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      Obesity Reduces Cognitive and Motor Functions across the Lifespan

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          Abstract

          Due to a sedentary lifestyle, more and more people are becoming obese nowadays. In addition to health-related problems, obesity can also impair cognition and motor performance. Previous results have shown that obesity mainly affects cognition and motor behaviors through altering brain functions and musculoskeletal system, respectively. Many factors, such as insulin/leptin dysregulation and inflammation, mediate the effect of obesity and cognition and motor behaviors. Substantial evidence has suggested exercise to be an effective way to improve obesity and related cognitive and motor dysfunctions. This paper aims to discuss the association of obesity with cognition and motor behaviors and its underlying mechanisms. Following this, mechanisms of exercise to improve obesity-related dysfunctions are described. Finally, implications and future research direction are raised.

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          An obesity-associated gut microbiome with increased capacity for energy harvest.

          Peter J Turnbaugh, Ruth E Ley, Michael A Mahowald … (2006)
          The worldwide obesity epidemic is stimulating efforts to identify host and environmental factors that affect energy balance. Comparisons of the distal gut microbiota of genetically obese mice and their lean littermates, as well as those of obese and lean human volunteers have revealed that obesity is associated with changes in the relative abundance of the two dominant bacterial divisions, the Bacteroidetes and the Firmicutes. Here we demonstrate through metagenomic and biochemical analyses that these changes affect the metabolic potential of the mouse gut microbiota. Our results indicate that the obese microbiome has an increased capacity to harvest energy from the diet. Furthermore, this trait is transmissible: colonization of germ-free mice with an 'obese microbiota' results in a significantly greater increase in total body fat than colonization with a 'lean microbiota'. These results identify the gut microbiota as an additional contributing factor to the pathophysiology of obesity.
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            Obesity alters gut microbial ecology.

            Ruth E Ley, Fredrik Bäckhed, Peter James Turnbaugh … (2005)
            We have analyzed 5,088 bacterial 16S rRNA gene sequences from the distal intestinal (cecal) microbiota of genetically obese ob/ob mice, lean ob/+ and wild-type siblings, and their ob/+ mothers, all fed the same polysaccharide-rich diet. Although the majority of mouse gut species are unique, the mouse and human microbiota(s) are similar at the division (superkingdom) level, with Firmicutes and Bacteroidetes dominating. Microbial-community composition is inherited from mothers. However, compared with lean mice and regardless of kinship, ob/ob animals have a 50% reduction in the abundance of Bacteroidetes and a proportional increase in Firmicutes. These changes, which are division-wide, indicate that, in this model, obesity affects the diversity of the gut microbiota and suggest that intentional manipulation of community structure may be useful for regulating energy balance in obese individuals. The sequences reported in this paper have been deposited in the GenBank database [accession nos. DQ 014552--DQ 015671 (mothers) and AY 989911--AY 993908 (offspring)].
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              Host-gut microbiota metabolic interactions.

              Jeremy Nicholson, Elaine Holmes, James Kinross … (2012)
              The composition and activity of the gut microbiota codevelop with the host from birth and is subject to a complex interplay that depends on the host genome, nutrition, and life-style. The gut microbiota is involved in the regulation of multiple host metabolic pathways, giving rise to interactive host-microbiota metabolic, signaling, and immune-inflammatory axes that physiologically connect the gut, liver, muscle, and brain. A deeper understanding of these axes is a prerequisite for optimizing therapeutic strategies to manipulate the gut microbiota to combat disease and improve health.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neural Plast
                Journal ID (iso-abbrev): Neural Plast
                Journal ID (publisher-id): NP
                Title: Neural Plasticity
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-5904
                ISSN (Electronic): 1687-5443
                Publication date (Print): 2016
                Publication date (Electronic): 12 January 2016
                Volume: 2016
                Electronic Location Identifier: 2473081
                Affiliations
                1Department of Neurology, The Affiliated Shenzhen Nanshan Hospital, Shenzhen University, Shenzhen 518000, China
                2Center for Brain Disorders and Cognitive Neuroscience, Shenzhen University, Shenzhen 518060, China
                3Department of Psychology, The Chinese University of Hong Kong, Shatin, Hong Kong
                4Department of Neurology, Shenzhen Second People's Hospital, Shenzhen University, Shenzhen 518035, China
                Author notes

                Academic Editor: Mauricio Arcos-Burgos

                Article
                DOI: 10.1155/2016/2473081
                PMC ID: 4737453
                PubMed ID: 26881095
                SO-VID: 03af7603-653e-4f0d-b29f-bd22441dd297
                Copyright © Copyright © 2016 Chuanming Wang et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 21 July 2015
                Date accepted : 15 October 2015
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Neurosciences
                Data availability:
                ScienceOpen disciplines: Neurosciences

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