Diet induced obesity is independent of metabolic endotoxemia and TLR4 signalling, but markedly increases hypothalamic expression of the acute phase protein, SerpinA3N

• Published in: Scientific reports Vol. 8; no. 1; pp. 15648 - 15
• Main Authors: Dalby, Matthew J., Aviello, Gabriella, Ross, Alexander W., Walker, Alan W., Barrett, Perry, Morgan, Peter J.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 23.10.2018; Nature Publishing Group
• Subjects: 13/51; 14/63; 38; 38/32; 38/39; 38/70; 38/77; 631/326/2565/2134; 631/378/1488/393; 64/60; Acute phase proteins; Acute-Phase Proteins - genetics; Adipose tissue; Animals; Body weight; Body weight gain; CD14 antigen; Diet; Diet, High-Fat - adverse effects; Endotoxemia; Endotoxemia - complications; Endotoxemia - genetics; Endotoxemia - immunology; Endotoxemia - pathology; Gastrointestinal Microbiome; Gene Expression Regulation; Genotype; High fat diet; Humanities and Social Sciences; Hybridization; Hypothalamus; Hypothalamus - immunology; Hypothalamus - pathology; Inflammation; Intestinal microflora; Lipopolysaccharides; Male; Metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; Microbiota; multidisciplinary; Obesity; Obesity - etiology; Obesity - genetics; Obesity - immunology; Obesity - pathology; Proteins; Science; Science (multidisciplinary); Serpins - genetics; Signal Transduction; TLR4 protein; Toll-Like Receptor 4 - genetics; Toll-Like Receptor 4 - immunology; Toll-like receptors; Up-Regulation; Metabolic Endotoxemia; Caecal Microbiota; Hypothalamic Inflammation; Microbiota Composition; Arcuate Nucleus

Hypothalamic inflammation is thought to contribute to obesity. One potential mechanism is via gut microbiota derived bacterial lipopolysaccharide (LPS) entering into the circulation and activation of Toll-like receptor-4. This is called metabolic endotoxemia. Another potential mechanism is systemic...