact of fructose on intestinal permeability in normo- and mal-absorptive fructose conditions
GENERAL CONCLUSION
BIBLIOGRAPHY
