The hypothalamus for whole-body physiology: from metabolism to aging

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Abstract

Obesity and aging are two important epidemic factors for metabolic syndrome and many other health issues, which contribute to devastating diseases such as cardiovascular diseases, stroke and cancers. The brain plays a central role in controlling metabolic physiology in that it integrates information from other metabolic organs, sends regulatory projections and orchestrates the whole-body function. Emerging studies suggest that brain dysfunction in sensing various internal cues or processing external cues may have profound effects on metabolic and other physiological functions. This review highlights brain dysfunction linked to genetic mutations, sex, brain inflammation, microbiota, stress as causes for whole-body pathophysiology, arguing brain dysfunction as a root cause for the epidemic of aging and obesity-related disorders. We also speculate key issues that need to be addressed on how to reveal relevant brain dysfunction that underlines the development of these disorders and diseases in order to develop new treatment strategies against these health problems.

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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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Neuroinflammation in Alzheimer's disease.

Michael T Heneka, Monica Carson, Joseph El Khoury … (2015)

Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease. Copyright © 2015 Elsevier Ltd. All rights reserved.

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The Microbiota-Gut-Brain Axis

John F. Cryan, Kenneth J. O'Riordan, Caitlin S M Cowan … (2019)

The importance of the gut-brain axis in maintaining homeostasis has long been appreciated. However, the past 15 yr have seen the emergence of the microbiota (the trillions of microorganisms within and on our bodies) as one of the key regulators of gut-brain function and has led to the appreciation of the importance of a distinct microbiota-gut-brain axis. This axis is gaining ever more traction in fields investigating the biological and physiological basis of psychiatric, neurodevelopmental, age-related, and neurodegenerative disorders. The microbiota and the brain communicate with each other via various routes including the immune system, tryptophan metabolism, the vagus nerve and the enteric nervous system, involving microbial metabolites such as short-chain fatty acids, branched chain amino acids, and peptidoglycans. Many factors can influence microbiota composition in early life, including infection, mode of birth delivery, use of antibiotic medications, the nature of nutritional provision, environmental stressors, and host genetics. At the other extreme of life, microbial diversity diminishes with aging. Stress, in particular, can significantly impact the microbiota-gut-brain axis at all stages of life. Much recent work has implicated the gut microbiota in many conditions including autism, anxiety, obesity, schizophrenia, Parkinson’s disease, and Alzheimer’s disease. Animal models have been paramount in linking the regulation of fundamental neural processes, such as neurogenesis and myelination, to microbiome activation of microglia. Moreover, translational human studies are ongoing and will greatly enhance the field. Future studies will focus on understanding the mechanisms underlying the microbiota-gut-brain axis and attempt to elucidate microbial-based intervention and therapeutic strategies for neuropsychiatric disorders.

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Author and article information

Contributors

Tiemin Liu:

ORCID: http://orcid.org/0000-0003-2077-7653

tiemin_liu@fudan.edu.cn

Qingchun Tong:

ORCID: http://orcid.org/0000-0002-4561-2540

qingchun.tong@uth.tmc.edu

Dongsheng Cai:

ORCID: http://orcid.org/0000-0002-0133-2125

dongsheng.cai@einsteinmed.org

Journal

Journal ID (nlm-ta): Protein Cell

Journal ID (iso-abbrev): Protein Cell

Title: Protein & Cell

Publisher: Higher Education Press (Beijing )

ISSN (Print): 1674-800X

ISSN (Electronic): 1674-8018

Publication date (Electronic): 7 April 2021

Publication date PMC-release: 7 April 2021

Publication date (Print): June 2022

Volume: 13

Issue: 6

Pages: 394-421

Affiliations

[1 ]GRID grid.8547.e, ISNI 0000 0001 0125 2443, State Key Laboratory of Genetic Engineering, Department of Endocrinology and Metabolism, Institute of Metabolism and Integrative Biology, Human Phenome Institute, and Collaborative Innovation Center for Genetics and Development, Zhongshan Hospital, School of Life Sciences, , Fudan University, ; Shanghai, 200438 China

[2 ]GRID grid.39382.33, ISNI 0000 0001 2160 926X, Children’s Nutrition Research Center, Department of Pediatrics, Department of Molecular and Cellular Biology, , Baylor College of Medicine, ; One Baylor Plaza, Houston, TX 77030 USA

[3 ]GRID grid.7177.6, ISNI 0000000084992262, Department of Endocrinology and Metabolism, Amsterdam University Medical Centers, Amsterdam Gastroenterology Endocrinology Metabolism, , University of Amsterdam, ; Meibergdreef 9, 1105AZ Amsterdam, Netherlands

[4 ]GRID grid.453726.1, ISNI 0000 0004 5906 7293, Brown Foundation Institute of Molecular Medicine, Department of Neurobiology and Anatomy, University of Texas McGovern Medical School, , Graduate Program in Neuroscience of MD Anderson UTHealth Graduate School of Biomedical Sciences, ; Houston, TX 77030 USA

[5 ]GRID grid.251993.5, ISNI 0000000121791997, Department of Molecular Pharmacology, , Albert Einstein College of Medicine, ; Bronx, New York, NY 10461 USA

Author information

Tiemin Liu http://orcid.org/0000-0003-2077-7653

Yong Xu http://orcid.org/0000-0002-4908-1572

Chun-Xia Yi http://orcid.org/0000-0003-1184-4615

Qingchun Tong http://orcid.org/0000-0002-4561-2540

Dongsheng Cai http://orcid.org/0000-0002-0133-2125

Article

Publisher ID: 834

DOI: 10.1007/s13238-021-00834-x

PMC ID: 9095790

PubMed ID: 33826123

SO-VID: 353c8555-0616-4706-8564-2ba17348d615

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

History

Date received : 3 December 2020

Date accepted : 1 March 2021

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Keywords: neuron,metabolism,hypothalamus,obesity,aging

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Keywords: neuron, metabolism, hypothalamus, obesity, aging

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The hypothalamus for whole-body physiology: from metabolism to aging

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Most cited references 325

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

Neuroinflammation in Alzheimer's disease.

The Microbiota-Gut-Brain Axis

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