Obesity associates with mood and anxiety disorders, cognitive dysfunction, and motor decline, whose major causes are puzzling, since obesogenic mechanisms are complex, including a marked intestinal dysbiosis and a sustained metabolic syndrome encompassing hyperglycemia, hyperinsulinemia, systemic inflammation and oxidative stress in both humans and animal models. We addressed whether the changes occurring in mood, cognitive and motor function in diet-induced pre-obese mice are linked to intestinal dysbiosis and body weight gain. Male and female Swiss mice were made pre-obese by feeding with a reinforced high-fat diet for 7 weeks, along which body weight and food intake were monitored. Then, holeboard, stress-induced hyperthermia, footprint, and vertical pole tests were performed to assess cognitive and motor functions. Animals were sacrificed and intestinal dysbiosis assessed: (i) by determining fecal pH and gram positive bacteria counts; (ii) by assessing bacterial infiltration to the jejunum using tissue gram stain; and (iii) by assessing jejunal tissue histopathological changes (H&E) and the immunohistochemical expression of the sustained inflammation marker CXCL10. Average increases in body weight were observed in males (37%) and females (49%), as well as increases in fecal pH, gram positive counts, bacterial infiltration and CXCL10 expression, particularly marked in females. For both sexes, HFD-fed animals with more marked changes in indicators of intestinal dysbiosis also gained weight faster and displayed more marked mood, cognitive and motor alterations. These results suggest that intestinal dysbiosis is a major driver of obesity-like cognitive and motor alterations in pre-obese mice.
Published in | Journal of Diseases and Medicinal Plants (Volume 2, Issue 3) |
DOI | 10.11648/j.jdmp.20160203.12 |
Page(s) | 26-42 |
Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
Copyright |
Copyright © The Author(s), 2016. Published by Science Publishing Group |
High-Fat Diet, Pre-obesity, Metabolic Syndrome, Gut Bacteria, Small Intestinal Bacterial Overgrowth, Central Nervous System Functional Alteration
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APA Style
Paul F. Seke Etet, Fayez K. Alharbi, Sayed Y. Osman, Rejo Jacob Joseph, Yahia M. Bushara, et al. (2016). Gut Dysbiosis Clinical Indicators Associate with Body Weight Gain and Cognitive Dysfunction in High-Fat Diet-Induced Pre-obese Mice. Journal of Diseases and Medicinal Plants, 2(3), 26-42. https://doi.org/10.11648/j.jdmp.20160203.12
ACS Style
Paul F. Seke Etet; Fayez K. Alharbi; Sayed Y. Osman; Rejo Jacob Joseph; Yahia M. Bushara, et al. Gut Dysbiosis Clinical Indicators Associate with Body Weight Gain and Cognitive Dysfunction in High-Fat Diet-Induced Pre-obese Mice. J. Dis. Med. Plants 2016, 2(3), 26-42. doi: 10.11648/j.jdmp.20160203.12
AMA Style
Paul F. Seke Etet, Fayez K. Alharbi, Sayed Y. Osman, Rejo Jacob Joseph, Yahia M. Bushara, et al. Gut Dysbiosis Clinical Indicators Associate with Body Weight Gain and Cognitive Dysfunction in High-Fat Diet-Induced Pre-obese Mice. J Dis Med Plants. 2016;2(3):26-42. doi: 10.11648/j.jdmp.20160203.12
@article{10.11648/j.jdmp.20160203.12, author = {Paul F. Seke Etet and Fayez K. Alharbi and Sayed Y. Osman and Rejo Jacob Joseph and Yahia M. Bushara and Lorella Vecchio and John C. Chijuka and Shama I. Y. Adam and Elhassan M. A. Saeed and Mohammed Farahna}, title = {Gut Dysbiosis Clinical Indicators Associate with Body Weight Gain and Cognitive Dysfunction in High-Fat Diet-Induced Pre-obese Mice}, journal = {Journal of Diseases and Medicinal Plants}, volume = {2}, number = {3}, pages = {26-42}, doi = {10.11648/j.jdmp.20160203.12}, url = {https://doi.org/10.11648/j.jdmp.20160203.12}, eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.jdmp.20160203.12}, abstract = {Obesity associates with mood and anxiety disorders, cognitive dysfunction, and motor decline, whose major causes are puzzling, since obesogenic mechanisms are complex, including a marked intestinal dysbiosis and a sustained metabolic syndrome encompassing hyperglycemia, hyperinsulinemia, systemic inflammation and oxidative stress in both humans and animal models. We addressed whether the changes occurring in mood, cognitive and motor function in diet-induced pre-obese mice are linked to intestinal dysbiosis and body weight gain. Male and female Swiss mice were made pre-obese by feeding with a reinforced high-fat diet for 7 weeks, along which body weight and food intake were monitored. Then, holeboard, stress-induced hyperthermia, footprint, and vertical pole tests were performed to assess cognitive and motor functions. Animals were sacrificed and intestinal dysbiosis assessed: (i) by determining fecal pH and gram positive bacteria counts; (ii) by assessing bacterial infiltration to the jejunum using tissue gram stain; and (iii) by assessing jejunal tissue histopathological changes (H&E) and the immunohistochemical expression of the sustained inflammation marker CXCL10. Average increases in body weight were observed in males (37%) and females (49%), as well as increases in fecal pH, gram positive counts, bacterial infiltration and CXCL10 expression, particularly marked in females. For both sexes, HFD-fed animals with more marked changes in indicators of intestinal dysbiosis also gained weight faster and displayed more marked mood, cognitive and motor alterations. These results suggest that intestinal dysbiosis is a major driver of obesity-like cognitive and motor alterations in pre-obese mice.}, year = {2016} }
TY - JOUR T1 - Gut Dysbiosis Clinical Indicators Associate with Body Weight Gain and Cognitive Dysfunction in High-Fat Diet-Induced Pre-obese Mice AU - Paul F. Seke Etet AU - Fayez K. Alharbi AU - Sayed Y. Osman AU - Rejo Jacob Joseph AU - Yahia M. Bushara AU - Lorella Vecchio AU - John C. Chijuka AU - Shama I. Y. Adam AU - Elhassan M. A. Saeed AU - Mohammed Farahna Y1 - 2016/06/16 PY - 2016 N1 - https://doi.org/10.11648/j.jdmp.20160203.12 DO - 10.11648/j.jdmp.20160203.12 T2 - Journal of Diseases and Medicinal Plants JF - Journal of Diseases and Medicinal Plants JO - Journal of Diseases and Medicinal Plants SP - 26 EP - 42 PB - Science Publishing Group SN - 2469-8210 UR - https://doi.org/10.11648/j.jdmp.20160203.12 AB - Obesity associates with mood and anxiety disorders, cognitive dysfunction, and motor decline, whose major causes are puzzling, since obesogenic mechanisms are complex, including a marked intestinal dysbiosis and a sustained metabolic syndrome encompassing hyperglycemia, hyperinsulinemia, systemic inflammation and oxidative stress in both humans and animal models. We addressed whether the changes occurring in mood, cognitive and motor function in diet-induced pre-obese mice are linked to intestinal dysbiosis and body weight gain. Male and female Swiss mice were made pre-obese by feeding with a reinforced high-fat diet for 7 weeks, along which body weight and food intake were monitored. Then, holeboard, stress-induced hyperthermia, footprint, and vertical pole tests were performed to assess cognitive and motor functions. Animals were sacrificed and intestinal dysbiosis assessed: (i) by determining fecal pH and gram positive bacteria counts; (ii) by assessing bacterial infiltration to the jejunum using tissue gram stain; and (iii) by assessing jejunal tissue histopathological changes (H&E) and the immunohistochemical expression of the sustained inflammation marker CXCL10. Average increases in body weight were observed in males (37%) and females (49%), as well as increases in fecal pH, gram positive counts, bacterial infiltration and CXCL10 expression, particularly marked in females. For both sexes, HFD-fed animals with more marked changes in indicators of intestinal dysbiosis also gained weight faster and displayed more marked mood, cognitive and motor alterations. These results suggest that intestinal dysbiosis is a major driver of obesity-like cognitive and motor alterations in pre-obese mice. VL - 2 IS - 3 ER -