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Biology
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Mitochondrial Homeostasis in Obesity
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Mitochondrial Homeostasis in Obesity

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 21521

Special Issue Editors

Prof. Dr. Katharina Timper

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Guest Editor
Obesity Research, Department of Biomedicine Basel, University Basel and University Hospital Basel, Hebelstrasse 20, 4031 Basel, Switzerland
Interests: central control of metabolism; obesity; mitochondrial homeostasis and integrity; lipid metabolism
Dr. Alexander Jais

E-Mail Website
Guest Editor
Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG) of the Helmholtz Zentrum München at the University of Leipzig and University Hospital Leipzig, Philipp-Rosenthal-Str. 27, 04103 Leipzig, Germany
Interests: obesity; energy homeostasis; immunometabolism; central control of metabolism

Special Issue Information

Dear Colleagues,

Accumulating evidence is highlighting the important role of mitochondrial homeostasis and integrity in the physiological regulation of energy homeostasis and indicating their critical role in the development of obesity and associated diseases such as type 2 diabetes mellitus, cardiovascular disease, and cancer. Over the last few decades, major advances have been made in the understanding of how mitochondria not only direct cellular but whole-body energy metabolism at various organ levels. While altered mitochondrial function was initially considered solely a result of obesity, major advances during the last few years have uncovered numerous mechanisms of how alterations in mitochondrial function not only promote but also prevent and balance metabolic deteriorations in the obese state. Thus, regulators of mitochondrial homeostasis and integrity have evolved as promising novel targets for the treatment of obesity and associated metabolic diseases.

With this Special Issue, we aim to integrate novel findings on the role of mitochondrial function and dysfunction in obesity development and prevention overall, highlighting the crucial role of mitochondria as integrative homeostastic regulators of whole-body energy homeostasis.

Prof. Dr. Katharina Timper
Dr. Alexander Jais
Guest Editors

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Keywords

  • mitochondria
  • energy homeostasis
  • obesity
  • metabolism

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Published Papers (4 papers)

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Review

18 pages, 941 KiB  
Review
Cardiolipin Alterations during Obesity: Exploring Therapeutic Opportunities
by Alexandre Prola and Fanny Pilot-Storck
Biology 2022, 11(11), 1638; https://doi.org/10.3390/biology11111638 - 9 Nov 2022
Cited by 6 | Viewed by 3010
Abstract
Cardiolipin is a specific phospholipid of the mitochondrial inner membrane that participates in many aspects of its organization and function, hence promoting proper mitochondrial ATP production. Here, we review recent data that have investigated alterations of cardiolipin in different tissues in the context [...] Read more.
Cardiolipin is a specific phospholipid of the mitochondrial inner membrane that participates in many aspects of its organization and function, hence promoting proper mitochondrial ATP production. Here, we review recent data that have investigated alterations of cardiolipin in different tissues in the context of obesity and the related metabolic syndrome. Data relating perturbations of cardiolipin content or composition are accumulating and suggest their involvement in mitochondrial dysfunction in tissues from obese patients. Conversely, cardiolipin modulation is a promising field of investigation in a search for strategies for obesity management. Several ways to restore cardiolipin content, composition or integrity are emerging and may contribute to the improvement of mitochondrial function in tissues facing excessive fat storage. Inversely, reduction of mitochondrial efficiency in a controlled way may increase energy expenditure and help fight against obesity and in this perspective, several options aim at targeting cardiolipin to achieve a mild reduction of mitochondrial coupling. Far from being just a victim of the deleterious consequences of obesity, cardiolipin may ultimately prove to be a possible weapon to fight against obesity in the future. Full article
(This article belongs to the Special Issue Mitochondrial Homeostasis in Obesity)
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17 pages, 2742 KiB  
Review
Is Brain-Derived Neurotrophic Factor a Metabolic Hormone in Peripheral Tissues?
by Elsie Chit Yu Iu and Chi Bun Chan
Biology 2022, 11(7), 1063; https://doi.org/10.3390/biology11071063 - 17 Jul 2022
Cited by 17 | Viewed by 7318
Abstract
Brain-derived neurotrophic factor (BDNF) is an important growth factor in the central nervous system. In addition to its well-known activities in promoting neuronal survival, neuron differentiation, and synaptic plasticity, neuronal BDNF also regulates energy homeostasis by modulating the hypothalamus’s hormonal signals. In the [...] Read more.
Brain-derived neurotrophic factor (BDNF) is an important growth factor in the central nervous system. In addition to its well-known activities in promoting neuronal survival, neuron differentiation, and synaptic plasticity, neuronal BDNF also regulates energy homeostasis by modulating the hypothalamus’s hormonal signals. In the past decades, several peripheral tissues, including liver, skeletal muscle, and white adipose tissue, were demonstrated as the active sources of BDNF synthesis in response to different metabolic challenges. Nevertheless, the functions of BDNF in these tissues remain obscure. With the use of tissue-specific Bdnf knockout animals and the availability of non-peptidyl BDNF mimetic, increasing evidence has reported that peripheral tissues-derived BDNF might play a significant role in maintaining systemic metabolism, possibly through the regulation of mitochondrial dynamics in the various tissues. This article reviews the autocrine/paracrine/endocrine functions of BDNF in non-neuronal tissues and discusses the unresolved questions about BDNF’s function. Full article
(This article belongs to the Special Issue Mitochondrial Homeostasis in Obesity)
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34 pages, 1413 KiB  
Review
Insulin and Its Key Role for Mitochondrial Function/Dysfunction and Quality Control: A Shared Link between Dysmetabolism and Neurodegeneration
by Giacoma Galizzi and Marta Di Carlo
Biology 2022, 11(6), 943; https://doi.org/10.3390/biology11060943 - 20 Jun 2022
Cited by 25 | Viewed by 5629
Abstract
Insulin was discovered and isolated from the beta cells of pancreatic islets of dogs and is associated with the regulation of peripheral glucose homeostasis. Insulin produced in the brain is related to synaptic plasticity and memory. Defective insulin signaling plays a role in [...] Read more.
Insulin was discovered and isolated from the beta cells of pancreatic islets of dogs and is associated with the regulation of peripheral glucose homeostasis. Insulin produced in the brain is related to synaptic plasticity and memory. Defective insulin signaling plays a role in brain dysfunction, such as neurodegenerative disease. Growing evidence suggests a link between metabolic disorders, such as diabetes and obesity, and neurodegenerative diseases, especially Alzheimer’s disease (AD). This association is due to a common state of insulin resistance (IR) and mitochondrial dysfunction. This review takes a journey into the past to summarize what was known about the physiological and pathological role of insulin in peripheral tissues and the brain. Then, it will land in the present to analyze the insulin role on mitochondrial health and the effects on insulin resistance and neurodegenerative diseases that are IR-dependent. Specifically, we will focus our attention on the quality control of mitochondria (MQC), such as mitochondrial dynamics, mitochondrial biogenesis, and selective autophagy (mitophagy), in healthy and altered cases. Finally, this review will be projected toward the future by examining the most promising treatments that target the mitochondria to cure neurodegenerative diseases associated with metabolic disorders. Full article
(This article belongs to the Special Issue Mitochondrial Homeostasis in Obesity)
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Graphical abstract

15 pages, 1079 KiB  
Review
How Do Hexokinases Inhibit Receptor-Mediated Apoptosis?
by Axel Schoeniger, Philipp Wolf and Frank Edlich
Biology 2022, 11(3), 412; https://doi.org/10.3390/biology11030412 - 8 Mar 2022
Cited by 11 | Viewed by 4977
Abstract
The regulated cell death apoptosis enables redundant or compromised cells in ontogeny and homeostasis to remove themselves receptor-dependent after extrinsic signaling or after internal stress by BCL-2 proteins on the outer mitochondrial membrane (OMM). Mitochondrial BCL-2 proteins are also often needed for receptor-mediated [...] Read more.
The regulated cell death apoptosis enables redundant or compromised cells in ontogeny and homeostasis to remove themselves receptor-dependent after extrinsic signaling or after internal stress by BCL-2 proteins on the outer mitochondrial membrane (OMM). Mitochondrial BCL-2 proteins are also often needed for receptor-mediated signaling in apoptosis. Then, the truncated BH3-only protein BID (tBID) blocks retrotranslocation of the pro-apoptotic BCL-2 proteins BAX and BAK from the mitochondria into the cytosol. BAX and BAK in turn permeabilize the OMM. Although the BCL-2 proteins are controlled by a complex regulatory network, a specific mechanism for the inhibition of tBID remained unknown. Curiously, it was suggested that hexokinases, which channel glucose into the metabolism, have an intriguing function in the regulation of apoptosis. Recent analysis of transient hexokinase interactions with BAX revealed its participation in the inhibition of BAX and also BAK by retrotranslocation from mitochondria to the cytosol. In contrast to general apoptosis inhibition by anti-apoptotic BCL-2 proteins, hexokinase I and hexokinase 2 specifically inhibit tBID and thus the mitochondrial apoptosis pathway in response to death receptor signaling. Mitochondrial hexokinase localization and BH3 binding of cytosolic hexokinase domains are prerequisites for protection against receptor-mediated cell death, whereas glucose metabolism is not. This mechanism protects cells from apoptosis induced by cytotoxic T cells. Full article
(This article belongs to the Special Issue Mitochondrial Homeostasis in Obesity)
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