Special Issue "Metabolomic Studies in Metabolic Diseases"

A special issue of Metabolites (ISSN 2218-1989).

Deadline for manuscript submissions: closed (30 March 2017)

Special Issue Editor

Guest Editor
Prof. Dr. Peter Meikle

Metabolomics Laboratory NHMRC, Baker Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia
Website | E-Mail
Interests: dyslipidemia associated with obesity, diabetes and cardiovascular disease and its relationship to the pathogenesis of these disease states; application of lipidomics to the early diagnosis, risk assessment and therapeutic monitoring of these most prevalent diseases

Special Issue Information

Dear Colleagues,

Obesity, diabetes and cardiovascular disease are part of a disease continuum involving metabolic dysregulation. These metabolic diseases represent a growing health burden on most countries and are the focus of much research. Metabolomic studies have the potential to inform on the altered metabolism preceding, or resulting from, these chronic diseases. Such studies can provide insight into the pathogenesis of disease, identify new biomarkers for disease risk stratification and/or new therapeutic targets. Here we call for manuscripts addressing all aspects of metabolomic studies into these chronic metabolic diseases.

Dr. Peter Meikle
Guest Editor

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 papers will be 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 quarterly 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 850 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.

Keywords

  • obesity
  • metabolic syndrome
  • insulin resistance
  • type 2 diabetes
  • cardiovascular disease

Published Papers (4 papers)

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Research

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Open AccessArticle Effects of Obesity on Pro-Oxidative Conditions and DNA Damage in Liver of DMBA-Induced Mammary Carcinogenesis Models
Metabolites 2017, 7(2), 26; https://doi.org/10.3390/metabo7020026
Received: 8 May 2017 / Revised: 31 May 2017 / Accepted: 5 June 2017 / Published: 8 June 2017
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Abstract
The prevalence of the overweight and obesity is on the rise worldwide. Obesity can increase the risk of certain cancers and liver steatosis development. Previously, we reported that obesity increased liver steatosis in a mammary tumor model, but little is known about the
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The prevalence of the overweight and obesity is on the rise worldwide. Obesity can increase the risk of certain cancers and liver steatosis development. Previously, we reported that obesity increased liver steatosis in a mammary tumor model, but little is known about the effects of obesity in the liver in regard to global DNA methylation, DNA damage, and oxidative/nitrosative stress. Using a mammary tumor model, we investigated the effects of obesity on oxidative stress and DNA reaction. Five-week-old lean and obese female rats were used. At 50 days of age, all rats received 7,12-dimethylbenz(α)anthracene (DMBA) and were sacrificed 155 days later. HPLC with electrochemical and ultraviolet detection and LC-MS were used. Obesity caused higher (p < 0.0004) methionine levels, had no effect (p < 0.055) on SAM levels, caused lower (p < 0.0005) SAH levels, caused higher (p < 0.0005) SAM/SAH ratios, and increased (p < 0.02) global DNA methylation. Levels of free reduced GSH were not significantly lower (p < 0.08), but free oxidized GSSG was higher (p < 0.002) in obese rats. The GSH/GSSG ratio was lower (p < 0.0001), and oxidized guanosine was higher (p < 0.002) in DNA of obese rats compared to lean rats. Obesity caused significant oxidative/nitrosative stress, oxidative DNA damage, and change of DNA methylation pattern in the liver, and these changes may contribute to the development of liver steatosis in breast cancer models. Full article
(This article belongs to the Special Issue Metabolomic Studies in Metabolic Diseases)
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Review

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Open AccessReview Lysophosphatidylinositol Signalling and Metabolic Diseases
Metabolites 2016, 6(1), 6; https://doi.org/10.3390/metabo6010006
Received: 11 December 2015 / Revised: 7 January 2016 / Accepted: 11 January 2016 / Published: 15 January 2016
Cited by 4 | PDF Full-text (580 KB) | HTML Full-text | XML Full-text
Abstract
Metabolism is a chemical process used by cells to transform food-derived nutrients, such as proteins, carbohydrates and fats, into chemical and thermal energy. Whenever an alteration of this process occurs, the chemical balance within the cells is impaired and this can affect their
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Metabolism is a chemical process used by cells to transform food-derived nutrients, such as proteins, carbohydrates and fats, into chemical and thermal energy. Whenever an alteration of this process occurs, the chemical balance within the cells is impaired and this can affect their growth and response to the environment, leading to the development of a metabolic disease. Metabolic syndrome, a cluster of several metabolic risk factors such as abdominal obesity, insulin resistance, high cholesterol and high blood pressure, and atherogenic dyslipidaemia, is increasingly common in modern society. Metabolic syndrome, as well as other diseases, such as diabetes, obesity, hyperlipidaemia and hypertension, are associated with abnormal lipid metabolism. Cellular lipids are the major component of cell membranes; they represent also a valuable source of energy and therefore play a crucial role for both cellular and physiological energy homeostasis. In this review, we will focus on the physiological and pathophysiological roles of the lysophospholipid mediator lysophosphatidylinositol (LPI) and its receptor G-protein coupled receptor 55 (GPR55) in metabolic diseases. LPI is a bioactive lipid generated by phospholipase A (PLA) family of lipases which is believed to play an important role in several diseases. Indeed LPI can affect various functions such as cell growth, differentiation and motility in a number of cell-types. Recently published data suggest that LPI plays an important role in different physiological and pathological contexts, including a role in metabolism and glucose homeostasis. Full article
(This article belongs to the Special Issue Metabolomic Studies in Metabolic Diseases)
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Open AccessFeature PaperReview Bioactive Plant Metabolites in the Management of Non-Communicable Metabolic Diseases: Looking at Opportunities beyond the Horizon
Metabolites 2015, 5(4), 733-765; https://doi.org/10.3390/metabo5040733
Received: 8 October 2015 / Revised: 2 December 2015 / Accepted: 9 December 2015 / Published: 12 December 2015
Cited by 6 | PDF Full-text (427 KB) | HTML Full-text | XML Full-text
Abstract
There has been an unprecedented worldwide rise in non-communicable metabolic diseases (NCDs), particularly cardiovascular diseases (CVD) and diabetes. While modern pharmacotherapy has decreased the mortality in the existing population, it has failed to stem the rise. Furthermore, a large segment of the world
[...] Read more.
There has been an unprecedented worldwide rise in non-communicable metabolic diseases (NCDs), particularly cardiovascular diseases (CVD) and diabetes. While modern pharmacotherapy has decreased the mortality in the existing population, it has failed to stem the rise. Furthermore, a large segment of the world population cannot afford expensive pharmacotherapy. Therefore, there is an urgent need for inexpensive preventive measures to control the rise in CVD and diabetes and associated co-morbidities. The purpose of this review is to explore the role of food bioactives in prevention of NCDs. To this end, we have critically analyzed the possible utility of three classes of food bioactives: (a) resistant starch, a metabolically resistant carbohydrate known to favorably modulate insulin secretion and glucose metabolism; (b) cyclo (His-Pro), a food-derived cyclic dipeptides; and (c) polyphenol-rich berries. Finally, we have also briefly outlined the strategies needed to prepare these food-bioactives for human use. Full article
(This article belongs to the Special Issue Metabolomic Studies in Metabolic Diseases)
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Open AccessReview Obesity-Related Chronic Kidney Disease—The Role of Lipid Metabolism
Metabolites 2015, 5(4), 720-732; https://doi.org/10.3390/metabo5040720
Received: 3 November 2015 / Revised: 1 December 2015 / Accepted: 8 December 2015 / Published: 11 December 2015
Cited by 19 | PDF Full-text (803 KB) | HTML Full-text | XML Full-text
Abstract
Obesity is an independent risk factor for chronic kidney disease (CKD). The mechanisms linking obesity and CKD include systemic changes such as high blood pressure and hyperglycemia, and intrarenal effects relating to lipid accumulation. Normal lipid metabolism is integral to renal physiology and
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Obesity is an independent risk factor for chronic kidney disease (CKD). The mechanisms linking obesity and CKD include systemic changes such as high blood pressure and hyperglycemia, and intrarenal effects relating to lipid accumulation. Normal lipid metabolism is integral to renal physiology and disturbances of renal lipid and energy metabolism are increasingly being linked with kidney disease. AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) are important regulators of fatty acid oxidation, which is frequently abnormal in the kidney with CKD. A high fat diet reduces renal AMPK activity, thereby contributing to reduced fatty acid oxidation and energy imbalance, and treatments to activate AMPK are beneficial in animal models of obesity-related CKD. Studies have found that the specific cell types affected by excessive lipid accumulation are proximal tubular cells, podocytes, and mesangial cells. Targeting disturbances of renal energy metabolism is a promising approach to addressing the current epidemic of obesity-related kidney disease. Full article
(This article belongs to the Special Issue Metabolomic Studies in Metabolic Diseases)
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