The Role of Nutrient Sensors in Energy Metabolism

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (15 April 2022) | Viewed by 6686

Special Issue Editors

1. Department of Cell Biology. Faculty of Medicine.University Complutense of Madrid, 28040 Madrid, Spain
2. Health Research Institute of the Hospital Clínico San Carlos, 28040 Madrid, Spain
Interests: PASK; metabolic sensors; diabetes; obestity; insulin resistance; feeding behaviour; hypothalamus; liver; adipose tissue; glucagon-like peptide 1
1. Department of Physiology. Faculty of Medicine.University Complutense of Madrid, 28040 Madrid, Spain
2. Health Research Institute of the Hospital Clínico San Carlos. 28040 Madrid, Spain
Interests: PASK; Metabolic sensors; Diabetes; Obestity; Insulin resistance; Feeding behaviour; Hypothalamus; Liver; Adipose tissue; Glucagon-like peptide 1

Special Issue Information

Dear Colleagues,

Cell survival depends on meeting the constant challenge of matching energy demands with nutrient availability. Nutrients such as carbohydrates, amino acids, fats, etc. are supplied by food intake, and act as metabolic substrates for energy production and for the synthesis of different macromolecules and cellular components. Accordingly, organisms have developed nutrient-sensing mechanisms to detect levels of specific nutrients to ensure that rates of growth, proliferation, and function coordinate properly and adjust to nutrient availability. Importantly, some of these mechanisms in multicellular organisms have also evolved for regulation by the endocrine system, allowing the coordination of nutrient-sensing activity among different cells/tissues in the body.

Therefore, an efficient and adequate coordination between cellular energy demand and nutrient availability is vital for a healthy physiological response related to the control of food intake, glycemic homeostasis, prevention of insulin resistance or weight gain, etc. However, its alteration triggers pathologies such as obesity, type 2 diabetes, metabolic syndrome, aging-related diseases (e.g., cancer and neurodegeneration) and others.

This Special Issue, "The Role of Nutrient Sensors in Energy Metabolism", focuses especially on the role of nutrient sensors such as PASK, AMPK, mTOR, GLUT2/GK, and others. It focuses on their role in the control of energy homeostasis in health and disease. Topics will include, among others, new findings on how these nutrient sensors control energy homeostasis in the body.

Dr. Carmen Sanz
Dr. Verónica Hurtado-Carneiro
Guest Editors

Manuscript Submission Information

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Keywords

  • PASK
  • nutrients sensing
  • AMPK
  • mTOR
  • energy storage
  • energy expenditure
  • glucose homeostasis

Published Papers (2 papers)

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Review

18 pages, 3786 KiB  
Review
Endosomal v-ATPase as a Sensor Determining Myocardial Substrate Preference
by Shujin Wang, Yinying Han, Miranda Nabben, Dietbert Neumann, Joost J. F. P. Luiken and Jan F. C. Glatz
Metabolites 2022, 12(7), 579; https://0-doi-org.brum.beds.ac.uk/10.3390/metabo12070579 - 22 Jun 2022
Cited by 3 | Viewed by 2549
Abstract
The heart is a metabolically flexible omnivore that can utilize a variety of substrates for energy provision. To fulfill cardiac energy requirements, the healthy adult heart mainly uses long-chain fatty acids and glucose in a balanced manner, but when exposed to physiological or [...] Read more.
The heart is a metabolically flexible omnivore that can utilize a variety of substrates for energy provision. To fulfill cardiac energy requirements, the healthy adult heart mainly uses long-chain fatty acids and glucose in a balanced manner, but when exposed to physiological or pathological stimuli, it can switch its substrate preference to alternative substrates such as amino acids (AAs) and ketone bodies. Using the failing heart as an example, upon stress, the fatty acid/glucose substrate balance is upset, resulting in an over-reliance on either fatty acids or glucose. A chronic fuel shift towards a single type of substrate is linked with cardiac dysfunction. Re-balancing myocardial substrate preference is suggested as an effective strategy to rescue the failing heart. In the last decade, we revealed that vacuolar-type H+-ATPase (v-ATPase) functions as a key regulator of myocardial substrate preference and, therefore, as a novel potential treatment approach for the failing heart. Fatty acids, glucose, and AAs selectively influence the assembly state of v-ATPase resulting in modulation of its proton-pumping activity. In this review, we summarize these novel insights on v-ATPase as an integrator of nutritional information. We also describe its exploitation as a therapeutic target with focus on supplementation of AA as a nutraceutical approach to fight lipid-induced insulin resistance and contractile dysfunction of the heart. Full article
(This article belongs to the Special Issue The Role of Nutrient Sensors in Energy Metabolism)
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15 pages, 1431 KiB  
Review
The Sensory Mechanisms of Nutrient-Induced GLP-1 Secretion
by Anna Pii Hjørne, Ida Marie Modvig and Jens Juul Holst
Metabolites 2022, 12(5), 420; https://0-doi-org.brum.beds.ac.uk/10.3390/metabo12050420 - 07 May 2022
Cited by 15 | Viewed by 3477
Abstract
The enteroendocrine system of the gut regulates energy homeostasis through the release of hormones. Of the gut-derived hormones, GLP-1 is particularly interesting, as analogs of the hormone have proven to be highly effective for the treatment of type 2 diabetes mellitus and obesity. [...] Read more.
The enteroendocrine system of the gut regulates energy homeostasis through the release of hormones. Of the gut-derived hormones, GLP-1 is particularly interesting, as analogs of the hormone have proven to be highly effective for the treatment of type 2 diabetes mellitus and obesity. Observations on increased levels of GLP-1 following gastric bypass surgery have enhanced the interest in endogenous hormone secretion and highlighted the potential of endogenous secretion in therapy. The macronutrients and their digestive products stimulate the secretion of GLP-1 through various mechanisms that we have only begun to understand. From findings obtained from different experimental models, we now have strong indications for a role for both Sodium-Glucose Transporter 1 (SGLT1) and the K+ATP channel in carbohydrate-induced GLP-1 secretion. For fat, the free fatty acid receptor FFA1 and the G-protein-coupled receptor GPR119 have been linked to GLP-1 secretion. For proteins, Peptide Transporter 1 (Pept1) and the Calcium-Sensing Receptor (CaSR) are thought to mediate the secretion. However, attempts at clinical application of these mechanisms have been unsuccessful, and more work is needed before we fully understand the mechanisms of nutrient-induced GLP-1 secretion. Full article
(This article belongs to the Special Issue The Role of Nutrient Sensors in Energy Metabolism)
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