Metabolic Imaging in Obesity

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (15 August 2022) | Viewed by 1714

Special Issue Editor


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Guest Editor
Institute of Clinical Physiology, National Research Council, Via Moruzzi 1, 56124 Pisa, Italy
Interests: imaging; positron emission tomography; obesity; type 2 diabetes; metabolism; fetal programming

Special Issue Information

Dear Colleagues,

Metabolic imaging has disclosed several organ-specific morphological and functional features that associate with obesity and its complications in humans and animal models. However, the common grouping of people based on BMI is distant from the approach required to achieve precision medicine, whose rationale is instead well-suited to the heterogeneity of obesity determinants, phenotypes and health risks. In addition, most studies are descriptive and cross-sectional, with insufficient coverage of mechanistic understanding and cause–effect demonstration.

This special issue of Metabolites, "Metabolic Imaging in Obesity," is aimed to generate a new vision of how metabolic imaging can contribute to the advancement of precision medicine in the field of obesity prevention and treatment, both from a fundamental and an applied point of view. The topics that will be covered by this Special Issue include (but are not limited to): metabolism in relevant organs, life-course changes, organ cross-talk, mechanistic understanding, cause–effect proof, tissue inflammation, biomarker development, personalized treatment, cutting-edge approaches, technology and probes, radiomics, omics, mathematical modeling, metabolic flux analysis, and regulatory science. Manuscripts dealing with other challenging issues are also highly desired.

Prof. Dr. Patricia Iozzo
Guest Editor

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Keywords

  • fatty acids
  • glucose
  • amino acids
  • inflammation
  • cross-talk
  • scanners
  • image (post) processing
  • new probes
  • risk stratification
  • disease models
  • drug/nutrient development
  • lifestyle, age, sex, and gender specificities

Published Papers (1 paper)

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Research

14 pages, 1689 KiB  
Article
Maternal High-Fat Diet Programs White and Brown Adipose Tissues In Vivo in Mice, with Different Metabolic and Microbiota Patterns in Obesity-Susceptible or Obesity-Resistant Offspring
by Maria Angela Guzzardi, Maria Carmen Collado, Daniele Panetta, Maria Tripodi and Patricia Iozzo
Metabolites 2022, 12(9), 828; https://doi.org/10.3390/metabo12090828 - 2 Sep 2022
Cited by 2 | Viewed by 1357
Abstract
Maternal obesity causes metabolic dysfunction in the offspring, including dysbiosis, overeating, obesity, and type 2 diabetes. Early-life phases are fundamental for developing subcutaneous (SAT) and brown adipose tissues (BAT), handling energy excesses. Imaging of 18F-fluorodeoxyglucose by positron emission tomography (PET) and radiodensity [...] Read more.
Maternal obesity causes metabolic dysfunction in the offspring, including dysbiosis, overeating, obesity, and type 2 diabetes. Early-life phases are fundamental for developing subcutaneous (SAT) and brown adipose tissues (BAT), handling energy excesses. Imaging of 18F-fluorodeoxyglucose by positron emission tomography (PET) and radiodensity by computerized tomography (CT) allows assessing adipose tissue (AT) whitening and browning in vivo and the underlying metabolic efficiency. Our aim was to examine these in vivo traits in SAT and BAT concerning gut microbiota composition in 1- and 6-month-old mice born to normal (NDoff) and high-fat diet-fed dams (HFDoff), accounting for body weight responses. We found low radiodensity (high lipids) in HFDoff SAT at 1 month, relating to an increased abundance of Dorea genus in the caecum and activation of the fatty acid biosynthetic pathway. Instead, low BAT radiodensity and glucose uptake were seen in adult HFDoff. Glucose was shifted in favor of BAT at 1 month and SAT at 6 months. In adults, unclassified Enterococcaceae and Rikenellaceae, and Bacillus genera were negatively related to BAT, whereas unclassified Clostridiales genera were related to SAT metabolism. Stratification of HFDoff based on weight-response, namely maternal induced obesity (MIO-HFDoff) or obesity-resistant (MIOR-HFDoff), showed sex dimorphism. Both subgroups were hyperphagic, but only obese mice had hyper-leptinemia and hyper-resistinemia, together with BAT dysfunction, whereas non-obese HFDoff had hyperglycemia and SAT hypermetabolism. In the caecum, unclassified Rikenellaceae (10-fold enrichment in MIO-HFDoff) and Clostridiales genera (4-fold deficiency in MIOR-HFDoff) were important discriminators of these two phenotypes. In conclusion, SAT whitening is an early abnormality in the offspring of HFD dams. In adult life, maternal HFD and the induced excessive food intake translates into a dimorphic phenotype involving SAT, BAT, and microbiota distinctively, reflecting maternal diet*sex interaction. This helps explain inter-individual variability in fetal programming and the higher rates of type 2 diabetes observed in adult women born to obese mothers, supporting personalized risk assessment, prevention, and treatment. Full article
(This article belongs to the Special Issue Metabolic Imaging in Obesity)
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