Insulin Resistance and Metabolic Disease: Mitochondria and Beyond

Dear Colleagues,

Tight regulation of core cellular metabolic pathways is essential for tissue homeostasis and resistance to stress. In this regard, mitochondria act as gatekeepers of metabolic homeostasis by integrating lipid, carbohydrate, and amino acids metabolism with energy production. Besides controlling respiration and ATP synthesis, mitochondria are also central regulators of many other cellular functions, such as calcium homeostasis, autophagy, apoptosis, phospholipid synthesis, and senescence. In addition, mitochondria act as hubs integrating responses to cellular stress. Importantly, the aforementioned processes controlled and modulated by mitochondria are altered in metabolic diseases, such as obesity, insulin resistance, and type 2 diabetes. However, the exact mechanisms behind these changes and whether they represent a compensation or a dysfunction are still unclear. Studies performed in humans and animal models have demonstrated a connection between deficient mitochondrial activity in different tissues and the development of metabolic diseases. However, although the implication of mitochondria in these diseases is clear, much less is known about the molecular mechanisms and specific mitochondrial alterations responsible of their development, and the crosstalk between these alterations and other metabolic pathways. Therefore, advances in this knowledge could facilitate the design and development of novel therapeutic tools for the prevention or treatment of these disorders.

In this Special Issue, we invite investigators to contribute original research articles as well as review articles addressing the role of metabolism and mitochondria in different tissues in the development of metabolic diseases. We encourage submissions that elucidate novel molecular mechanisms regarding mitochondria (mitochondrial function, dynamics, and quality), mitochondrial-derived metabolites, and metabolic regulation in mammalian cells, mouse models or humans, and their potential role in the pathogenesis and/or diagnosis of the aforementioned diseases.

Dr. David Sebastián
Dr. Maria Isabel Hernández-Alvarez
Dr. Laura Herrero
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• Mitochondria
• Obesity
• Insulin resistance
• Type 2 diabetes
• Mitophagy
• Mitochondrial metabolites